gastrins and Gastritis

Gastric cancer, a disease with a reduced frequency for decades, now appears to be on the rise again in young Americans. The epidemiology of gastric cancer differs between tumors in the cardia and those of the more distal parts of the stomach. The tumors are divided into the intestinal type showing glandular growth pattern and the diffuse type with a different pattern. The latter often expresses neuroendocrine and more specifically ECL-cell markers suggesting that they originate from the ECL cell, the target cell for the antral hormone, gastrin. Helicobacter pylori gastritis is accepted as the major cause of gastric cancer, but only after having induced oxyntic atrophy which reduces gastric acid secretion and thus induces hypoacidity leading to hypergastrinemia. Long-term hypergastrinemia is known to induce malignant neoplasia in the stomach of animals as well as man. Recently treatment with proton pump inhibitor after Helicobacter pylori eradication in patients with gastroesophageal reflux disease, has been reported to predispose to gastric cancer. Since profound acid inhibition is a well-known cause of gastric neoplasia, it is to be expected that Helicobacter pylori infection and profound acid inhibition has an additive or possibly potentiating effect on the development of gastric cancer.

Topics: Animals; Enterochromaffin-like Cells; Gastrins; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Proton Pump Inhibitors; Stomach Neoplasms

Gastrin acts physiologically as a gut hormone to stimulate acid secretion after meal and as a cell-growth factor of oxyntic mucosa. Increase in serum gastrin level happens under various conditions including Zollinger-Ellison syndrome, antral G cell hyperplasia, autoimmune gastritis, atrophic gastritis, renal failure, vagotomy, Helicobacter pylori infection and acid suppressive therapy. As acid suppressive therapy causes hypergastrinemia, the association between acid suppressive therapy and gastric neuroendocrine cell tumor (NET) has been discussed during the past 30 years. In this review article, the definition of hypergastrinemia and the related disorders including acid suppressive therapy and gastric NET are discussed.

Topics: Carcinogenesis; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Neuroendocrine Tumors; Proton Pump Inhibitors; Stomach Neoplasms

Gastric cancer occurs almost exclusively in patients with gastritis. Since Helicobacter pylori (Hp) was proved to cause gastritis, Hp was also expected to play a role in gastric carcinogenesis. Despite extensive studies, the mechanisms by which Hp cause gastric cancer are still poorly understood. However, there is evidence that the anatomical site of Hp infection is of major importance. Infection confined to the antral mucosa protects against gastric cancer but predisposes to duodenal ulcer, whereas Hp infection of the oxyntic mucosa increases the risk of gastric cancer. Hp infection does not predispose to cancers in the gastric cardia. In patients with atrophic gastritis of the oxyntic mucosa, the intragastric pH is elevated and the concentration of microorganisms in the stomach is increased. This does not lead to increased risk of gastric cancer at all anatomical sites. The site specificity of Hp infection in relation to cancer risk indicates that neither Hp nor the changes in gastric microflora due to gastric hypoacidity are carcinogenic per se. However, reduced gastric acidity also leads to hypergastrinemia, which stimulates the function and proliferation of enterochromaffin-like (ECL) cells located in the oxyntic mucosa. The ECL cell may be more important in human gastric carcinogenesis than previously realized, as every condition causing long-term hypergastrinemia in animals results in the development of neoplasia in the oxyntic mucosa. Patients with hypergastrinemia will far more often develop carcinomas in the gastric corpus. In conclusion, hypergastrinemia may explain the carcinogenic effect of Hp.

Topics: Animals; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Risk; Stomach Neoplasms

Gastrin has been identified as the principal effector of gastric secretion, but several studies have demonstrated its role as a biomarker of cancer risk and as a growth factor for colorectal, stomach, liver, and pancreatic cancer. Hypergastrinemia characterizes autoimmune gastritis, with body and fundic gland atrophy and increased risk for both gastric adenocarcinoma and neuroendocrine tumors. Gastric type I carcinoids develop in the context of autoimmune gastritis because of the stimulus exerted by gastrin on enterochromaffin-like cells and remain gastrin-sensitive for long durations because the removal of hypergastrinemia leads to tumor regression. The treatment of gastric carcinoid is still open to debate, but when the disease frequently relapses, or is multicentric or infiltrating, surgery is advocated or, in the alternative, a costly and long-lasting treatment with long-acting somatostatin analogues is prescribed. A technology allowing the preparation of an immunogen eliciting an immune system response with generation of antibodies against G17 has been developed. This vaccine has been tested in patients with colorectal, pancreatic or advanced gastric cancer. The vaccine has also been used in the treatment of gastric type I carcinoids, and the administration of G17DT in patients harboring these lesions leads to carcinoid regression. Antigastrin vaccination in the treatment of gastrointestinal cancer obviously needs validation, but this immunotherapy may well represent a simple, inexpensive, and active 'adjuvant' treatment.

Topics: Adenocarcinoma; Autoimmune Diseases; Cancer Vaccines; Carcinoid Tumor; Colorectal Neoplasms; Gastrins; Gastritis; Humans; Liver Neoplasms; Pancreatic Neoplasms; Stomach Neoplasms

Gastric exocrine secretion, both acid and non-acid, is required for micronutrients absorption, such as iron, calcium and vitamin B12, drugs absorption, protein digestion. Clinical presentation of a gastric secretion impairment might be then characterized by the presence of both gastrointestinal and non-gastrointestinal specific symptoms (i.e. anemia) or to a non-response to therapies. The main factor that impairs gastric exocrine secretion homeostasis is mucosal chronic inflammation that principally occurs after colonization by Helicobacter pylori (Hp). The extent and distribution of gastritis ultimately determine the clinical outcome linked to differences in gastric acid secretion status, the involvement of gastric body leading to a decrease in gastric exocrine secretion with possible progression to mucosal atrophy towards cancer. A correct clinical strategy in the management of Hp infected patients should be then to early identify body involvement, a diagnosis generally missed in that body biopsies are not routinely performed. The use of gastric serological markers, gastrin and pepsinogens, are helpful in suspecting the presence of mucosal atrophy but their diagnostic accuracy for non-atrophic chronic gastritis topography is not adequate despite a good specificity due to the low sensitivity, of all the available biomarkers. Gastric serology associated to anemia/iron-deficiency screening might nevertheless been helpful in the framing of patients that undergo endoscopy in order to highlight the need of extensive mucosal biopsies sampling.

Topics: Absorption; Anemia; Biomarkers; Biopsy; Gastric Acid; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Intrinsic Factor; Micronutrients; Models, Biological; Parietal Cells, Gastric; Pepsinogens; Secretory Rate; Stomach

Chronic infection of the gastric mucosa with Helicobacter pylori has long been recognized as a significant risk factor for gastric cancer, and indeed, this model represents the prototypical inflammation-associated cancer. In this review, we present the latest clinical and experimental evidence showing that gastrin peptides and their receptors [the cholecystokinin (CCK2) receptors] potentiate the progression of gastric cancer and other gastrointestinal malignancies in the presence of inflammation.. We highlight the feed-forward mechanisms by which gastrin and CCK2 receptor expression are upregulated during inflammation and in gastrointestinal cancers, summarize gastrin's proinflammatory role by inducing the production of cyclooxgenase-2 (COX-2) and interleukin-8 (IL-8), and relate evidence suggesting that gastrin and their receptors modulate the function of immune cells and fibroblasts following cellular stress, injury, repair, as well as during cancer progression.. We discuss trends for future studies directed toward the elucidation of gastrin peptides' role in regulating intercellular molecular signaling mechanisms between local and circulating immune cells, fibroblasts, epithelial cells, and other cell types in the microenvironments of inflammation-related cancers. Elucidation of the molecular and cellular pathways that relate inflammation with cancer may provide additional opportunities to develop complementary therapies that target the inflammatory microenvironment of the cancer.

Topics: Animals; Cocarcinogenesis; Colorectal Neoplasms; Cytokines; Feedback, Physiological; Gastrins; Gastritis; Gastrointestinal Neoplasms; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation Mediators; Leukocytes; Receptor, Cholecystokinin B

Gastrin release is affected by gastric inflammatory conditions. Antral G cells respond to inflammatory mediators by increasing gastrin secretion. Accumulating experimental evidence suggests that gastrin exerts immunomodulatory and proinflammatory effects. Gastrin could be a contributing factor to these pathologies, which may constitute a new justification for pharmacological blockade of gastrin action.

Topics: Animals; Cell Proliferation; Gastric Acid; Gastrin-Secreting Cells; Gastrinoma; Gastrins; Gastritis; Humans; Immunomodulation; Protein Precursors; Receptors, Cholecystokinin; Signal Transduction

This review summarizes the past year's literature regarding the regulation and assessment of gastric acid secretion.. Gastric acid secretion is regulated by biologic agents produced and released by enteroendocrine cells and neurons as well as by exogenously administered substances and infection. Too much acid can lead to gastroesophageal reflux disease, peptic ulcer disease, and stress-related erosion/ulcer disease. Too little acid can interfere with the absorption of certain nutrients, predispose to enteric infection, and interfere with the absorption of some medications. Gastrin, histamine, gastrin-releasing peptide, ghrelin, orexin, and glucocorticoids stimulate whereas leptin, glucagon-like peptide 1, and Helicobacter pylori inhibit acid secretion. Helicobacter pylori inhibits the transcriptional activity of HK-ATPase, the proton pump of the parietal cell.. A better understanding of the pathways and mechanisms regulating gastric acid secretion should lead to improved management of patients with acid-induced disorders as well as those who secrete too little acid.

Topics: Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Humans

Proton pump inhibitors are being increasingly used and for longer periods of time, especially in patients with gastroesophageal reflux disease. Each of these trends has led to numerous studies and reviews of the potential risk-benefit ratio of the long-term use of proton pump inhibitors. Both long-term effects of hypergastrinaemia due to the profound acid suppression caused by proton pump inhibitors as well as the effects of hypo-/achlorhydria per se have been raised and studied. Potential areas of concern that have been raised in the long-term use of proton pump inhibitors, which could alter this risk-benefit ratio include: gastric carcinoid formation; the development of rebound acid hypersecretion when proton pump inhibitor treatment is stopped; the development of tolerance; increased oxyntic gastritis in H. pylori patients and the possibility of increasing the risk of gastric cancer; the possible stimulation of growth of non-gastric tumours due to hypergastrinaemia; and the possible effect of the hypo/achlorhydria on nutrient absorption, particularly iron and vitamin B12. Because few patients with idiopathic gastro-oesophageal reflux disease/peptic ulcer disease have been treated long-term (i.e., >10 years), there is little known to address the above areas of potential concern. Most patients with gastrinomas with Zollinger-Ellison syndrome have life-long hypergastrinaemia, require continuous proton pump inhibitors treatment and a number of studies report results of >5-10 years of tratment and follow-up. Therefore, an analysis of Zollinger-Ellison syndrome patients can provide important insights into some of the safety concerns raised above. In this paper, results from studies of Zollinger-Ellison syndrome patients and other recent studies dealing with the safety concerns above, are briefly reviewed.

Topics: Animals; Carcinoid Tumor; Cell Transformation, Neoplastic; Drug Tolerance; Enterochromaffin-like Cells; Gastric Acid; Gastric Mucosa; Gastrinoma; Gastrins; Gastritis; Gastroesophageal Reflux; Gastrointestinal Agents; Helicobacter pylori; Humans; Malabsorption Syndromes; Peptic Ulcer; Proton Pump Inhibitors; Stomach Neoplasms; Time Factors; Zollinger-Ellison Syndrome

Classifications of chronic gastritis and neoplastic gastric diseases, developed in recent years (1996 Houston update of 1990 Sidney classification system, 2002 New Orlean classification of atrophic gastritis according to recommendations of International Group for Atrophy Studies; 1998 Padova classification of gastric displasia, and 1998 Vienna classification of gastrointestinal neoplasia) allow to statandardize international research and perform more objective diagnostics of pathological changes in the gastric mucosa. Studies carried out in recent years have established that morphological manifestations of chronic gastritis caused by Helicobacter pylori infection can be reduced after its eradication. Longterm treatment with proton pump inhibitors have been demonstrated not to cause atrophic changes in the gastric mucosa when undertaken after successful eradicational therapy. It has been established that corporal gastritis intensifies in patients treated with proton pump inhibitors. The studies show that measurement of serum levels of Helicobacter pylori antibodies, gastrine, pepsinogen I and II can be used in non-invasive serologic diagnostics of atrophic gastritis. Achievements in diagnostics and treatment of chronic gastritis create the necessary prerequisites for the development of gastric cancer preventing measures.

Topics: Antibodies, Bacterial; Biopsy; Chronic Disease; Dyspepsia; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Gastrointestinal Neoplasms; Helicobacter Infections; Helicobacter pylori; Humans; Pepsinogen A; Pepsinogen C; Proton Pump Inhibitors; Stomach; Stomach Neoplasms; Time Factors

In 1984, Reg protein was shown to be stimulated during the regeneration of pancreatic islets. Since then, many Reg-related proteins have been identified in humans and other animals. These Reg-related proteins are classified into four subfamilies according to their amino-acid sequences, but they share a similar structure and physiological function. The role of Reg in gastric tissue was investigated, and Reg I was found to be expressed mainly in gastric fundic enterochromaffin-like (ECL) cells. Reg I production in ECL cells is stimulated by gastrin, as well as by the proinflammatory cytokine, cytokine-induced neutrophil chemoattractant (CINC)-2Beta. In patients with chronic hypergastrinemia, Reg production is stimulated, with the increased proliferation of gastric mucosal cells. Patients with Helicobacter pylori infection also showed increased Reg production in the gastric mucosa, partly via increased plasma gastrin concentration and partly via increased proinflammatory cytokine production. Thus, Reg protein induced by H. pylori infection may be partly responsible for the increased proliferation of gastric epithelial cells in H. pylori-infected patients. Reg protein is also produced in many gastric cancer cells, especially in poorly differentiated and advanced cancers. Reg protein stimulates the proliferation of several gastric cancer cell types, and gastric cancers with Reg protein expression tend to show a poorer clinical outcome. In summary, Reg protein may be a growth factor that regulates the proliferation and differentiation of normal and neoplastic gastric epithelial cells.

Topics: Animals; Cell Division; Chronic Disease; Enterochromaffin-like Cells; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; In Situ Hybridization; Stomach Neoplasms

The recent discovery of gastric leptin has initiated several investigations on the possible role of leptin in digestive physiology. The following clues are currently suggested: leptin might control meal size in cooperation with Cholecystokinin, help cytoprotection of the gastric mucosa, play a role in gut inflammatory processes, regulate secretion of gastric hormones such as gastrin and somatostatin, and modulate intestinal transport of small peptides. The present review is a brief survey of the most significant advances in these issues.

Topics: Animals; Appetite Regulation; Biological Transport; Cholecystokinin; Cytoprotection; Gastric Mucosa; Gastrins; Gastritis; Humans; Leptin; Peptides; Somatostatin

Proton pump inhibitors are potent drugs for the treatment of acid-related diseases. The moderate hypergastrinaemia observed during therapy is a physiological response to low intragastric pH and the increase is limited to the first months of therapy with no further changes thereafter. Reports on endocrine cell changes in the antral mucosa under chronic PPI therapy are controversial and lack clinical relevance. In contrast, in the oxyntic mucosa hyperplastic argyrophil cell changes have been reported, dependent on the degree and duration of hypergastrinaemia, the severity of oxyntic mucosal gastritis, especially atrophy, and the presence of H. pylori infection. Current data do not support a progression from hyperplastic to dysplastic argyrophil cell lesions in humans in the absence of additional genetic factors. Data on the progression of oxyntic gastritis under chronic PPI treatment in comparison to untreated controls could not be confirmed in more recent studies including a well-matched control population. The main factor for gastritis progression is the presence of Helicobacter pylori infection. The bacterium not only causes a chronic inflammation of the gastric mucosa, resulting in atrophy and intestinal metaplasia, but also influences endocrine cell populations involved in the regulation of gastric acid secretion. The clinical benefit of H. pylori eradication in reflux esophagitis patients is still a matter of debate. The complex relations in humans between hypergastrinaemia, (oxyntic) gastritis and atrophy, H. pylori infection, argyrophil cell hyperplasia, and the effects of long-term PPI treatment of acid-related diseases do not allow a quantification of the contribution of each single factor for the observed changes.

Topics: Anti-Ulcer Agents; Atrophy; Enzyme Inhibitors; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Metaplasia; Proton Pump Inhibitors

Duodenal ulcer patients are characterized by an antrum-predominant, body-sparing, nonatrophic Helicobacter pylori (H. pylori) gastritis, which results in increased gastrin release and increased acid secretion. The increased gastrin release is caused by the infection impairing the acid-mediated inhibitory control of gastrin release. The elevated levels of the gastrin stimulate the healthy uninflamed, non-atrophic acid-secreting region of the stomach to secrete excess amounts of acid. The increased gastrin also exerts trophic effects on the oxyntic mucosa, causing hyperplasia of both the enterochromaffin-like cells and the parietal cells. These trophic changes in the mucosa further enhance its ability to secrete acid. The increased acid secretion results in an increased duodenal acid load, causing gastric metaplasia of the duodenal bulb and eventually the development of ulceration. In H. pylori-infected subjects without duodenal ulceration, a different pattern of gastritis is seen. This includes atrophy of the antrum, which reduces the number of G-cells and thus the degree of hypergastrinaemia induced by the antral infection. There are usually also varying degrees of inflammation and atrophy of the acid-secreting mucosa, which impair its ability to secrete acid in response to gastrin stimulation. The combined effects of the atrophy of the antrum and the inflammation of the antrum of the body mucosa therefore prevent H. pylori-induced acid hypersecretion and may result in varying degrees of hypochlorhydria. The particular pattern of gastritis that a subject develops in response to H. pylori infection and their likelihood of developing a duodenal ulcer is likely to be determinded by host genetic factors plus dietary factors.

Topics: Duodenal Ulcer; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Metaplasia; Parietal Cells, Gastric

Helicobacter pylori infection affects the concentration of regulatory peptides such as gastrin, somatostatin and cholecystokinin and the concentration and activity of glutathione and glutathione S-transferases in the gastric mucosa.. Literature review.. Although some of these peptides have been known since the beginning of this century, their action has changed since the discovery of H. pylori infection in 1983. Chronic infection with H. pylori might lead to an increased risk in developing gastric cancer. Glutathione S-transferases are involved in the cellular detoxification of xenobiotics and other toxic compounds. Since there is a close inverse relationship between the activity of glutathione S-transferase and incidence of malignancies in the gastrointestinal tract, the possible relation between H. pylori infection and activity of glutathione S-transferases in the gastric mucosa is discussed.. The effect of H. pylori infection on regulatory peptides and glutathione/glutathione S-transferases might play a role in the development of neoplastic changes of the H. pylori-infected gastric mucosa.

Topics: Animals; Biomarkers; Cholecystokinin; Chronic Disease; Disease Progression; Gastric Mucosa; Gastrins; Gastritis; Glutathione; Glutathione Transferase; Helicobacter Infections; Helicobacter pylori; Humans; Somatostatin; Stomach Neoplasms

Helicobacter pylori (H. pylori) infection leads to profound changes in gastric physiology. Several clinical and animal studies have been performed to clarify the influence of H. pylori on gastric acid secretion. Published data, however, are not consistent throughout. Infection of the gastric antrum, which can be observed mainly in duodenal ulcer patients, increases gastrin release and consecutively acid output. The net effect of corpus and antrum gastritis, such as in patients with gastric cancer, is to decrease acid secretion. Chronic H. pylori infection may finally promote gastric atrophy with irreversibly diminished acid secretion but in earlier stages of this infection eradication of H. pylori normalizes gastric secretory activity.

Topics: Animals; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Peptic Ulcer; Somatostatin

Topics: Animals; Cell Division; Colonic Neoplasms; Gastrins; Gastritis; Gastrointestinal Diseases; Humans; Receptors, Cholecystokinin

An analysis carried out in 1994 by the WHO International Agency for Research on Cancer (IARC) resulted in Helicobacter pylori being designated as a Group 1 carcinogen and thus clearly having an association with the development of gastric cancer. In the case of H. pylori, the evaluation was made solely on the basis of epidemiological results. In Japan, in 1993, only 235,000 of the 60 million people with H. pylori had gastric cancer. This represents only 0.4% of the infected population. Each individual reacts in a unique way to H. pylori infection in terms of the inflammatory response. The probability of developing cancer will be determined by environmental factors such as diet, duration of or age at acquisition of H. pylori infection, the virulence of H. pylori strains, and host factors including genetic make-up.

Topics: Antibodies, Bacterial; Diet; Environment; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Prevalence; Stomach Neoplasms

Helicobacter pylori is the cause of chronic type B gastritis and occurs in almost all patients with duodenal ulcers. Infection with H. pylori is characterized by an increased production of several inflammatory cytokines. Increasing evidence suggests a central role of these cytokines in the pathogenesis of H. pylori-associated gastritis and peptic ulcer disease. Cytokines may be crucial in the recruitment and activation of inflammatory cells and in stimulation of gastrin release. In addition to their proinflammatory properties, cytokines may also inhibit the ulcer occurrence by stimulation of prostaglandins and somatostatin release and by direct impairment of acid secretion. The balance of these factors may determine the clinical outcome of H. pylori infection.

Topics: Animals; Cytokines; Duodenal Ulcer; Gastrins; Gastritis; Genes, MHC Class II; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation; Intestinal Mucosa; Peptic Ulcer; Somatostatin

There are three main types of blood test available for the management of Helicobacter pylori infection: those that detect an antibody response; tests of the pathophysiological state of the stomach; and those that indicate an active infection. Enzyme linked immunosorbent assay (ELISA) based kits are the most numerous of the commercially available tests. Originally the kits used crude antigen preparations but many of the newer kits use a more purified antigen preparation giving increased specificity but a lower sensitivity. The sensitivity, specificity, and predictive values of the tests can also be affected by the population under test and coexistent disease in the patients. Near patient test kits are based on either latex agglutination or immunochromatography. Generally, they have low sensitivities compared with laboratory tests. Commercial western blotting kits have also been developed and are used to detect the presence of specific virulence markers. The exact role of serology in the management of Helicobacter infection has still to be defined, although there is evidence that, used as a screening procedure, it can reduce endoscopy cost and workload. Gastrin and pepsinogen blood concentrations may provide valuable information on the pathophysiological state of the stomach--for example, the presence of inflammation or gastric atrophy. A combination of serology and serum concentrations of gastrin and pepsinogen may be used effectively to detect serious gastroduodenal disease in patients.

Topics: Antibodies, Bacterial; Biomarkers; Enzyme-Linked Immunosorbent Assay; Evaluation Studies as Topic; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Pepsinogens; Reagent Kits, Diagnostic; Sensitivity and Specificity; Serologic Tests

It is now widely recognized that H. pylori gastritis can produce marked alterations in gastric acid secretion. In subjects with an antral predominant gastritis there is increased release of gastrin and consequently increased acid secretion. Such subjects are at risk of developing duodenal ulcers. In other subjects the infection produces a marked body gastritis and this is associated with marked hyposecretion of acid or complete achlorhydria. These subjects have an increased risk of developing gastric cancer. Between these two ends of the disease spectrum lie the majority of H. pylori-infected subjects who have gastritis of both the antrum and body and no overall change in acid secretion. The reason why the infection exerts these divergent effects on gastric morphology and function remains unclear and is a challenge for ongoing research.

Topics: Cell Count; Duodenal Ulcer; Gastric Acid; Gastric Fundus; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Pyloric Antrum; Risk Factors

Topics: Betazole; Duodenal Ulcer; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastritis; Humans; Stomach Neoplasms; Stomach Ulcer; Zollinger-Ellison Syndrome

Helicobacter pylori infection increases gastric acid secretion in patients with duodenal ulcers but diminishes acid output in patients with gastric cancer and their relatives. Investigation of the basic mechanisms may show how H. pylori causes different diseases in different persons. Infection of the gastric antrum increases gastrin release. Certain cytokines released in H. pylori gastritis, such as tumor necrosis factor alpha and specific products of H. pylori, such as ammonia, release gastrin from G cells and might be responsible. The infection also diminishes mucosal expression of somatostatin. Exposure of canine D cells to tumor necrosis factor alpha in vitro reproduces this effect. These changes in gastrin and somatostatin increase acid secretion and lead to duodenal ulceration. But the acid response depends on the state of the gastric corpus mucosa. The net effect of corpus gastritis is to decrease acid secretion. Specific products of H. pylori inhibit parietal cells. Also, interleukin 1 beta, which is overexpressed in H. pylori gastritis, inhibits both parietal cells and histamine release from enterochromaffin-like cells. H. pylori also promotes gastric atrophy, leading to loss of parietal cells. Factors such as a high-salt diet and a lack of dietary antioxidants, which also increase corpus gastritis and atrophy, may protect against duodenal ulcers by decreasing acid output. However, the resulting increase of intragastric pH may predispose to gastric cancer by allowing other bacteria to persist and produce carcinogens in the stomach.

Topics: Animals; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans

The dictum "no acid-no ulcer" had, in the past, summarized the thinking concerning the pathogenesis of peptic ulcer disease. It is now recognized that infection with Helicobacter pylori is the major causal factor leading to both duodenal and gastric ulceration. Infection is associated with many of the acid secretory abnormalities that have traditionally characterized peptic ulcer disease; indeed, acid secretory physiology returns to normal following bacterial eradication. Since not all individuals infected with H. pylori develop ulcers, host susceptibility, bacterial virulence, and/or specific environmental factors must determine the response to infection and the ultimate clinical outcome. The relative importance of these factors and their complex interactions remain to be determined. H. pylori infection produces tissue damage indirectly because the organism does not directly invade gastroduodenal tissue. A variety of bacterial enzymes, toxins, and inflammatory mediators produced in response to bacterial colonization challenge the integrity of host mucosal defenses. In a susceptible host, breached defenses render epithelium more vulnerable to acid injury and ulcer development. Eradication of H. pylori leads to rapid ulcer healing and reversal of tissue injury, thereby obviating ulcer recurrence.

Topics: Duodenal Ulcer; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Peptic Ulcer; Stomach Ulcer

Helicobacter pylori is probably the commonest bacterial infection worldwide and is now accepted as the cause of chronic active type B gastritis. Most patients continue through life with a chronic superficial gastritis while some develop either duodenal or gastric ulcer. In a very small proportion the lymphoid reaction to H. pylori infection appears to progress to become a mucosal associated lymphoid tissue (MALT) lymphoma, while in others the evidence suggests that chronic superficial gastritis progresses to atrophy, the loss of gastric acid secretory capacity and the development of gastric cancer. The mechanisms involving H. pylori infection in peptic ulceration are increasingly well understood and H. pylori is now accepted as having a critical role in duodenal ulcer, where the prevalence of infection is 90 to 95%. More important is the dramatic reduction in duodenal ulcer recurrence after successful eradication of the organism to about 4% in a year compared to recurrences of up to 80% in those who ulcers have been healed but in whom the infection persists. There is also increasing evidence for the involvement of H. pylori in gastric ulcer, where infection is seen in between 60 and 80%, and there is a similar dramatic reduction in recurrence following cure of H. pylori infection. The progression of H. pylori gastritis from the acute infection to chronic superficial gastritis, predominantly antral gastritis or a pangastritis with increasing atrophy appears to be associated with the differing outcomes seen in this disease. Moreover, there is increasing data on the roles played by bacterial heterogeneity and the virulence of the organism, host factors such as the HLA genotype and immune response, environmental factors and the age of acquisition of infection play in determining these clinical outcomes of the disease.

Topics: Gastric Acid; Gastrins; Gastritis; Gastrointestinal Diseases; Helicobacter Infections; Helicobacter pylori; Humans; Lymphoma, B-Cell, Marginal Zone; Somatostatin; Stomach Neoplasms

Unlike the stimulation of gastric acid secretion, which clearly involves the release of gastrin, the mechanisms of inhibition of this secretory process are poorly defined although recent studies in animals with the use of highly selective cholecystokinin (CCK) antagonists indicate that CCK may play a crucial role in this inhibition. Duodenal ulcer patients (DU) differ from healthy controls by higher total acid secretory rates and diminished inhibition of acid secretion. Several possible pathomechanisms of the abnormal gastric secretory function in DU patients were previously proposed. The deficiency of CCK-induced gastric inhibition in DU patients together with the somatostatin hypothesis appear to be attractive, particularly so the suggestion that a deficiency of somatostatin activity exists in DU patients.

Topics: Animals; Cholecystokinin; Duodenal Ulcer; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Humans; Reference Values; Somatostatin

Topics: Bacterial Proteins; Breath Tests; Carbon Radioisotopes; Child; Chronic Disease; Gastric Juice; Gastrins; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Pepsinogens; Predictive Value of Tests; Prevalence; Sensitivity and Specificity; Staining and Labeling; Urease

Etiologic role for HP appears to be best established in histologically proven gastritis. The major factors mediating gastritis induced by the colonization of the "gastric type" mucosa with HP are probably cytotoxins, cytokines and free radicals activated by this organisms. The deficiency of negative feedback in somatostatin-gastrin link in antral gastritis may result in an excessive gastrin release and increased gastric acid secretion with increased duodenal acid load under basal state and after meal. Recent NIH consensus 1994 proposes that: (1) ulcer patients with HP require treatment with antimicrobial agents whether on first presentation or on recurrence; (2) the value of treatment of HP infection in non-ulcer dyspepsia remains to be determined and (3) the asymptomatic subjects with HP infection do not require treatment with antimicrobial agents.

Topics: Bacteriological Techniques; Bicarbonates; Duodenal Ulcer; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Peptic Ulcer

Topics: Analgesics; Blood Group Antigens; Diet; Duodenitis; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Metaplasia; Peptic Ulcer; Risk Factors; Smoking; Stress, Physiological; Twin Studies as Topic

Topics: Duodenal Diseases; Duodenal Ulcer; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Models, Biological; Somatostatin; Stomach Diseases; Stomach Neoplasms; Stomach Ulcer

ECL cells are argyrophilic endocrine cells of the stomach. Their distribution is species specific, however they are consistently located in the oxyntic mucosa and, in particular, in very close contact with the adenomeres of acidopeptic glands. ECL cells store histamine and are considered a key element in the mechanisms of gastric acid secretion as controlled by gastrin stimulus. Their peculiar anatomical disposition and secretory properties strongly suggest that ECL cells exert their function by a paracrine mechanism, i.e. by releasing histamine in the extracellular spaces surrounding acid-producing parietal cells. ECL cell activity is strongly stimulated by gastrin, which, once applied as a long-standing stimulus, also exerts a potent proliferating effect. Long-lasting hypergastrinaemia has been demonstrated to elicit ECL cell proliferation in laboratory animals, inducing ECL cell hyperplasia, dysplasia and ECL cell tumours, i.e. argyrophilic gastric carcinoids. However, in experimental rodents it is believed that hypergastrinaemia is not per se a stimulus capable of inducing ECL cell transformation, a predisposing genetic background being required for tumour development in endocrine organs. In man, long-standing hypergastrinaemia exerts the same proliferative pressure on ECL cells and is associated with hyperplasia with or without dysplastic changes and carcinoid development. Clinical evidence suggests that other factors, both genetic and environmental, are required to induce ECL cell transformation and carcinoid development. For this reason human gastric argyrophilic ECL carcinoids are subdivided into three main groups depending on their clinical background: (1) gastric carcinoids in patients with chronic atrophic gastritis; (2) gastric carcinoids in patients with Zollinger-Ellison and multiple endocrine neoplasia type 1 syndrome (MEN-ZES); and (3) solitary, sporadic gastric carcinoids. The clinical assessment of carcinoid-bearing patients is strongly recommended for better diagnosis and management of patients.

Topics: Animals; Carcinoid Tumor; Enterochromaffin Cells; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Histamine Release; Humans; Multiple Endocrine Neoplasia; Omeprazole; Parietal Cells, Gastric; Stomach Neoplasms; Zollinger-Ellison Syndrome

There is general agreement that motility, urease activity, and association with gastric mucosal cells are important virulence factors of H. pylori. Urease activity is perhaps the best characterized of these factors. Presumably, urease activity creates a "cloud" of ammonia around the bacterium, thus neutralizing the lethal effects of gastric acid. Motility allows the bacterium to penetrate the mucus layer and promotes specific association of the bacteria with epithelial cells, further allowing evasion of gastric acidity. The association between gastrin levels and H. pylori infection is currently the most thoroughly studied feature relating to pathogenesis in vivo. Prolonged hypergastrinemia associated with H. pylori infection may contribute to increased parietal cell mass and chronically increased secretion of gastric acid; however, long-term studies are needed to validate this hypothesis. The identification of mucosal gamma delta T cells and immunologic cross-reactivity between H. pylori and gastric cells implies that the immune response contributes significantly to the pathogenesis of H. pylori. The role of the immune system in modulating H. pylori infection requires further study. Although many putative pathogenic factors have been identified on the basis of in vitro phenomena alone, their significance in vivo is not known. Ultimately, it will be necessary to evaluate the significance of these factors in animal models by using isogenic strains of H. pylori that differ only in a single genotypic characteristic.

Topics: Bacterial Toxins; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans

At present at least seven different endocrine cell types have been identified in the stomach. According to their relative frequency and secretion products the antral gastrin producing G cell and somatostatin producing D cell and the fundic histamine producing ECL cell are the best characterized cell types. Total endocrine cell mass is controlled by various factors from inside and outside the stomach. Density of antral G and D cells depends on the presence and absence of food, on the antral pH and on additional humoral and/or neural factors. Gastrin and not gastric pH has been identified as the most important factor regulating the density of fundic ECL cells. Adaptation of gastric endocrine cells to gastric pH and to the presence, abundance or absence of humoral and neural regulators are well known phenomena though only partially understood. Antral G cells increase and antral D cells decrease during long-term achlorhydria which as a consequence leads to hypergastrinaemia. Examples are pernicious anaemia in man and drug-induced acid suppression under experimental conditions. Interestingly, achlorhydria-induced G cell hyperplasia never progresses to gastrinomas. Fundic ECL cell density increases markedly in the presence of long-lasting hypergastrinaemia independently of gastric pH. In contrast to G cells ECL cell hyperplasia may progress to rarely occurring ECLomas. However, this depends on additional conditioning factors as the presence of severe atrophic gastritis as in pernicious anaemia or a specific genetic trait present in patients with gastrinomas associated with the MEN I syndrome.

Topics: Adaptation, Physiological; Enterochromaffin Cells; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Hormones; Humans; Hyperplasia; Stomach

Although Helicobacter pylori is now accepted as the major aetiological factor in chronic gastritis in man, many of the factors which determine its pathogenicity are unknown. The organism has adapted to survive in the low-pH environment of the stomach, partly through its ability to buffer hydrogen ion by the hydrolysis of urea and by the presence of lectins on its surface, which bind to gastric mucosa and epithelial cells. After attachment, harmful toxins and enzymes have access to the gastric cells and cellular damage and an immune response ensues. In patients with duodenal ulceration, Helicobacter pylori-related gastritis predominantly affects the gastric antrum and has a high prevalence. Excessive gastrin production has been suggested as a potential aetiological factor linking infection with duodenal ulcer development. Perhaps more important is the association between gastric metaplasia of the duodenal epithelium, which is correlated with acid load and is more extreme in H. pylori positive patients with duodenitis. Organisms may subsequently spread from the gastric antrum into areas of gastric metaplasia in the duodenal bulb, leading to areas of chronic duodenitis and ultimately frank ulceration. It should not be overlooked, however, that other factors such as genetic predisposition, blood group, stress, drugs and smoking all have a role to play in the outcome, given the comparatively small number of patients in the general population infected with H. pylori who develop ulcer disease.

Topics: Duodenal Ulcer; Duodenitis; Duodenum; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Intestinal Mucosa

Achlorhydria has been discussed as a possibly dangerous consequence of therapeutic inhibition of gastric acid secretion since the introduction of H2-receptor antagonists. The risk of long-term hypergastrinaemia has only been considered for about 5 years. The reason for this was the demonstration that gastric carcinoids (ECLomas) observed after life-long treatment of rats with the proton pump inhibitor omeprazole could also be produced in rats by other methods leading to long-lasting profound hypergastrinaemia. Such methods were the 80% resection of the oxyntic mucosa or feeding of ranitidine (2000 mg/day) for 2 years. The endocrine tumours corresponded to the gastric carcinoids found in patients with long-lasting hypergastrinaemia due to pernicious anaemia or with a gastrinoma as part of the MEN I syndrome. Neither in animals nor in man could other endocrine tumours or adenocarcinomas of the gastrointestinal tract be related to hypergastrinaemia. Epidemiologic data do not support gastrin dependence of adenocarcinoma of the stomach or the colon. Experimental findings of gastrin effects on tumour growth in vivo and in vitro have been contradictory and may be explained by the presence of gastrin receptors on tumour cells and the role of gastrin as an autocrine growth factor in some of these tumours. Since acid blockade by proton pump inhibitors or H2-receptor blockers dose-dependently increase serum gastrin levels, patients with ranitidine-resistant peptic ulceration receiving long-term treatment with high-dose omeprazole have been followed up with serial gastric biopsy specimens for up to 5 years. Complete healing, moderate hypergastrinaemia, and a slight hyperplasia but no dysplasia of the ECL cells in the oxyntic mucosa have been observed, which seemed to be correlated to chronic gastritis progressing over the years. Despite these negative findings excessive hypergastrinaemia by overdosage of potent drugs for inhibition of gastric secretion should be avoided and monitoring of plasma gastrin levels is recommended in case of long-term treatment.

Topics: Achlorhydria; Adenocarcinoma; Colonic Neoplasms; Enterochromaffin Cells; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Histamine H2 Antagonists; Humans; Stomach Neoplasms

Topics: Cimetidine; Duodenal Ulcer; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged; Ranitidine; Recurrence

There is a significant inverse relationship between intragastric acidity and plasma gastrin concentration. All generally available gastric acid antisecretory drugs induce a release of gastrin into the circulation. The more potent the gastric antisecretory dosage regimen or drug, the greater the rise of plasma gastrin concentration. The drug-induced rise of plasma gastrin concentration is of no direct clinical concern, although it may be partly responsible for the phenomenon of tolerance to H2-blockade. Drug-induced hypergastrinemia could stimulate the proliferation of certain cell lines associated with the gastrointestinal tract, for example, the gastric epithelium, ECL cells, or colonic neoplasms.

Topics: Adenocarcinoma; Animals; Campylobacter Infections; Gastric Acid; Gastrins; Gastritis; Gastrointestinal Neoplasms; Humans

Although carcinoid tumors only infrequently (2-6%) have a gastric localization, in recent years several cases have been described of this tpe of neoplasm in association with atrophic gastritis (with or without pernicious anemia). A possible carcinogenetic effect of sustained hypergastrinemia on the enterochromaffin-like cells (ECL) of the gastric mucosa has been postulated. A new case of these characteristics in reported, and a review is made of the pathogenic hypotheses in the literature on this peculiar type of tumors and their possible clinical implications.

Topics: Adult; Carcinoid Tumor; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Male; Stomach Neoplasms

The accumulating evidence of an association between antrum-sparing hypergastrinaemic atrophic gastritis, frequently associated with pernicious anaemia, and the occurrence of gastric carcinoid tumours is briefly reviewed. The development of argyrophil cell carcinoid tumours in the atrophic fundic mucosa seems to be related to argyrophil cell hyperplasia caused by hypergastrinaemia. Epidemiologic considerations indicate that the gastric carcinoid generally is underdiagnosed and that the incidence of this tumour is higher than previously recognized. The clinical relevance of minute gastric carcinoids, or endocrine cell 'adenomas', is obscure. However, larger tumours should be regarded as potentially malignant. These findings are relevant to the aspect of long-term medically induced achlorhydria leading to hypergastrinaemia.

Topics: Achlorhydria; Adenoma; Anemia, Pernicious; Atrophy; Carcinoid Tumor; Cell Division; Epidemiologic Methods; Gastrins; Gastritis; Humans; Stomach Neoplasms

Topics: Duodenum; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Histamine; Hormones; Humans; Insulin; Pepsin A; Pepsinogens; Secretin; Secretory Rate; Somatostatin; Vagus Nerve

Topics: Animals; Digestive System; Digestive System Physiological Phenomena; Duodenal Ulcer; Gastric Acid; Gastrins; Gastritis; Histamine; Histamine H2 Antagonists; Humans; Intrinsic Factor; Liver Circulation; Pepsinogens; Receptors, Histamine; Receptors, Histamine H1; Receptors, Histamine H2; Regional Blood Flow; Stomach; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Acute Kidney Injury; Bile; Digestive System Diseases; Gastrins; Gastritis; Humans; Kidney; Kidney Failure, Chronic; Peptic Ulcer

Topics: Acromegaly; Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastroesophageal Reflux; Gastrointestinal Motility; Humans; Hyperparathyroidism; Ileal Diseases; Pyloric Antrum; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Biopsy; Chronic Disease; Digestion; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Gastrointestinal Hormones; Humans; Pepsin A

Development of histamine H2-receptor antagonists has enhanced the understanding of histamine physiology and pharmacology. The effect of H2-receptor antagonists on gastrointestinal physiology has been studied extensively. These compounds inhibit gastric acid secretion in response to all known secretagogues and, in contrast to anticholinergic drugs, markedly inhibit food-stimulated acid secretion in duodenal ulcer patients. The relative roles of H2-receptor antagonists, anticholinergic drugs and antacids in the treatment of duodenal ulcer remain to be defined. Cimetidine currently is under investigation for the treatment of duodenal ulcer, gastric ulcer, reflux esophagitis, gastrointestinal bleeding and hypersecretory states. Although the long-term safety of cimetidine has not been established, in short-term clinical trials there have been no significant subjective or objective side-effects. Assuming that toxic effects do not develop, H2-receptor antagonists should improve the treatment of acid-peptic disease.

Topics: Cimetidine; Cyclic AMP; Duodenal Ulcer; Esophagitis, Peptic; Gastric Juice; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Histamine; Histamine H2 Antagonists; Humans; Intrinsic Factor; Metiamide; Pepsin A; Stomach Ulcer

Topics: Digestion; Esophageal Achalasia; Esophagitis, Peptic; Gastric Inhibitory Polypeptide; Gastric Mucosa; Gastrins; Gastritis; Glucagon; Humans; Ileum; Islets of Langerhans; Jejunum; Kidney Failure, Chronic; Liver; Protein Hydrolysates; Pyloric Antrum; Somatostatin; Vagotomy; Vasoactive Intestinal Peptide; Zollinger-Ellison Syndrome

With combined immunofluorescent, cytochemical and electron microscopic investigations the enterochromaffin cell system has been differentiated into 5 distinct endocrine cell types in the human stomach and into 8 cell types in the intestine. These endocrine cells are probably of neuroectodermal origin and belong to the APUD (amine precursor uptake and decarboxylation)-system. Maximal gastrointestinal hormone concentrations as determined by tissue extracts correlate fairly well to the location of each endocrine cell type in various segments of the gastrointestinal tract. In certain gastroenteropathies the pathophysiological disturbances can be explained by pathomorphological alterations of the disseminated endocrine cells. 1. The gastrin-producing G-cell is the predominating endocrine cell in the gastric antrum. Besides immunocytochemistry the G-cell can be demonstrated with argyrophilic reaction (Grimelius, 1968), masked metachromasia and leadhematoxylin. The ultrastructural features are variable, depending on functional activity. The secretory granules are usually only slightly osmiophilic, measuring 200 till 250 nm in diameter. By some working groups a positive immunofluorescence with gastrin-antisera has been demonstrated in A1- or D-cells of the pancreatic islets. However, numerous negative results have been reported, too. Considering physiological conditions, a gastrin-secretion of the human pancreatic islets has not been secured without doubt. 2. The EC-cell produces serotonin and in the intestine motilin, too. Besides the formaldehyde-induced fluorescence, these cells can be demonstrated with diazonium and argentaffin reactions, less specific with argyrophilic methods. Ultrastructurally the EC-granules are easily differeniated from the other endocrine cells by their pronounced osmiophilia and pleomorphism. In experimental conditions the EC-cells demonstrate species- and site-specific alterations. With reserpine no ultrastructural changes were demonstrable in EC-cells of the rat. However, marked ultrastructural alterations with an increase of the hormone-producing organelle system were noticed after administration of parachlorophenylalanine (PCPA) which interferes with serotonine synthesis; 5. The gastric D-cells are characterized by large secretory granules similar to pancreatic D-cells. They secrete the HCl-inhibitory peptide somatostatin. 4. The D1-cell is a cell type with unknown function. The cytoplasm contains small granules with variable elect

Topics: Adenoma, Islet Cell; Anemia, Pernicious; Chromaffin System; Digestive System; Duodenal Ulcer; Endocrine System Diseases; Enterochromaffin Cells; Esophagitis, Peptic; Gastrectomy; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Hormones; Gastrointestinal Neoplasms; Humans; Intestinal Mucosa; Metabolic Diseases; Serotonin; Somatostatin; Stomach Neoplasms; Stomach Ulcer; Syndrome; Zollinger-Ellison Syndrome

Topics: Anemia, Pernicious; Calcium; Dietary Proteins; Duodenal Ulcer; Gastric Juice; Gastrins; Gastritis; Glucagon; Humans; Hyperplasia; Intestine, Small; Kidney Failure, Chronic; Pyloric Antrum; Pyloric Stenosis; Secretin; Stomach Neoplasms; Stomach Ulcer; Vagotomy; Zollinger-Ellison Syndrome

The patient with gastric ulcer (GU) has abnormal reflux of bile-containing duodenal contents into the stomach. Antral gastritis is prominently associated with GU and is more extensive with severe reflux and with ulcer chronicity and probably when bile salts are accompanied by other constituents of duodenal fluids. Smoking is significantly associated with GU, and it produces reflux in normal subjects and in patients with duodenal ulcer, which in turn is commonly associated with GU. Reflux has not been shown to precede either the gastritis or the gastric ulcer and probably persists despite ulcer healing. The pyloric spincter in the patient with GU probably contracts subnormally to endogenous or exogenous secretin or CCK. This can be explained by associated hypergastrinemia since antral acidification improves the response. Because the pylorus may be usually open, abnormal reflux may be related as much or more to disturbances of other gastroduodenal functions known to control the movement of chyme through what may be a relatively passive pyloric zone. Speculation from animal models implicates bile reflux in aspirin-induced and shock-related gastric ulceration and assigns to bile a possible explanation, in part at least, for the apparent therapeutic efficacy of a carbenoxalone derivative and an antipepsin agent. Similar speculation warrants a search in the patient with GU for abnormalities of gastroduodenal peristalsis-related electric activity and for impaired release of secretin, possibly from antral cells of production. Possible abnormal purinergic inhibition of the gastric fundus and pylorus also warrants further study.

Topics: Animals; Bile; Cholecystokinin; Disease Models, Animal; Duodenum; Gastric Mucosa; Gastrins; Gastritis; Gastroesophageal Reflux; Humans; Pyloric Antrum; Pylorus; Secretin; Stomach Ulcer

Topics: Adrenal Cortex Hormones; Anemia, Pernicious; Animals; Antigen-Antibody Complex; Antigens; Autoantibodies; Autoimmune Diseases; Chronic Disease; Dogs; Female; Gastric Mucosa; Gastrins; Gastritis; Guinea Pigs; Haplorhini; Humans; Immunity, Cellular; Intrinsic Factor; Male; Rabbits; Rats; Vitamin B 12 Deficiency

Topics: Adrenal Cortex Hormones; Adult; Anemia, Pernicious; Atrophy; Autoantibodies; Autoimmune Diseases; Binding Sites, Antibody; Child; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Immunity, Cellular; Immunoglobulin A; Immunoglobulin G; Intrinsic Factor; Vitamin B 12

Topics: Acetylcholine; Anemia, Pernicious; Atrophy; Calcium; Carcinoma; Catecholamines; Circadian Rhythm; Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Diseases; Hormones, Ectopic; Humans; Ligation; Pancreatic Ducts; Secretin; Stimulation, Chemical; Stomach Diseases; Stomach Neoplasms; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Cholecystokinin; Duodenal Ulcer; Duodenum; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Motility; Humans; Hydrogen-Ion Concentration; Hypertrophy; Intestinal Mucosa; Pepsin A; Secretory Rate; Vagus Nerve; Zollinger-Ellison Syndrome

Topics: Bile; Duodenal Ulcer; Gastric Mucosa; Gastrins; Gastritis; Humans; Hydrogen-Ion Concentration; Intestinal Mucosa; Ischemia; Permeability; Stomach Ulcer

Topics: Animals; Cats; Chronic Disease; Creatinine; Dogs; Duodenal Ulcer; Esophageal Achalasia; Esophageal Diseases; Gastric Mucosa; Gastrins; Gastritis; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Peptic Ulcer; Pyloric Antrum; Rats; Scleroderma, Localized; Stomach Neoplasms; Vagotomy; Zollinger-Ellison Syndrome

Topics: Animals; Aspirin; Atropine; Bile Acids and Salts; Cell Membrane Permeability; Ethanol; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Humans; Hydrogen; Hydrogen-Ion Concentration; Ion Exchange; Membrane Potentials; Pentagastrin; Pepsin A; Pyloric Antrum; Smoking; Sodium; Stomach Neoplasms

Topics: Anxiety Disorders; Aspirin; Bile Acids and Salts; Blood Group Antigens; Diet; Duodenal Ulcer; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Motility; Histamine; Humans; Hyperplasia; Male; Pentagastrin; Peptic Ulcer; Radioimmunoassay; Stomach Ulcer; Vagotomy

Topics: Adolescent; Adult; Aged; Anemia, Hypochromic; Anemia, Pernicious; Atrophy; Autoantibodies; Autoimmune Diseases; Chronic Disease; Female; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Postgastrectomy Syndromes; Stomach Neoplasms; Stomach Ulcer

Topics: Anemia, Pernicious; Autoantibodies; Chronic Disease; Diagnosis, Differential; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Intrinsic Factor; Schilling Test

Topics: Digestion; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Diseases; Gastrointestinal Neoplasms; Humans; Intestine, Small; Pancreas; Paraneoplastic Endocrine Syndromes; Stomach Neoplasms; Zollinger-Ellison Syndrome

Topics: Adrenal Cortex Hormones; Anemia, Pernicious; Animals; Antibodies; Autoantibodies; Biopsy; Chronic Disease; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Intrinsic Factor; Schilling Test; Stomach; Stomach Neoplasms; Stomach Ulcer; Vitamin B 12

Topics: Amino Acid Sequence; Anemia, Pernicious; Chronic Disease; Duodenal Ulcer; Duodenum; Esophagus; Feedback; Gastric Juice; Gastrins; Gastritis; Gastrointestinal Motility; Humans; Intestinal Mucosa; Jejunum; Muscle Tonus; Pancreas; Pyloric Antrum; Radioimmunoassay; Vagus Nerve; Zollinger-Ellison Syndrome

Topics: Diagnosis, Differential; Duodenal Ulcer; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Hydrogen-Ion Concentration; Hypertrophy; Intubation, Gastrointestinal; Stomach Neoplasms

Topics: Anemia, Pernicious; Chemical Phenomena; Chemistry; Duodenal Ulcer; Gastric Mucosa; Gastrins; Gastritis; Humans; Research; Zollinger-Ellison Syndrome

Topics: Anemia, Pernicious; Antibodies; Atrophy; Autoimmune Diseases; Capillaries; Chronic Disease; Dyspepsia; Gastrectomy; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Hypertrophy; Intrinsic Factor; Metaplasia; Mitosis; Pentagastrin; Pepsin A; Peptic Ulcer; Pyloric Antrum; Radiography; Stomach; Stomach Neoplasms; Thyroid Diseases; Vagotomy

Topics: Aspirin; Atropine; Bile Acids and Salts; Biological Transport; Cell Membrane Permeability; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Histamine; Humans; Hydrochloric Acid; Membrane Potentials; Peptic Ulcer; Potassium; Sodium; Stomach; Vagus Nerve

Topics: Acetylcholine; Achlorhydria; Adenoma; Anemia, Pernicious; Atrophy; Duodenal Ulcer; Endocrine System Diseases; Gastrectomy; Gastric Juice; Gastric Mucins; Gastric Mucosa; Gastrins; Gastritis; Humans; Hyperplasia; Intrinsic Factor; Stomach Ulcer; Vagus Nerve; Zollinger-Ellison Syndrome

Topics: Gastric Acidity Determination; Gastric Juice; Gastrins; Gastritis; Histamine; Humans; Inhalation; Intubation, Gastrointestinal; Methods; Peptic Ulcer; Radio; Radioisotopes; Radionuclide Imaging; Stomach; Stomach Neoplasms; Technetium; Vagotomy; Zollinger-Ellison Syndrome

Topics: Age Factors; Anemia, Pernicious; Antibodies; Atrophy; Bethanechol Compounds; Carbachol; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Histamine; Humans; Insulin; Intrinsic Factor; Methacholine Compounds; Vitamin B 12; Vitamin B 12 Deficiency

Prolonged gastric acid suppression leads to hypergastrinaemia, which promotes hyperplasia of the enterochromaffin-like (ECL) cells of the oxyntic mucosa. The objective was to determine the effects of 5 years of treatment with rabeprazole or omeprazole on the gastric mucosa.. Two hundred and forty-three patients received rabeprazole (20 mg or 10 mg) or omeprazole (20 mg) once daily for up to 5 years, for gastro-oesophageal reflux disease and 51% completed the whole 5 year period. Gastric biopsy specimens were taken and examined for gastritis, Helicobacter pylori infection, and ECL cell status.. H. pylori infection in the gastric corpus was more common than in the antrum, and remained constant, whereas antral H. pylori infection became less common as the study progressed. H. pylori infection was a highly significant predictor of higher gastritis scores, which were similar among the three treatment groups. ECL cell hyperplasia occurred in a minority of patients, and was associated with serum gastrin concentrations. No ECL cell dysplasia or tumours were observed. There were no significant differences among the treatment groups in gastritis or ECL cell hyperplasia grades.. This study has confirmed the link between ECL cell hyperplasia and elevated serum gastrin concentrations, but has found no evidence that this progresses to high grades of hyperplasia during 5 years of treatment with rabeprazole or omeprazole.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Anti-Ulcer Agents; Benzimidazoles; Biopsy; Disease Progression; Dose-Response Relationship, Drug; Double-Blind Method; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Hyperplasia; Male; Metaplasia; Middle Aged; Omeprazole; Prospective Studies; Proton Pump Inhibitors; Rabeprazole; Severity of Illness Index

To assess the possibility of non-invasive screening of atrophic chronic gastritis for preventing further development of gastric cancer.. One hundred and seventy-eight consecutive Helicobacter pylori (H pylori)-positive dyspeptic patients after detection of serum levels of pepsinogen-1 (PG-1) and gastrin-17 (G-17) by enzyme immunoassay were proposed for endoscopy and histology. The serologic and morphologic results were compared with estimating the sensitivity, specificity and prognostic values of the tests.. There was statistically significant reverse dependence between the grade of stomach mucosal antral or corpus atrophy and the proper decreasing of serum G17 or PG1 levels. The serologic method was quite sensitive in the diagnosis of non-atrophic and severe antral and corpus gastritis. Also, it was characterized by the high positive and negative prognostic values.. Detection of serum G-17 and PG1 levels can be offered as the screening tool for atrophic gastritis. The positive serologic results require further chromoendoscopy with mucosal biopsy, for revealing probable progressing of atrophic process with development of intestinal metaplasia, dysplasia or gastric cancer.

Topics: Atrophy; Biomarkers; Biopsy; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Mass Screening; Pepsinogen A; Precancerous Conditions; Sensitivity and Specificity

To explore the prevalence of autoimmune gastritis in chronic hepatitis C virus (HCV) patients and the influence of alpha-interferon (IFN) treatment on autoimmune gastritis.. We performed a prospective study on 189 patients with positive anti-HCV and viral RNA enrolled in a 12-month IFN protocol. We evaluated: a) the baseline prevalence of autoimmune gastritis, b) the impact of IFN treatment on development of biochemical signs of autoimmune gastritis (at 3, 6 and 12 months), c) the evolution after IFN withdrawal (12 months) in terms of anti-gastric-parietal-cell antibodies (APCA), gastrin, anti-thyroid, and anti-non-organ-specific antibodies.. APCA positivity and 3-fold gastrin levels were detected in 3 (1.6 %) and 9 (5 %) patients, respectively, at baseline, in 25 (13 %) and 31 (16 %) patients at the end of treatment (both P<0.001, vs baseline), and in 7 (4 %) and 14 (7 %) patients 12 months after withdrawal (P=0.002 and P=0.01 respectively, vs baseline; P=not significant vs end of treatment). The development of autoimmune gastritis was strictly associated with the presence of autoimmune thyroiditis (P =0.0001), no relationship was found with other markers of autoimmunity.. In HCV patients, IFN frequently precipitates latent autoimmune gastritis, particularly in females. Following our 12-month protocol, the phenomenon generally regressed. Since APCA positivity and high gastrin levels are associated with the presence of antithyroid antibodies, development of autoimmune thyroiditis during IFN treatment may provide a surrogate preliminary indicator of possible autoimmune gastritis to limit the need for invasive examinations.

Topics: Adult; Aged; Antiviral Agents; Autoimmune Diseases; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Hepatitis C, Chronic; Humans; Interferon-alpha; Male; Middle Aged; Organ Specificity; Parietal Cells, Gastric; Prevalence; Prospective Studies; Thyroid Gland; Treatment Outcome

We investigated an antiinflammatory effect of rebamipide [2-(4-chlorobenzoylamino)-3-[2(1H)-quinolinon-4-yl] propionic acid], a gastroprotective agent, in H. pylori-associated gastritis. Eighty-six patients with H. pylori-positive chronic gastritis were enrolled: 53 were treated with rebamipide (300 mg daily for 12 months) and 33 served as controls. Significant decreases in mononuclear cell infiltration into the antrum and corpus were noted in the rebamipide treatment group (before vs after, 1.42 +/- 0.15 vs 1.02 +/- 0.15; P < 0.01 and 1.60 +/- 0.15 vs 1.21 +/- 0.14; P < 0.05, respectively). Levels of infiltrating neutrophil were also decreased in the antrum (before vs after, 0.98 +/- 0.14 vs 0.70 +/- 0.13; P < 0.05) and were associated with a decrease in iNOS production. Sera from patients treated with rebamipide showed a significant decrease in gastrin (276.3 +/- 58.3 pg/ml vs 173.0 +/- 34.2 pg/ml; P < 0.05), whereas no change was observed in the control group. These suggest that long-term rebamipide treatment improved histologic gastritis and decreased serum gastrin levels in H. pylori-associated gastritis.

Topics: Alanine; Anti-Ulcer Agents; Drug Administration Schedule; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; Pepsinogens; Quinolones; Stomach

Pantoprazole is the third proton pump inhibitor to become available. When this study was started, there were few data on its long-term use. Our aim was to investigate this aspect and, because powerful inhibitors of acid secretion can cause hypergastrinemia and, in experimental animals, enterochromaffin-like cell hyperplasia, we also monitored serum gastrin and endocrine cell histology.. One hundred fifty patients refractory to H2-receptor antagonists, running an aggressive course or with complications, were entered into a 5-yr treatment program. We performed serial endoscopy, checked for adverse events, and laboratory values. We also monitored serum gastrin, gastric endocrine cell histology, and antral and corpus gastritis.. This report presents results from up to 3 yr of treatment. Cumulative healing on 40-80 mg of pantoprazole was 82% at 4 wk and 92% by 12 wk. Most patients became asymptomatic within 4 wk. Remission on maintenance treatment with 40 mg (n = 111) was 85% at 12 months and 78% at 24 months. Treatment was safe; only four patients had adverse events definitely related to pantoprazole. Elevations in gastrin were modest and there were no significant changes in gastric endocrine cells. The number of enterochromaffin-like cells tended to decrease.. Pantoprazole is effective, safe, and does not seem to be associated with large increases in serum gastrin or alterations in gastric endocrine cells.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adolescent; Adult; Aged; Anti-Ulcer Agents; Benzimidazoles; Cell Count; Drug Resistance; Enteroendocrine Cells; Enzyme Inhibitors; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole; Pantoprazole; Peptic Ulcer; Proton Pump Inhibitors; Recurrence; Sulfoxides

Gastric lipase contributes significantly to overall lipolysis and is regulated by interacting neuro-hormonal mechanisms. Patients with alcoholic chronic pancreatitis (ACP) have low, or even absent, activity of pancreatic lipases. In that state the secretion of gastric lipase could be essential and compensate for the pancreatic defect. However, conflicting studies have not resolved the order of magnitude of gastric lipase secretion in these patients. This could be explained by differences in regulatory mechanisms, gastric mucosal changes, and abdominal vagal tone.. Nasogastric intubation with modified sham feeding and upper endoscopy including biopsies for histologic classification and Helicobacter pylori infection status were performed in eight ACP patients, and eight healthy volunteers were studied on separate occasions. Vagal nerve function was assessed by calculation of heart rate variability in ACP patients. Gastric lipase was measured in aspirates by means of enzyme-linked immunosorbent assay and an enzyme kinetic assay. Plasma concentrations of gastrin, secretin, cholecystokinin, and pancreatic polypeptide were measured throughout the study.. Sham feeding rapidly and significantly increased gastric lipase secretion in healthy volunteers, whereas ACP patients did not respond to sham feeding. Two of eight patients were infected with H. pylori and had mucosal changes accordingly. The lack of lipase response could not be ascribed to dysfunction of the abdominal vagus.. The cephalic phase of gastric lipase secretion is impaired in ACP patients. Although their fundic cells continue to secrete gastric lipase, they are not subject to normal neuro-hormonal regulation.

Topics: Adult; Biopsy; Chronic Disease; Endoscopy, Digestive System; Enteral Nutrition; Exocrine Pancreatic Insufficiency; Female; Gastric Acid; Gastrins; Gastritis; Humans; Lipase; Lipolysis; Male; Middle Aged; Pancreatitis, Alcoholic

To determine the accuracy of blood tests in predicting normal gastric mucosa confirmed by histological examination of gastric biopsy specimens.. In total, 207 consecutive patients referred for upper endoscopy were included. Two biopsy specimens each from the antrum and corpus were assessed histologically for the presence of Helicobacter pylori, gastritis, and atrophy. Serum samples were studied for H. pylori antibodies by enzyme immunoassay (Pyloriset EIA-G and EIA-A) and by a rapid latex agglutination test (Pyloriset Dry); pepsinogen I was measured by an immunoenzymometric assay (Gastroset PGI), gastrin by radioimmunoassay, and parietal cell antibodies by indirect immunofluorescence.. In 101 (49%) of 207 patients, the gastric mucosa on histologic examination was normal. In the 63 patients aged 45 years or less, H. pylori IgG serology was negative in all 47 patients with normal gastric mucosa and none had low serum pepsinogen I levels. Among 144 patients over age 45 years, 72 had negative H. pylori IgG serology. Combining the serum pepsinogen I assay with the results of H. pylori IgG serology, 12 patients with normal serology but low serum pepsinogen I were found. Thus, 60 patients, 52 of whom showed normal gastric histology, had normal IgG serology and serum pepsinogen 1. In the remaining eight patients with normal blood tests, the histologic changes were very mild.. Although negative H. pylori IgG serology alone in younger patients, and in combination with normal serum pepsinogen I levels in older patients, reliably predicted the presence of normal gastric mucosa, gastroscopy is still recommended for patients over 45 years.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Biopsy, Needle; Blood Chemical Analysis; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Helicobacter pylori; Humans; Immunoglobulin G; Immunohistochemistry; Male; Middle Aged; Pepsinogen A; Predictive Value of Tests; Reference Values; Sensitivity and Specificity; Serologic Tests

Gastric acid secretion, gastrin release, gastric emptying, and gastroesophageal acid reflux were measured in asymptomatic individuals before and after elimination of Helicobacter pylori gastritis. After basal gastric acid secretion and serum gastrin concentrations were measured, meal-stimulated gastric acid secretion and gastrin release were assessed during in vivo intragastric titration to pH 3. Experiments were repeated 4 wk after treatment with lansoprazole, amoxicillin, and clarithromycin. Esophageal pH was also monitored for 24 h before and after therapy. Basal gastric acidity increased approximately 20 mmol/l in subjects whose infection was eradicated (P < 0.05) but not in those with persistent infection. Basal and meal-stimulated gastric acid secretion did not change after H. pylori eradication, despite a 41% reduction in meal-stimulated gastrin release (P < 0.05). Gastroesophageal acid reflux increased two- to threefold after successful treatment (P < 0. 05) but did not change in subjects with persistent infection. Thus elimination of H. pylori gastritis increases gastric acidity, probably by reducing nonparietal alkaline secretion, and this may facilitate gastroesophageal acid reflux.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Amoxicillin; Anti-Bacterial Agents; Anti-Ulcer Agents; Clarithromycin; Esophagitis; Female; Food; Gastric Acid; Gastric Emptying; Gastric Mucosa; Gastrins; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Lansoprazole; Male; Middle Aged; Monitoring, Physiologic; Omeprazole; Penicillins; Polyethylene Glycols; Postprandial Period; Solvents

The gastric irritation potential of orally administered coffee (150 ml) was investigated in four healthy volunteers by continuous measurement of gastric potential difference (GPD) and intragastric pH. Furthermore, serum gastrin concentrations were measured up to 45 min after administration of the coffee. One of the coffees, untreated, had to be compared with a pretreated coffee. The evaluation of the target parameters Reiz-Index, AUB, Pdmax and ttot revealed a significant difference between untreated coffee and specially treated coffee: the improved coffee processing produced significantly less mucosal irritation. Regarding the intragastric pH, no significant differences between the treatments were observed and no stimulation of gastric acid secretion following coffee was measurable. No consistent effect on serum gastrin concentration was seen: two of the four subjects had a steep increase in serum gastrin following administration with a clear difference between the differently processed coffees, whereas the other two subjects showed no change in serum gastrin. The results of this pilot study confirm the findings of former experiments on the reliability of continuous transmural GPD measurement when investigating the mucosal irritation potential of barrier breakers.

Topics: Coffee; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Humans; Hydrogen-Ion Concentration; Membrane Potentials; Reference Values

To date, it is unclear whether Helicobacter pylori infection is associated with disturbances of gastric emptying or acid secretion in patients with functional dyspepsia (FD). Our aim was to investigate whether, in the long run, cure of H. pylori infection significantly influences gastric emptying of solids, acid secretion, and gastrin and pepsinogen I (PGI) release in patients with FD.. Thirty-eight consecutive H. pylori-positive patients with FD, whose complaints were scored for severity and frequency on the basis of a validated symptom questionnaire, were initially enrolled in the study. They were randomized to receive an eradicating regimen consisting of omeprazole plus clarithromycin and tinidazole for 1 week or full-dose ranitidine for 3 weeks. In 33 patients (18 H. pylori-cured and 15 with persistent infection) basal and pentagastrin-stimulated acid secretion, fasting and meal-induced gastrin concentrations, fasting serum PGI levels, and gastric emptying of solids were determined before and 6 months after therapy.. In the 18 H. pylori-cured patients meal-induced gastrin and fasting PGI levels were significantly reduced after 6 months as compared with pretreatment values (peak serum gastrin, 76.0 +/- 23.4 versus 111.9+/-37.4 pg/ml; PGI, 57.1+/-23.4 versus 72.9+/-29.1 ng/ml), whereas they remained virtually unchanged in the 15 patients with persistent infection. In contrast, both basal and stimulated acid secretion and gastric emptying time of solids remained unmodified over time in both groups of patients.. We confirm that also in patients with functional dyspepsia H. pylori eradication in the long run significantly reduces gastrin and PGI release as a result of improvement in the underlying antral gastritis, but this is not accompanied by modifications of gastric emptying of solids or acid secretion.

Topics: Adult; Anti-Bacterial Agents; Anti-Ulcer Agents; Clarithromycin; Drug Therapy, Combination; Dyspepsia; Female; Gastric Acid; Gastric Emptying; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole; Pepsinogens; Prospective Studies; Ranitidine; Tinidazole; Treatment Outcome

Twelve patients with active duodenal ulcer disease and Helicobacter pylori infection were treated with 1 g sucralfate q.d.s. for 1 month. Ulcers healed in 8 of the 12 patients without an alteration in the H. pylori-associated antral gastritis. Sucralfate produced a significant fall in basal acid output in all the patients, from a median of 4.8 (range 2.1-12.1) to 1.6 (0.4-8) mmol/h, P less than 0.01, whereas peak acid output was unchanged from 41 (21-59) before to 38 (24-55) mmol/h after treatment. Basal plasma gastrin concentrations and the meal-stimulated integrated gastrin response were not altered significantly by sucralfate: 8 (2-17) pmol/L and 732 (188-1045) pmol. min/L pre-treatment and 6 (2-17) pmol/L and 600 (140-1302) pmol. min/L post-treatment, respectively. The fall in basal acid output observed may contribute to prolonged duodenal ulcer remission after treatment with sucralfate.

Topics: Adult; Aged; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pyloric Antrum; Sucralfate

Achlorhydric atrophic gastritis occurs in approximately 25% of patients with dermatitis herpetiformis (DH). The effect of gluten withdrawal on the gastric condition was studied in 35 patients, with a control group of 20 patients continuing their habitual diet. Gastrointestinal examinations were performed initially and repeated after about 1 3/4 years. Adherence to the diet was confirmed by dietary interviews, improvement of malabsorption test results and intestinal villous structure, and decreased dapsone requirement. Neither the non-restricted diet nor the gluten-free diet had any effect on gastric morphology, the ability to secrete gastric acid, serum gastrin levels, or the frequency or titres of circulating parietal cell antibodies. The findings indicate that gluten is not responsible for the perpetuation of the gastric affection in DH, in contrast to the enteropathy.

Topics: Adolescent; Adult; Aged; Antibodies; Dapsone; Dermatitis Herpetiformis; Female; Follow-Up Studies; Gastric Acid; Gastrins; Gastritis; Gastritis, Atrophic; Glutens; Humans; Intestinal Absorption; Intestine, Small; Male; Middle Aged; Parietal Cells, Gastric; Stomach

The clinical and physiological relevance of the relationship between gastrin and calcitonin has been investigated in normal subjects and in patients suffering from gastritis or duodenal ulcer. Basal plasma levels of calcitonin are increased in these patients but there is no significant relationship between calcitonin and gastrin levels. Acute pentagastrin injection in normal male subjects increased significantly (P less than 0.05) plasma calcitonin levels whereas lower doses of pentagastrin which are known to stimulate gastric secretion are without effect on calcitonin levels. Moreover, stimulation of gastrin secretion by a protein test meal and by intragastric administration of a calcium chloride solution is not followed by any significant increase of plasma calcitonin levels. These results suggest that the stimulation of calcitonin secretion by gastrin and its synthetic analogue pentagastrin is a pharmacological rather than a physiological phenomenon.

Topics: Adult; Anemia, Pernicious; Calcitonin; Calcium Chloride; Dietary Proteins; Duodenal Ulcer; Gastrins; Gastritis; Humans; Injections, Intravenous; Male; Pentagastrin

The effect of carbenoxolone on the healing of gastric ulcer and erosions was compared with that of placebo. The series consisted of 20 patients with chronic gastric ulcers and 20 patients with superficial erosions of the stomach. The diagnosis as well as the follow-up of the lesions were based on gastroscopic examinations. The ulcers were measured gastroscopically. A double-blind method was used. Besides carbenoxolone 50 mg or placebo three times daily, all the patients received antacids in fixed dosage for six weeks. Subjective symptoms and cardiovascular side-effects were recorded. Maximal acid output and serum gastrin levels were measured before and after the treatment. No difference was seen between carbenoxolone and placebo groups with regard to the healing rate of the ulcers of disappearance of the erosions. The subjective symptoms subsided significantly faster in the treatment groups than in the control groups. No cardiovascular side-effects were evident during the treatment with carbenoxolone. One patient needed potassium supplements. Carbenoxolone had no effect on the pentagastrin-stimulated gastric acid secretion nor on the serum gastrin values.

Topics: Carbenoxolone; Clinical Trials as Topic; Double-Blind Method; Drug Evaluation; Follow-Up Studies; Gastric Juice; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Humans; Stomach Ulcer; Triterpenes

The effect of continuous versus interrupted high-dose aspirin (ASA) for 14 days was evaluated in a randomized double-blind study in 8 rheumatoid arthritis patients. Acute gastric mucosal injury was measured by serial gastroscopy and gastric biopsy. Significant gross mucosal damage was seen in all patients following 3 days of ASA (P less than 0.01) and persisted without significant change in severity to the end of the study. Histologic gastritis in areas free of hemorrhages and erosions was not increased significantly by ASA. In spite of gross mucosal injury, symptoms occurred infrequently. Serum pepsinogen I, but not serum gastrin, increased significantly following 3 days of ASA, and the elevation persisted to the end of the study. The extent of mucosal injury at 14 days was not significantly different in those receiving ASA continuously from those on an interrupted schedule. Thus, gastric mucosal adaptation to ASA in man was not demonstrated.

Topics: Arthritis, Rheumatoid; Aspirin; Clinical Trials as Topic; Dose-Response Relationship, Drug; Drug Evaluation; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Male; Middle Aged; Pepsinogens; Pyloric Antrum; Time Factors

Topics: Adolescent; Adult; Aged; Benzamides; Clinical Trials as Topic; Drug Evaluation; Duodenal Ulcer; Female; Gastrins; Gastritis; Gastrointestinal Agents; Glutarates; Humans; Male; Middle Aged; Peptic Ulcer; Stomach Ulcer

Stomach cancer is a leading cause of cancer death. Helicobacter pylori is a bacterial gastric pathogen that is the primary risk factor for carcinogenesis, associated with its induction of inflammation and DNA damage. Dicarbonyl electrophiles are generated from lipid peroxidation during the inflammatory response and form covalent adducts with amine-containing macromolecules. 2-hydroxybenzylamine (2-HOBA) is a natural compound derived from buckwheat seeds and acts as a potent scavenger of reactive aldehydes. Our goal was to investigate the effect of 2-HOBA on the pathogenesis of H. pylori infection. We used transgenic FVB/N insulin-gastrin (INS-GAS) mice as a model of gastric cancer. First, we found that 2-HOBA is bioavailable in the gastric tissues of these mice after supplementation in the drinking water. Moreover, 2-HOBA reduced the development of gastritis in H. pylori-infected INS-GAS mice without affecting the bacterial colonization level in the stomach. Further, we show that the development of gastric dysplasia and carcinoma was significantly reduced by 2-HOBA. Concomitantly, DNA damage were also inhibited by 2-HOBA treatment in H. pylori-infected mice. In parallel, DNA damage was inhibited by 2-HOBA in H. pylori-infected gastric epithelial cells in vitro. In conclusion, 2-HOBA, which has been shown to be safe in human clinical trials, represents a promising nutritional compound for the chemoprevention of the more severe effects of H. pylori infection.

Topics: Animals; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Mice; Stomach Neoplasms

Gastric polyps represent an abnormal proliferation of the gastric mucosa. Chronic atrophic autoimmune gastritis (CAAG) targets parietal cells and results in hypo-achlorhydria and hypergastrinemia, which exerts a proliferative effect on the gastric mucosa.. We investigate the incidence of gastric polyps in CAAG patients.. This is a single-center retrospective study examining patients with confirmed CAAG from January 1990 until June 2022. Demographic, clinical, biochemical, and serological data were collected for each included patient. The histopathological characteristics of the detected polyps were recorded.. A total of 176 CAAG patients were included. Eighty-nine (50.5%) had 163 incidental polyps. Seventy-six patients (85%) had 130 non-endocrine lesions, among which 118 (90.7%) were inflammatory, 6 (4.6%) adenomatous, and 4 (3%) fundic; 33 patients (37%) had gastric neuroendocrine neoplasms (gNENs), and 21 (23.6%) both; one had MALToma and one gastric adenocarcinoma. Higher circulating levels of gastrin and chromogranin A were observed among patients with polyps (median 668 vs 893 pg/ml p = 0.0237, 146 vs 207 ng/ml p = 0.0027, respectively).. CAAG implies a high incidence of gNENs and exocrine lesions. Gastrin plays a possible trophic role on the mucosa. Further evidence is needed to validate its predictive role for increased polyp risk in CAAG.

Topics: Autoimmune Diseases; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Polyps; Precancerous Conditions; Retrospective Studies; Stomach Neoplasms

The ABC method, which combines the pepsinogen method and anti-Helicobacter pylori antibody titers, has been used for risk screening for gastric cancer in Japan. However, it has been reported that there are cases of gastritis and carcinogenesis risk even in group A, which is considered to be a low-risk group based on the ABC method. Currently, in group A, endoscopic examination is needed to strictly discriminate "patients without gastritis" (defined as true A patients) from those "with gastritis." A simple and minimally invasive diagnostic criterion for gastritis using serological markers is desirable. In this study, we aimed to identify the normal serum gastrin concentrations in normal stomach cases based on pathological diagnosis and investigate the usefulness of serum gastrin concentrations in diagnosing gastritis.. Patients who underwent endoscopy and blood tests at Hiroshima University Hospital were enrolled in the study and categorized into the "pathologically-evaluated group" and "endoscopically-evaluated group," according to the evaluation method of atrophic gastritis. Initially, we measured serum gastrin concentrations in the normal stomach cases in the pathologically-evaluated group and calculated the normal range of serum gastrin concentrations. We used the upper limit of this normal range of serum gastrin concentrations and performed a validation study to determine its usefulness as a diagnostic marker for distinguishing between cases of gastritis and true A in the endoscopically-evaluated group.. The 95th percentile of serum gastrin concentrations in pathologically-evaluated normal stomach cases was 34.12-126.03 pg/mL. Using the upper limit of this normal range of serum gastrin concentrations, the sensitivity, specificity, positive predictive value, and negative predictive value for gastritis were 52.8%, 92.6%, 97.0%, and 31.0%, respectively. Additionally, the receiver operating characteristic (ROC) curve for the endoscopically-evaluated group showed an area under the ROC curve of 0.80.. The gastrin cut-off value of 126 pg/mL has a good positive predictive value (97.0%) for detecting gastritis positing its use as a marker for cases requiring endoscopy. However, the identification of patients with gastritis having normal serum gastrin concentrations due to insufficient sensitivity remains a challenge for the future.

Topics: Biomarkers; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Humans; Pepsinogen A; Reference Values; Retrospective Studies; Stomach Neoplasms

To elucidate the chemical profile and the pharmacological mechanism by which Jinlingzi powder (, JLZP) treats bile reflux gastritis (BRG).. A BRG model was established in rats by oral administration of the model solution. JLZP was orally administered for 35 d. Residual gastric rate and tumor necrosis factor (TNF)-α, interleukin (IL)-6, and gastrin levels in the serum were measured, and stomach tissues were collected for histopathological analysis. We used ultra-high performance liquid chromatography coupled with Q Exactive Focus mass spectrometry to identify the chemical ingredients in JLZP. Then, protein-protein interaction and herb-compound-target networks were constructed to screen potential bioactive compounds and targets. Kyoto Encyclopedia of Genes and Genomes pathway analysis was then performed to elucidate the pathway involved in the JLZP-mediated treatment of BRG. After constructing the core compound-target-pathway interaction network, molecular docking was performed to study the binding free energy of core bioactive compounds and two candidate targets [RAC-alpha serine/threonine-protein kinase (AKT1) and phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform (PIK3CA)].. JLZP extracts significantly promoted gastric emptying, regulating the release of cytokines (TNF-α and IL-6) and improving gastrin secretion and mucosal repair. Fifty-six compounds were tentatively characterized in JLZP. Moreover, the network pharmacology and molecular docking results showed that alkaloids and flavonoids might be the bioactive compounds in JLZP that treat BRG. JLZP might improve mucosal repair during BRG progression by modulating the phosphatidylinositol-4,5-bisphosphate 3-kinase-protein kinase B, hypoxia inducible factor-1, mitogen-activated protein kinase, forkhead box O, TNF, and IL-17 signaling pathways.. We elucidated the chemical constituents and the pharmacological mechanism of JLZP in treating BRG and provided a basis for clinical application.

Topics: Animals; Bile Reflux; Chromatography, High Pressure Liquid; Drugs, Chinese Herbal; Gastrins; Gastritis; Molecular Docking Simulation; Network Pharmacology; Phosphatidylinositols; Powders; Rats; Tumor Necrosis Factor-alpha

The aims of the present study are to evaluate non-invasive screening tests for autoimmune gastritis (AIG) and re-evaluate histopathological classification.. We screened candidates of AIG in JCHO Shiga Hospital between May 2012 and January 2020. The screening criteria were as follows: endoscopic O-p atrophy with Updated Kimura-Takemoto classification, 3 + pepsinogen (PG) test, low serum vitamin B. Twenty-two of 28 (78.6%) patients who met the screening criteria were histopathologically confirmed as AIG. Common clinical findings in the AIG patients were 10 × or greater anti-PC antibody, elevated serum gastrin greater than 172 pg/mL and endoscopic atrophy O-1 or greater. The areas under the curve of PG I, PG II and PG I/II ratio were 0.81, 0.29 and 0.98, respectively. Among histopathologically confirmed AIG patients, 4 and 18 patients were histopathologically classified into florid and end stages, respectively, while no patients into early stage. We could not find a significant difference between florid and end stages in the screening items studied.. Florid and end stages in histopathological classification are both advanced-stage AIG in clinical aspects. Our screening criteria without biopsy are applicable to screen clinically-advanced AIG with 78.6% positive predictive value. PG I and PG I/II ratio may be useful to screen AIG. However, we may need other criteria to screen early stage of AIG.

Topics: Atrophy; Autoimmune Diseases; Gastrins; Gastritis; Humans; Japan; Pepsinogen A

The clinical spectrum of autoimmune gastritis is silent in the early stages of the disease and no specific symptom is related to this entity. Although gastroscopic findings of this entity are well defined, data regarding colonoscopic findings are limited. The aims of this study were to determine the prevalence of colonoscopic findings and to explore factors that might affect these findings. This is a retrospective chart review of patients with autoimmune gastritis (n=240). Data regarding colonoscopic findings, serum gastrin and chromogranin A (CgA) levels and gastric histopathological results were extracted and compared with 550 patients positive for

Topics: Adult; Aged; Chromogranin A; Colonoscopy; Colorectal Neoplasms; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Precancerous Conditions; Prevalence; Retrospective Studies

PPI use,

Topics: Aged; Amino Acid Sequence; Animals; Arthropod Proteins; Cloning, Molecular; Endoscopy, Digestive System; Fasting; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Invertebrate Hormones; Male; Middle Aged; Nerve Tissue Proteins; Ovary; Penaeidae; Precancerous Conditions; Proton Pump Inhibitors; Stomach Neoplasms; Vitellogenesis; Vitellogenins

Patients with autoimmune atrophic gastritis (AAG) often complain of acid reflux symptoms, despite the evidence of hypo-achlorhydria. Rome IV criteria are used to define functional esophageal disorders. Our aim was to characterize gastroesophageal reflux disease (GERD) phenotypes in patients with AAG.. Between 2017-2018, 172 AAG patients were evaluated at Gastro-Oncology outpatient clinic of University of Padua. Of them, 38 patients with reflux symptoms underwent high-resolution manometry (HRM) and multichannel intraluminal impedance-pH monitoring (MII-pH). Seventy-six AAG consecutive patients asymptomatic for gastroesophageal reflux were selected as age and gender matched controls. Serum biomarkers (pepsinogens, gastrin-17 and Helicobacter pylori antibodies), upper endoscopy, histology and clinical data were compared.. Out of 38/172 (22%) AAG patients with reflux symptoms, 2/38 had a GERD diagnosis based on abnormal esophageal acid exposure and 6/38 had a major motility disorder (i.e. outflow obstruction). Among the 30/38 patients with normal endoscopic findings, 9/30 had reflux hypersensitivity, 19 functional heartburn, 1 functional globus, 1 functional chest pain according to the Rome IV criteria. Antral atrophy, advanced corpus atrophy and OLGA stage were more frequent in controls than in reflux patients (p=0.01, p=0.031, p=0.01, respectively). No differences were found for serum biomarkers and symptom presentation. Most of the patients received proton pump inhibitors (PPIs) treatment (87%), with a minority (34%) reporting clinical benefit.. Reflux symptoms are relatively common in AAG patients, but a firm diagnosis of GERD is rare (5%), whereas most of the patients have a functional disorder. PPI treatment is mostly clinical ineffective and should not be largely indicated.

Topics: Aged; Antibodies, Bacterial; Autoimmune Diseases; Biomarkers; Endoscopy, Digestive System; Gastrins; Gastritis; Gastroesophageal Reflux; Helicobacter pylori; Humans; Italy; Male; Middle Aged; Pepsinogens; Prospective Studies; Proton Pump Inhibitors

Gastrin regulates gastric acid secretion, and gastrin secretion itself is regulated by the negative feedback system of gastric acidity. Autoimmune gastritis (AG) is a disease where parietal cells are destroyed, resulting in decreased acid production and an elevated serum gastrin level. We herein report 2 AG cases with marked hypergastrinemia (>5,000 pg/mL). In both cases, 24-hour gastric pH monitoring showed no time when gastric pH was <2, and immunohistochemistry revealed more than 140 gastrin-positive cells per linear millimeter at the antral mucosa. This is the first report to confirm the relationship between marked hypergastrinemia and G-cell hyperplasia with AG.

Topics: Aged; Autoimmune Diseases; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Hyperplasia; Immunohistochemistry

The glycoprotein chromogranin A (CgA) is expressed by endocrine and neuroendocrine cells. High levels of serum CgA serve as markers of neuroendocrine tumors (NET), but its role in autoimmunity has not been assessed.. To investigate CgA utility as a marker of endocrine autoimmunity.. CgA serum levels were evaluated in 807 consecutive unselected participants (cross-sectional study) with the time-resolved amplified cryptate emission technology.. Serum CgA concentrations were increased in 66%, 39%, 38%, and 24% of patients with NET, type 1 diabetes (T1D), autoimmune gastritis (AG) and autoimmune polyendocrinopathy (AP), respectively. Compared with healthy participant controls (C), the odds of positive CgA measurement were up to 28 times higher in the disease groups. In detail, the odds ratios (ORs) for positive CgA levels were 27.98, 15.22, 7.32 (all P < 0.0001) and 3.89 (P = 0.0073) in patients with NET, T1D, AG, and AP, respectively. In AG, CgA and serum gastrin correlated positively (r = 0.55; P < 0.0001). The area under the receiver operating characteristic curve to predict AG was higher for parietal cell antibody (PCA) positivity than for CgA (0.84 vs 0.67; P < 0.0001). However, in combination with PCA and intrinsic factor autoantibodies, CgA independently improved prediction of AG (OR 6.5; P = 0.031). An impact of age on CgA positivity and on CgA value was detected (P < 0.0001) while current smoking significantly increased CgA serum levels by 25% (P = 0.0080).. CgA qualifies as a novel biomarker for T1D, AP, and AG.

Topics: Adolescent; Adult; Aged; Autoantibodies; Autoimmunity; Biomarkers; Chromogranin A; Cross-Sectional Studies; Diabetes Mellitus, Type 1; Female; Gastrins; Gastritis; Healthy Volunteers; Humans; Male; Middle Aged; Neuroendocrine Tumors; Polyendocrinopathies, Autoimmune; Predictive Value of Tests; ROC Curve; Young Adult

Chronic autoimmune gastritis (CAG) is a continuum of histological changes in gastric mucosa including: atrophy, intestinal metaplasia, dysplasia and finally, the occurrence of a neoplasm (gastric Neuroendocrine Tumors -NETs- and adenocarcinoma). The association with Hashimoto and Graves-Basedow disease is known as the thyrogastric autoimmune syndrome. While Helicobacter pylori (Hp) infection may be associated with CAG, the role of the gastric microbiota is ill-defined. The gastric hypochlorhydria determines a malabsorption of different micronutrients (iron, magnesium, calcium, vitamin B12) as well as drugs (thyroxine, etc.). Pernicious anemia is favoured by the deficit of parietal intrinsic factor that contributes to B12 malabsorption. Serology for Hp, serum pepsinogen I/II, increased gastrin levels, the presence of parietal cell antibodies and intrinsic factor antibodies may reveal CAG. High definition endoscopy associated with virtual chromoendoscopy seems promising for CAG diagnosis and follow-up. NETs type 1 treatment includes: endoscopic and surgical resection, somatostatin analogues and the recent availability of netazepide, a gastrin antagonist. We review herein advances in the treatment and diagnosis of CAG and associated autoimmune disorders, which may involve, in a multidisciplinary way, all practitioners.. La gastrite chronique auto-immune (GAI) est un continuum d’altérations de la muqueuse gastrique incluant : atrophie, métaplasie intestinale, dysplasie et, enfin, la survenue d’une néoplasie (tumeurs neuroendocrines [NETs] gastriques et adénocarcinome). L’association avec la maladie de Hashimoto et de Graves-Basedow est connue comme syndrome thyrogastrique auto-immun. Alors que l’Helicobacter pylori (Hp) peut s’associer avec la GAI, le rôle du microbiote gastrique est mal défini. L’hypochlorhydrie gastrique détermine une malabsorption de micronutriments (fer, magnésium, calcium, vitamine B12) et de médicaments (thyroxine et autres). L’anémie de Biermer est favorisée par le déficit de production du facteur intrinsèque pariétal, contribuant à la malabsorption de B12. Un rapport diminué de pepsinogène I/II, une augmentation de la gastrine, la présence d’anticorps anti-cellule pariétale, les anticorps anti-facteur intrinsèque et la sérologie pour Hp contribuent à révéler précocement le diagnostic de GAI. L’endoscopie haute définition, associée à la chromoendoscopie virtuelle, semble prometteuse dans le diagnostic et dans le suivi. Le traitement des NETs gastriques de type 1, favorisées par la GAI, inclut : la résection endoscopique/chirurgicale, les analogues de la somatostatine et l’antagoniste de la gastrine nétazépide. Nous résumons ici les avancées diagnostiques et thérapeutiques dans la GAI et dans les affections associées : elles impliquent, de façon multidisciplinaire, l’ensemble des praticiens.

Topics: Autoimmune Diseases; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans

Autoimmune gastritis patients may have autonomic nerve dysfunction. The goal of our study was to explore the predictive value of two scoring systems in the differentiation of altered autonomic nerve function in autoimmune gastritis patients.. Seventy-five patients with autoimmune gastritis were evaluated by using cardiovascular reflex tests in order to delineate autonomic nerve function. Data were analyzed by using two laboratory-based scoring systems: "global score" (hemoglobin, mean corpuscular volume, gastrin, vitamin B12, and chromogranin A) and "simple score" (hemoglobin, mean corpuscular volume, gastrin) in order to discriminate deranged and normal autonomic nerve function.. Mean "simple" and "global" scores were significantly higher in subjects with altered autonomic dysfunction than in subjects with normal autonomic function (3.55±1.88 vs. 0.908±0.409, p<0.001 and 5.95±2.07 vs 2.46±1.28, p<0.001, respectively). Receiver operatör characteristic (ROC) analysis revealed that the optimum "simple score" cutoff point was 0.75 with a sensitivity of 86.7% and specificity of 92.3% for discriminating autoimmune gastritis patients with autonomic nerve dysfunction from patients with normal autonomic nerve function [area under the curve (AUC): 88.3, positive predictive value (PPV): 97.5% and negative predictive value (NPV): 66.6%; 95% confidence interval (CI), 88.4-99.7].. Simple score and global score have a high predictive value in the assessment of autoimmune gastritis patients with autonomic nerve dysfunction. These scoring systems may help physicians while evaluating autoimmune gastritis patients for the existence of autonomic nerve dysfunction instead of complex cardiovascular reflex tests.

Topics: Area Under Curve; Autoimmune Diseases; Autonomic Nervous System; Autonomic Nervous System Diseases; Chromogranin A; Erythrocyte Indices; Gastrins; Gastritis; Hemoglobins; Humans; Predictive Value of Tests; ROC Curve; Sensitivity and Specificity; Severity of Illness Index; Vitamin B 12

Nano TiO

Topics: Animals; Cyclooxygenase 2; Cytokines; Gastrins; Gastritis; Gene Expression Regulation; Male; Metal Nanoparticles; Mice; Mice, Inbred ICR; Myocytes, Smooth Muscle; NF-kappa B; Stomach; Titanium; Trefoil Factor-1; Trefoil Factor-2; Tumor Necrosis Factor-alpha

Topics: Biological Assay; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans

Topics: Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Pepsinogen A

Elderly patients with autoimmune gastritis might have different symptoms than those of young patients. The aim of the present study was to compare presented symptoms and laboratory parameters associated with autoimmune gastritis in both old and young age groups.. A total of 355 patients with autoimmune gastritis were stratified into two groups: 65 years or older (n = 119, mean age 69.47 ± 5.027 years), and under 65 years (n = 236, mean age 45.79 ± 10.51 years). These two groups were then evaluated and compared by means of clinical symptoms, concurrent autoimmune diseases, serum gastrin, vitamin B

Topics: Adult; Age Distribution; Aged; Analysis of Variance; Autoimmune Diseases; Cohort Studies; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Multivariate Analysis; Prevalence; Prognosis; Retrospective Studies; Risk Assessment; Severity of Illness Index; Statistics, Nonparametric; Vitamin B 12

To assess characteristics of oxyntic gastric atrophy (OGA) in autoimmune gastritis (AIG) compared with OGA as a consequence of Helicobacter pylori infection.. Patients undergoing oesophagogastroduodenoscopy from July 2011 to October 2014 were prospectively included (N=452). Gastric biopsies were obtained for histology and H. pylori testing. Serum gastrin-17 (G17), pepsinogen (PG) I, PGII and antibodies against H. pylori and cytotoxin-associated gene A protein were determined in all patients. Antibodies against parietal cells and intrinsic factor were determined in patients with advanced (moderate to severe) OGA. Areas under the receiver operating characteristic curves (AUCs) were calculated for serum biomarkers and compared with histology.. Overall, 34 patients (8.9%) had advanced OGA by histology (22 women, age 61±15 years). Current or past H. pylori infection and AIG were present in 14/34 and 22/34 patients, respectively. H. pylori-negative AIG patients (N=18) were more likely to have another autoimmune disease (OR 6.3; 95% CI 1.3 to 29.8), severe corpus atrophy (OR 10.1; 95% CI 1.9 to 54.1) and corpus intestinal metaplasia (OR 26.9; 95% CI 5.3 to 136.5) compared with H. pylori-positive patients with advanced OGA. Antrum atrophy was present in 39% of H. pylori-negative AIG patients. The diagnostic performance of G17, PG I and PGI/II was excellent for AIG patients (AUC=0.83, 0.95 and 0.97, respectively), but limited for H. pylori-positive patients with advanced OGA (AUC=0.62, 0.75 and 0.67, respectively).. H. pylori-negative AIG has a distinct clinical, morphological and serological phenotype compared with advanced OGA in H. pylori gastritis.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Atrophy; Autoimmune Diseases; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Humans; Male; Middle Aged; Pepsinogen A; Prospective Studies; Young Adult

Green tea catechins (GTCs) have been implicated in various physiological effects, including anti-carcinogenic activities. In the present study, we evaluated the effects of GTCs specifically on the development of gastritis and pre-malignant lesions in insulin-gastrin mice. Nine-week-old male INS-GAS mice (n=38) were supplemented with GTCs for 4 and 28 weeks, and their body weights, serum gastrin levels, histopathology and pro-inflammatory cytokine levels in gastric tissue and mucosal cell proliferation were monitored. Body weights of the GTC-treated mice were significantly lower than those of the untreated controls (P≤0.05). Serum gastrin levels were suppressed at the age of 37-weeks (P≤0.05). The histopathological scores indicated that the extent of dysplasia was significantly diminished (P≤0.05), although GTC supplementation did not affect the inflammation scores. The messenger RNA levels of interferon (IFN)-γ were significantly reduced at the age of 13 weeks (P≤0.05), although the changes did not reach statistical significance at the age of 37 weeks (P=0.056). The labeling index of Ki-67 immunohistochemistry was significantly decreased (P≤0.05). These results demonstrated that GTCs may play a protective role in the development of gastritis and pre-malignant lesions via an IFN-γ, gastrin, and mucosal cell proliferation-dependent mechanism in this rodent model and potentially in humans.

Topics: Animals; Anticarcinogenic Agents; Body Weight; Camellia sinensis; Catechin; Cell Proliferation; Drug Evaluation, Preclinical; Epithelial Cells; Gastric Mucosa; Gastrins; Gastritis; Interferon-gamma; Male; Mice; Stomach Neoplasms

Collagenous gastritis is a rare condition defined histologically by a superficial subepithelial collagen layer. This study further characterizes the morphologic spectrum of collagenous gastritis by evaluating a multi-institutional series of 40 patients (26 female and 14 male). The median age at onset was 16 years (range 3-89 years), including 24 patients (60%) under age 18. Twelve patients (30%) had associated celiac disease, collagenous sprue, or collagenous colitis. Hematoxylin and eosin slides were reviewed in biopsies from all patients and tenascin, gastrin, eotaxin, and IgG4/IgG immunohistochemical stains were applied to a subset. The distribution of subepithelial collagen favored the body/fundus in pediatric patients and the antrum in adults. There were increased surface intraepithelial lymphocytes (>25 lymphocytes/100 epithelial cells) in five patients. Three of these patients had associated celiac and/or collagenous sprue/colitis, while the remaining two had increased duodenal lymphocytosis without specific etiology. An eosinophil-rich pattern (>30 eosinophils/high power field) was seen in 21/40 (52%) patients. Seven patients' biopsies demonstrated atrophy of the gastric corpus mucosa. Tenascin immunohistochemistry highlighted the subepithelial collagen in all 21 specimens evaluated and was a more sensitive method of collagen detection in biopsies from two patients with subtle subepithelial collagen. No increased eotaxin expression was identified in 16 specimens evaluated. One of the twenty-three biopsies tested had increased IgG4-positive cells (100/high power field) with an IgG4/IgG ratio of 55%. In summary, collagenous gastritis presents three distinct histologic patterns including a lymphocytic gastritis-like pattern, an eosinophil-rich pattern, and an atrophic pattern. Eotaxin and IgG4 were not elevated enough to implicate these pathways in the pathogenesis. Tenascin immunohistochemistry can be used as a sensitive method of collagen detection.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Celiac Disease; Chemokine CCL11; Child; Child, Preschool; Colitis, Collagenous; Collagen; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Immunoglobulin G; Male; Middle Aged; Stomach; Tenascin; Young Adult

Gastric acidic abnormalities are related to various types of diseases in Helicobacter pylori (H. pylori) infection status. However, no studies have shown correlations between many tiny endoscopic findings and the acid secretion level simultaneously. In the present study, we investigated predictive tiny endoscopic findings of hyperchlorhydria and hypochlorhydria.. A total of 223 subjects without organic diseases who underwent esophagogastroduodenoscopy and endoscopic gastrin test (EGT) for estimating gastrin-stimulated gastric acid secretory response between 1999 and 2012 at our institution were retrospectively analyzed. Two blinded expert endoscopists reviewed the images independently and recorded the endoscopic findings.. According to the EGT values, the enrolled subjects were categorized into hyperchlorhydria, normal acid secretion, and hypochlorhydria groups. In all subjects, hematin (odds ratio [95% confidence interval] = 3.32 [1.40-7.84]) and antral erosion(2.88 [1.24-6.70]) were the predictive endoscopic findings for hyperchlorhydria, and swelling of areae gastricae (14.4 [5.74-36.1]) and open-type atrophy (15.1 [7.35-31.1]) were those for hypochlorhydria. In addition, the predictive endoscopic findings for hyperchlorhydria differed according to the H. pylori infection status, hematin in H. pylori-positive subjects and antral erosion in H. pylori-negative subjects, in contrast to those for hypochlorhydria, which were the same irrespective of the H. pylori infection status.. We could predict the acid secretion status based on the endoscopic findings regardless of H. pylori infection status, which would be of some help for evaluating the risk for acid-related diseases.

Topics: Adult; Aged; Aged, 80 and over; Endoscopy, Gastrointestinal; Female; Follow-Up Studies; Gastric Acid; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Humans; Male; Middle Aged; Reproducibility of Results; Retrospective Studies; ROC Curve; Young Adult

The antibacterial and anti-inflammatory activities, and protective effects of extracts (flavonoid glycosides) of Polygonum capitatum were investigated to detect the evidence for the utilization of the herb in the clinical therapy of gastritis caused by H. pylori. A mouse gastritis model was established using H. pylori. According to treating methods, model mice were random assigned into a model group (MG group), a triple antibiotics group (TG group, clarithromycin, omeprazole and amoxicillin), low/middle/high concentrations of flavonoid glycosides groups (LF, MF and HF groups) and low/middle/high concentrations of flavonoid glycosides and amoxicillin groups (LFA, MFA and HFA groups). A group with pathogen-free mice was regarded as a control group (CG group). The eradicate rates of H. pylori were 100%, 93%, 89% in TG, MFA and HF groups. The serum levels of IFN-gamma and gastrin were higher in a MG group than those from all other groups (P < 0.05). The serum levels of IFN-gamma and gastrin were reduced significantly in LF, MF and HF groups (P < 0.05) while little changes were observed in LFA, MFA and HFA groups. In contrast, the serum levels of IL-4 were lower and higher in MG and CG groups compared with other groups (P<0.05). The serum levels of IL-4 were increased significantly in LF, MF and HF groups (P < 0.05) while little changes were found in LFA, MFA and HFA groups. According to pathological scores, flavonoid glycosides therapy showed better protection for gastric injuries than the combination of flavonoid glycoside and amoxicillin (P < 0.05). The results suggested that flavonoid glycoside has repairing functions for gastric injuries. The results suggest that the plant can treat gastritis and protect against gastric injuries. The flavonoid glycosides from Polygonum capitatum should be developed as a potential drug for the therapy of gastritis caused by H. pylori.

Topics: Animals; Anti-Bacterial Agents; Female; Flavonoids; Gastrins; Gastritis; Glycosides; Helicobacter Infections; Helicobacter pylori; Inflammation; Interferon-gamma; Male; Mice; Mice, Inbred C57BL; Phytotherapy; Polygonum

Toll-like receptor 4 is a part of the innate immune system and recognizes Helicobacter pylori lipopolysaccharide. The goal of this study was to analyze the role of Toll-like receptor 4 polymorphisms +896 (rs4986790) and +1196 (rs4986791) in the pathogenesis of Helicobacter pylori related gastroduodenal diseases in relation to gastric secretion and inflammation. Toll-like receptor 4 polymorphisms, serum gastrin-17 and pepsinogen I and II concentrations were determined, and gastroscopies with histopathological analyses were performed to 216 dyspeptic patients. As genotype controls, 179 controls and 61 gastric cancer patients were studied. In our study, the Toll-like receptor 4 +896 and +1196 polymorphisms were in total linkage disequilibrium. The homozygous wild types displayed higher gastrin-17 serum concentrations than the mutants (p = 0.001) and this effect was independent of Helicobacter pylori. The homozygous wild types also displayed an increased risk for peptic ulcers (OR: 4.390). Toll-like receptor 4 genotypes did not show any association with Helicobacter pylori positivity or the features of gastric inflammation. Toll-like receptor 4 expression was seen in gastrin and somatostatin expressing cells of antral mucosa by immunohistochemistry. Our results suggest a role for Toll-like receptor 4 in gastric acid regulation and that the Toll-like receptor 4 +896 and +1196 wild type homozygozity increases peptic ulcer risk via gastrin secretion.

Topics: Adult; Aged; Aged, 80 and over; Female; Gastrins; Gastritis; Gene Frequency; Genetic Predisposition to Disease; Genotype; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Peptic Ulcer; Polymorphism, Single Nucleotide; Risk Factors; Stomach Neoplasms; Toll-Like Receptor 4; Young Adult

To detect the clinical diagnostic criteria for non-invasive diagnosis of erosive gastritis in children with juvenile arthritis have been studied the 92 children aged 9 to 16 years (mean age-13,9 ± 2,3 years) with verified diagnosis of juvenile arthritis, of whom 10 had erosive gastritis (group 1) and 82 without erosions (group 2). A comparison of the groups on 23 grounds by analysis of contingency tables and the subsequent discriminant analysis, has developed a new non-invasive method for determining the erosive lesions of the mucous membrane of the stomach in children with juvenile arthritis, including a score of history, complaints and the results of laboratory studies the level of the G-17, pepsinogen I, pepsinogen II, and the ratio of pepsinogen I to pepsinogen II, the presence of autoantibodies to the H+, K+/ATPase of the parietal cells of the stomach, the test for occult blood "Colon View Hb and Hb/Hp". Developed a diagnostic table, including 11 features with scores each. The total score 27 or higher allows a high degree of probability to determine the erosive lesions of the gastric mucosa in children with juvenile arthritis.

Topics: Adolescent; Arthritis, Juvenile; Autoantibodies; Child; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Pepsinogen A; Pepsinogen C

The analysis of noninvasive diagnostics of a phenotype of gastritis among 1050 people aged from 18 till 80 years which consistently addressed to policlinic is presented in the article. The instrument of diagnostics was a <>, including a complex of biomarkers - so-called <> (pepsinogen I, pepsinogen II, gastrin-17 and IgG- antibodies to Helicobacter Pylori). High frequency of different variants of atrophic gastritis (25%) with a gastric cancer risk and conditions with a risk of erosive and ulcer damages of the stomach mucous (26 %) was shown. Clinical and economical expediency of noninvasive screening of a phenotype of gastritis is postulated.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Female; Gastrins; Gastritis; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Retrospective Studies

The aim of this study was to investigate the prevalence of autoimmune gastritis, enterochromaffin-like cell (ECL-cell) hyperplasia and gastric neuroendocrine neoplasms type 1 (GNEN1) in patients with autoimmune thyroid disease.. Prospective observational study in a single institutional study.. One hundred and twenty patients with autoimmune thyroid disease were consecutively recruited from the Endocrine Unit. Upper gastrointestinal tract endoscopy (UGE) and biochemical parameters for autoimmune thyroid disease and autoimmune gastritis were assessed at recruitment and annually thereafter in patients with a mean follow-up of 37·5 ± 14·4 months. Autoimmune gastritis was defined by the presence of antiparietal cell antibodies (APCA) and histological confirmation after UGE. Serum gastrin and chromogranin Α were also measured.. One hundred and eleven patients had Hashimoto's thyroiditis and nine Graves' disease. Autoimmune gastritis was identified in 40 (38 with Hashimoto's thyroiditis and two with Graves' disease) patients all of whom had increased levels of gastrin and chromogranin Α; Helicobacter pylori infection was histologically identified in 15 of 40 (37·5%) patients. Six patients had isolated nodular ECL-cell hyperplasia and one mixed nodular and linear ECL-cell hyperplasia [7 of 40 (17·5%)]. Only increased gastrin (P = 0·03) levels predicted the presence ECL-cell hyperplasia. A GNEN1 developed in one patient with nodular ECL-cell hyperplasia after 39 months of follow-up.. Concomitant autoimmune gastritis was found in 33·3% of patients with autoimmune thyroid disease, 17·5% of whom had ECL-cell hyperplasia that evolved to GNEN1 in one (2·5%). Larger studies with longer follow-up are needed to define the incidence of GNEN1 in patients with autoimmune thyroid disease and ECL-cell hyperplasia and potential implications.

Topics: Aged; Autoimmune Diseases; Chromogranin A; Endoscopy; Enterochromaffin-like Cells; Female; Gastrins; Gastritis; Hashimoto Disease; Helicobacter Infections; Humans; Male; Middle Aged; Neuroendocrine Tumors; Phenotype; Prevalence; Prospective Studies; Risk; Stomach Neoplasms; Thyroid Diseases

Bone marrow-derived mesenchymal stem cells (MSCs) sustain cancer cells by creating a microenvironment favorable for tumor growth. In particular, MSCs have been implicated in gastric cancer development. There is extensive evidence suggesting that Hedgehog signaling regulates tumor growth. However, very little is known regarding the precise roles of Hedgehog signaling and MSCs in tumor development within the stomach. The current study tests that hypothesis that Sonic Hedgehog (Shh), secreted from MSCs, provides a proliferative stimulus for the gastric epithelium in the presence of inflammation. Red fluorescent protein-expressing MSCs transformed in vitro (stMSCs) were transduced with lentiviral constructs containing a vector control (stMSC(vect)) or short hairpin RNA (shRNA) targeting the Shh gene (stMSC(ShhKO)). Gastric submucosal transplantation of wild-type MSCs (wtMSCs), wild-type MSCs overexpressing Shh (wtMSC(Shh)), stMSC(vect), or stMSC(ShhKO) cells in C57BL/6 control (BL/6) or gastrin-deficient (GKO) mice was performed and mice analyzed 30 and 60 days posttransplantation. Compared with BL/6 mice transplanted with wtMSC(Shh) and stMSC(vect) cells, inflamed GKO mice developed aggressive gastric tumors. Tumor development was not observed in mouse stomachs transplanted with wtMSC or stMSC(ShhKO) cells. Compared with stMSC(ShhKO)-transplanted mice, within the inflamed GKO mouse stomach, Shh-expressing stMSC(vect)- and wtMSC(Shh)-induced proliferation of CD44-positive cells. CD44-positive cells clustered in gland-like structures within the tumor stroma and were positive for Patched (Ptch) expression. We conclude that Shh, secreted from MSCs, provides a proliferative stimulus for the gastric epithelium that is associated with tumor development, a response that is sustained by chronic inflammation.

Topics: Animals; Cell Proliferation; Cell Transformation, Neoplastic; Epithelial Cells; Gastric Mucosa; Gastrins; Gastritis; Hedgehog Proteins; Mesenchymal Stem Cells; Mice; Mice, Inbred C57BL; Signal Transduction; Stomach Neoplasms

Gastric cancer (GC) is the second cause of cancer related death in the world. It may develop by progression from its precancerous condition, called gastric atrophy (GA) due to gastritis. The aim of this study was to evaluate the accuracy of serum levels of pepsinogens (Pg) and gastrin-17 (G17) as non-invasive methods to discriminate GA or GC (GA/GC) patients.. Subjects referred to gastrointestinal clinics of Golestan province of Iran during 2010 and 2011 were invited to participate. Serum levels of PgI, PgII and G17 were measured using a GastroPanel kit. Based on the pathological examination of endoscopic biopsy samples, subjects were classified into four groups: normal, non-atrophic gastritis, GA, and GC. Receiver operating curve (ROC) analysis was used to determine cut-off values. Indices of validity were calculated for serum markers.. Study groups were normal individuals (n=74), non-atrophic gastritis (n=90), GA (n=31) and GC patients (n=30). The best cut-off points for PgI, PgI/II ratio, G17 and HP were 80 μg/L, 10, 6 pmol/L, and 20 EIU, respectively. PgI could differentiate GA/GC with high accuracy (AUC=0.83; 95%CI: 0.76-0.89). The accuracy of a combination of PgI and PgI/II ratio for detecting GA/GC was also relatively high (AUC=0.78; 95%CI: 0.70-0.86).. Our findings suggested PgI alone as well as a combination of PgI and PgI/II ratio are valid markers to differentiate GA/GC. Therefore, Pgs may be considered in conducting GC screening programs in high-risk areas.

Topics: Adult; Antibodies, Bacterial; Case-Control Studies; Cross-Sectional Studies; Early Detection of Cancer; Female; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Iran; Male; Middle Aged; Pepsinogen A; Pepsinogen C; ROC Curve; Sensitivity and Specificity; Stomach Neoplasms

The aim of this study was to investigate the value of serum gastric markers to differentiate between patients with precancerous lesions and nonatrophic chronic gastritis.. Serum samples of 128 patients with dyspepsia who were candidates for endoscopic examination were tested for pepsinogen (PG I and PG II), PG I/II ratio, gastrin 17(G-17), anti-Helicobacter pylori (anti-H pylori ) and anti- CagA antibodies. Two sample t-tests, chi-square tests and Pearson's correlation analyses were used for analysis using SPSS (version 20).. PGI, PG I/II ratio values were decreased significantly in the precancerous lesion group (0.05, 0.001 respectively). The frequency of H pylori infection was significantly (p=0.03) different between the two groups ofthe study.. We suggest PGI and the PG I/II ratio as valuable markers for screening of premalignant gastric lesions.

Topics: Aged; Antibodies, Bacterial; Antigens, Bacterial; Bacterial Proteins; Biomarkers; Chronic Disease; Cross-Sectional Studies; Dyspepsia; Female; Follow-Up Studies; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Iran; Male; Pepsinogen A; Pepsinogen C; Precancerous Conditions; Prognosis; Stomach Neoplasms

In Japan, the prevalence of Helicobacter pylori infection is decreasing and the number of patients who receive eradication therapy is increasing. Although the serum level of gastrin is affected by H. pylori infection, the normal level has been unchanged for more than 20 years. The aim of this study was to study whether the present normal range for the serum gastrin level is appropriate for Japanese at present or in the near future.. We studied 810 adults (40-80 years old) who participated in a health survey in 2012. We measured H. pylori stool antigen, titer of serum antibody to H. pylori, and serum level of gastrin. The patient's H. pylori status was defined as positive or negative when the results of both stool antigen and serology were concordant. Subjects who were taking proton-pump inhibitor and had a previous history of gastric surgery were excluded.. Mean serum level of gastrin was 66.2±49.6 pg/mL in 281 H. pylori-negative subjects and 69.7±42.2 pg/mL in 115 patients who had H. pylori eradicated at least 2 years ago. The level of gastrin was 134.4±145.6 pg/mL in 224 patients with H. pylori infection and the level was significantly higher when compared with those in uninfected subjects and eradicated patients (P<0.01).. Because the situation of H. pylori infection has changed remarkably in Japan, a new appropriate normal range of gastrin should be established using current Japanese populations.

Topics: Adult; Aged; Aged, 80 and over; Asian People; Biomarkers; Disease Eradication; Duodenal Diseases; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Japan; Male; Middle Aged; Prevalence; Reference Values; Stomach Diseases

Mucosal alterations after Roux-en-Y gastric bypass for morbid obesity have not been clearly evaluated. This study aims to analyze the mucosal alterations (proliferative status (Ki-67); apoptosis (caspase-3 and BCL-2); hormonal function (gastrin)) in the excluded stomach.. Double-balloon enteroscopy was performed in 35 patients who underwent Roux-en-Y gastric bypass longer than 36 months. Multiple biopsies of the proximal pouch and the excluded gastric mucosa were collected. Gastric biopsies from 32 non-operated obese patients were utilized as controls. Endoscopic biopsies were cut from tissue blocks fixed in formalin and embedded in paraffin. Sections 4 μm thick were examined for immunoexpression using the streptavidin-biotin-peroxidase method.. The two groups were comparable for age, gender, gastritis, intestinal metaplasia, and Helicobacter pylori. The mean number of positive gastrin cells was 55.5 (standard deviation (SD) = 11.7) in the control group and 29.6 (SD = 7.9) in the cases, p = 0.0003. Ki-67 proliferative index in cases (body = 24.7%, antrum = 24.9%) was significantly higher compared to controls (body = 15.0% and antrum = 17.7%), p = 0.002 and 0.01, respectively. Caspase-3 immunoexpression was higher in the controls compared to the excluded stomach (46 vs. 31%), p = 0.02. There was no statistical difference between CD3, CD8, and Bcl-2 immunoexpressions in the control and cases.. Cell proliferation is increased and apoptosis is downregulated in the excluded gastric mucosa compared to the non-operated obese controls. Alterations in cell turnover and in hormonal secretions in these conditions may be of relevance in long-term follow-up.

Topics: Adolescent; Adult; Aged; Brazil; Caspase 3; Cell Proliferation; Double-Balloon Enteroscopy; Down-Regulation; Epithelial Cells; Female; Gastric Bypass; Gastric Mucosa; Gastric Stump; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Ki-67 Antigen; Male; Middle Aged; Obesity, Morbid

The thyrogastric autoimmune syndrome (TAS) was described in patients in whom the serum cross-reacted both with gastric parietal cells antigens and thyroid antigens. We report two cases illustrating the spectrum of pathogical features of TAS. The first case associates Hashimoto's thyroiditis and anemia perniciosa,and develops a gastric neuroendocrine tumor during follow up. The second case presents with a Graves' disease and an autoimmune reversible gastritis, secondary to Helicobacter pylori. Whereas type III autoimmune polyendocrinopathy is rare, TAS is frequent in our experience. Some 13% (32/240) of patients that we have prospectively followed affected with thyroiditis have also autoimmune gastritis. Helicobacter pylori is clearly implicated in 16% of autoimmune gastritis cases. Infection, malabsorption and gastritis are potentially reversible after bacterial eradication treatment. In the other 84% of gastritis patients, no histological or serological proof of Helicobacter pylori is found. Gastric autoimmunity is then irreversible, leading to gastric severe atrophy, hypochlorhydria and hypergastrinemia. Hypergastrinemia stimulates enterochromaffin cell hyperplasia, possibly progressing to neuroendocrine tumors. We propose a diagnostic approach to improve the characterization of TAS. We review the literature on the subject and discuss some interesting animal models of infectious gastric autoimmunity.

Topics: Enterochromaffin-like Cells; Gastrins; Gastritis; Humans; Hyperplasia; Neuroendocrine Tumors; Stomach Neoplasms; Thyroiditis, Autoimmune

Gastrin is a growth factor for the gastric epithelial cells. However, it is unknown how gastric receptor (GR) expression is regulated in the gastric mucosa. We studied GR expression using a newly raised antibody and investigated the relationship between GR expression and gastritis.. Gastric receptor expression in 63 human gastric mucosa was studied. Helicobacter pylori infection and histological gastritis status were evaluated in gastric biopsy samples. In gastric ulcer cases, additional biopsy specimens were taken from injured mucosa. Fasting sera were collected and serum gastrin level evaluated. MKN-28 cells were cultured at various pH conditions, and the change in GR expression was determined.. Gastric receptor expression was detected in the foveolar epithelium of the gastric mucosa, and its expression was stronger in patients infected with H. pylori. In particular, higher expression was detected in regenerating injured mucosa. There was no association between gastritis score/serum gastrin level and GR expression in H. pylori-positive cases. In MKN-28 cells, GR protein expression was lower in neutral conditions than in acidic or alkaline conditions.. Gastric mucosal injury with H. pylori infection destroys the pH barrier on the foveolar epithelium and may induce GR expression through pH changes.

Topics: Adenocarcinoma; Aged; Biopsy; Cell Line, Tumor; Female; Gastric Mucosa; Gastrins; Gastritis; Gene Expression Regulation; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Receptor, Cholecystokinin B; Stomach Neoplasms

The aim of this study was to investigate the association between serum pepsinogens, serum gastrin, serum vascular endothelial growth factor, serum interleukin-1 Beta, serum toll-like receptor-4 levels and Helicobacter pylori Cag A status in patients with various gastric precancerous lesions.. One hundred and sixty two consecutive patients with various gastric lesions [38 (23.5%) H. pylori positive chronic non-atrophic gastritis, 45 (27.8%) autoimmune gastritis, 42 intestinal metaplasia and 37 dysplasia] were enrolled into the study. Serum pepsinogen I and II, gastrin 17, vascular endothelial growth factor, interleukin-1 Beta, toll-like receptor-4 levels, H. pylori Cag A status were evaluated.. H. pylori was positive in 98 (60.5%) patients and 38 of these patients were Cag A positive. Serum pepsinogen level was significantly lower in patients with autoimmune atrophic gastritis compared to the patients with non-atrophic chronic gastritis (p<0.001), intestinal metaplasia (P<0.001) and dysplasia (P=0.002). Mean serum gastrin was 1209.6±268.48 pg/mL in patients with autoimmune atrophic gastritis and 234.95±184.018 pg/mL in patients with chronic non-atrophic gastritis. Mean toll-like receptor-4 level was 0.56±0.098 ng/mL in patient with dysplasia, and this value was higher compared to patients with chronic non-atrophic gastritis (P=0.007), autoimmune atrophic gastritis (P=0.003) and intestinal metaplasia (P=0.006). Interleukin-1 Beta level was significantly lower in patients with dysplasia compared to patients with chronic non-atrophic gastritis (P=0.034).. Serum pepsinogens, serum gastrin and H. pylori Cag A status are important tests in detecting gastric precancerous lesions. However, toll-like receptor-4 may be a sensitive test to differentiate the patients with dysplasia from the other precancerous gastric lesions. Non-invasive tests are sensitive in the diagnosis of gastric precancerous lesions.

Topics: Adult; Aged; Antigens, Bacterial; Bacterial Proteins; Biomarkers; Female; Gastrins; Gastritis; Helicobacter pylori; Humans; Interleukin-1beta; Male; Metaplasia; Middle Aged; Pepsinogen A; Pepsinogen C; Precancerous Conditions; Sensitivity and Specificity; Stomach; Stomach Neoplasms; Toll-Like Receptor 4; Vascular Endothelial Growth Factor A

Previous studies have suggested that dietary folic acid (FA) can protect against certain types of cancers. However, the findings have varied, and the mechanisms by which FA exerts chemopreventive effects remain to be clarified. We examined the effects of FA supplementation on DNA methylation, gene expression, and gastric dysplasia in a transgenic mouse model that is etiologically and histologically well matched with human gastric cancers.. Hypergastrinemic mice infected with Helicobacter felis were studied at multiple stages of gastric dysplasia and early cancer with FA supplementation initiated both at weaning and later in life. Global DNA methylation was assessed by a methylation sensitive cytosine incorporation assay, bisulfite pyrosequencing of B1 repetitive elements, and immunohistochemistry with anti-5-methylcytosine. We also profiled gene expression in the same tissues.. We found a decrease in global DNA methylation and tissue folate and an increase in serum homocysteine with progression of gastric dysplasia. FA supplementation prevented this loss of global DNA methylation and markedly reduced gastric dysplasia and mucosal inflammation. FA protected against the loss of global DNA methylation both in the dysplastic gastric epithelial cells and in gastric stromal myofibroblasts. In addition, FA supplementation had an anti-inflammatory effect, as indicated by expression profiling and immunohistochemistry for lymphocyte markers.. We conclude that FA supplementation is chemopreventive in this model of Helicobacter-associated gastric cancer. The beneficial effect of FA is likely due to its ability to prevent global loss of methylation and suppress inflammation.

Topics: Animals; Anti-Inflammatory Agents; Anticarcinogenic Agents; Disease Models, Animal; DNA Methylation; Folic Acid; Gastric Mucosa; Gastrins; Gastritis; Gene Expression Profiling; Gene Expression Regulation; Helicobacter felis; Helicobacter Infections; Homocysteine; Immunohistochemistry; Lymphocytes; Male; Mice; Mice, Transgenic; Myofibroblasts; Stomach; Stomach Neoplasms; Stromal Cells; Up-Regulation

The aim of this study was to determine serum gastrin levels and gastroduodenal lesions in children with chronic renal failure (CRF) on continuous ambulatory peritoneal dialysis (CAPD).. A total of 19 patients (mean age: 11.7±3.9 years, M/F: 1.37) with CRF on CAPD and 20 age-matched and sex-matched patients (mean age: 10.2±1.4 years, M/F: 1.5) with peptic ulcers were included in the study. Serum gastrin, creatinine, phosphate, and parathormone levels were determined. Upper gastrointestinal endoscopy was performed in all patients.. The basal gastrin concentrations of CAPD patients were significantly higher than those of patients with peptic ulcer disease without CRF (124.2±59.1 and 53.0±9.4 pg/ml, respectively) (P<0.001). A significant correlation was found between age, duration of uremia, and serum gastrin levels (r=0.59, P<0.01; r=0.60, P<0.01, respectively). No correlation was found between the duration of CAPD and serum gastrin levels in the patient group. Of the patients, 73.6% had abnormal upper gastrointestinal endoscopic findings. The gastroduodenal lesion observed was hemorrhagic gastritis (31.5%), followed by hemorrhagic gastroduodenitis (26.3%), gastric nodular gastritis (10.5%), and polyps (10.5%).. On the basis of our findings, such as higher serum gastrin levels in patients with CRF than those of the control group and the frequent endoscopic findings of gastroduodenal lesions in most of the patients, we recommend that an endoscopic examination should be considered for all the children with CRF on CAPD awaiting renal transplantation even if they are asymptomatic.

Topics: Adolescent; Case-Control Studies; Child; Child, Preschool; Creatinine; Duodenitis; Endoscopy, Gastrointestinal; Female; Gastrins; Gastritis; Humans; Incidence; Intestinal Polyps; Kidney Failure, Chronic; Male; Parathyroid Hormone; Peritoneal Dialysis, Continuous Ambulatory; Phosphates

Helicobacter pylori (HP) has been associated with neuroendocrine tumors of the stomach and duodenum. Gastric enterochromaffin-like (ECL) cell tumors and duodenal gastrinomas have also been associated with HP gastritis in separate series but have not been reported together. With other possible causes excluded, we present a patient with HP-associated atrophy of the oxyntic mucosa that ultimately resulted in stimulation and reactive hyperplasia of gastrin-producing cells in both the antrum and proximal duodenum, the latter progressing to formation of a gastrin-producing cell nodule (gastrinoma). Both of these sources of gastrin resulted in ECL hyperplasia in the atrophied oxyntic mucosa with progression to microcarcinoids and well-differentiated neuroendocrine tumors, along with hypertrophy of residual proximal gastric parietal cells. As atrophy tends to spread from the antrum proximally, residual oxyntic mucosa was still infected with HP and offers 1 explanation for the apparent paradox of atrophic gastritis with ECL hyperplasia and neoplasia in the distal oxyntic mucosa, with proximal oxyntic mucosa showing mild hypertrophic changes in a background of typical HP gastritis.

Topics: Aged; Atrophy; Chronic Disease; Duodenal Neoplasms; Gastrectomy; Gastrinoma; Gastrins; Gastritis; Helicobacter Infections; Humans; Intestinal Mucosa; Male; Neoplasms, Multiple Primary; Neuroendocrine Tumors; Stomach Neoplasms

Autoimmune gastritis (AIG) may predispose to gastric carcinoid tumors or adenocarcinomas and may also cause unexplained iron and/or vitamin B(12) deficiency. The aims of this study were to explore clinical manifestations, endoscopic findings and laboratory features of patients with AIG.. 109 patients with AIG were enrolled into the study. In addition to demographic and clinical data, gastric lesions, serum gastrin, vitamin B(12), antiparietal cell antibody (APA), current Helicobacter pylori status, and anti-H. pylori IgG were also investigated.. The mean age of the patients was 53.06 ± 12.7 years (range 24-81; 72 (66.1%) women). The most common main presenting symptom was abdominal symptoms in 51 patients, consultation for iron and/or vitamin B(12) deficiency in 36, and non-specific symptoms including intermittent diarrhea in 15 patients. Endoscopic lesions were detected in 17 patients, hyperplastic polyps in 8, gastric carcinoid tumor in 4, fundic gland polyps in 3, and adenomatous polyps in 2 patients. H. pylori was negative in all patients in biopsy specimens; however, anti-H. pylori IgG was positive in 30 (27.5%) patients. 91 patients (83.4%) were positive for APA.. In patients with AIG, the main symptoms prompted for clinical investigation were: abdominal symptoms, iron/B(12) deficiency and non-specific symptoms. 20% of patients with AIG had various gastric lesions including type I gastric carcinoids. None of the patients were positive for H. pylori by means of invasive tests; however, anti-H. pylori IgG was found in 27.5% of patients. Patients referring with non-specific abdominal symptoms such as bloating, diarrhea and iron/B(12) deficiency should be investigated for the presence of AIG.

Topics: Adenomatous Polyps; Adult; Age Factors; Aged; Aged, 80 and over; Antibodies, Bacterial; Autoimmune Diseases; Carcinoid Tumor; Diarrhea; Female; Gastrins; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Iron; Iron Deficiencies; Male; Middle Aged; Parietal Cells, Gastric; Polyps; Sex Factors; Stomach Neoplasms; Vitamin B 12 Deficiency; Young Adult

The aim of the study was to assess the accuracy of some specific biochemical indicators in discriminating between Helicobacter pylori-associated gastritis and H. pylori-associated stomach cancer (serum gastrin level, serum soluble E-cadherin and tissue COX-2 activity, as well as serodiagnostic markers for H. pylori infection) in order to find a simple diagnostic test that can reasonably predict the development of gastric cancer. The study participants comprised 20 patients with gastric carcinoma, 20 patients with positive H. pylori-associated gastritis and 20 individuals as the control group. Standard procedures and quality control measures were followed. Using cut-off values and ROC analysis to assess the diagnostic abilities of the biochemical indicators, E-cadherin showed the highest sensitivity (100%). We suggest that close follow-up together with periodic endoscopic examination for all patients with persistent H. pylori infection and serum soluble E-cadherin level above 5 microg/mL is essential.

Topics: Biomarkers, Tumor; Cadherins; Case-Control Studies; Cyclooxygenase 2; Diagnosis, Differential; Early Diagnosis; Egypt; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Risk Assessment; Sensitivity and Specificity; Stomach Neoplasms

Gastrin has a cholecystokinetic action on gallbladder motility, and cholecystokinin and gastrin act directly on the smooth muscle of the gallbladder. The aim of this study was to investigate the effect of endogenous hypergastrinemia on gallbladder motility in patients with autoimmune gastritis.. Forty-one patients (29 females, 12 males; mean age, 46 years) with autoimmune gastritis and 29 healthy subjects (17 females, 12 males; mean age, 44.8 years) were enrolled in the study. Fasting and postprandial gallbladder volumes were measured ultrasonographically with the ellipsoid technique and the ejection fraction of the gallbladder was calculated from fasting and postprandial volumes. All subjects were investigated after 12 hours of fasting and 30 minutes after a standard test meal.. The gallbladder ejection fraction (%) of the patients with autoimmune gastritis was lower than that of the control group (46.06+/-18.28% vs 55.03+/-14.67%, P=0.032). There was no difference between patients with autoimmune gastritis and the control group in terms of the mean fasting gallbladder volume (30.38+/-12.85 vs 29.27+/-9.91 cm3, P=0.189) and the mean postprandial gallbladder volume (15.67+/-8.32 vs 13.44+/-7.69 cm3, P=0.258). Logistic regression analysis of baseline parameters revealed that "abdominal bloating" was a risk factor for the low gallbladder ejection fraction in autoimmune gastritis patients (P=0.045, F=4.40). In addition, logistic regression analysis of baseline parameters revealed that smoking (n=5, P=0.025, F=5.44) is a predictor of low gallbladder ejection fraction in patients with autoimmune gastritis.. Patients with endogenous hypergastrinemia have a low gallbladder ejection fraction compared with healthy controls. This study shows that at least part of upper gastrointestinal symptoms observed in this patient population may be due to altered gallbladder motility.

Topics: Adult; Aged, 80 and over; Autoimmune Diseases; Female; Gallbladder; Gastrins; Gastritis; Humans; Male; Middle Aged

Transgenic FVB/N insulin-gastrin (INS-GAS) mice have high circulating gastrin levels, and develop spontaneous atrophic gastritis and gastrointestinal intraepithelial neoplasia (GIN) with 80% prevalence 6 months after Helicobacter pylori infection. GIN is associated with gastric atrophy and achlorhydria, predisposing mice to nonhelicobacter microbiota overgrowth. We determined if germfree INS-GAS mice spontaneously develop GIN and if H pylori accelerates GIN in gnotobiotic INS-GAS mice.. We compared gastric lesions, levels of messenger RNA, serum inflammatory mediators, antibodies, and gastrin among germfree and H pylori-monoinfected INS-GAS mice. Microbiota composition of specific pathogen-free (SPF) INS-GAS mice was quantified by pyrosequencing.. Germfree INS-GAS mice had mild hypergastrinemia but did not develop significant gastric lesions until 9 months old and did not develop GIN through 13 months. H pylori monoassociation caused progressive gastritis, epithelial defects, oxyntic atrophy, marked foveolar hyperplasia, dysplasia, and robust serum and tissue proinflammatory immune responses (particularly males) between 5 and 11 months postinfection (P<0.05, compared with germfree controls). Only 2 of 26 female, whereas 8 of 18 male, H pylori-infected INS-GAS mice developed low to high-grade GIN by 11 months postinfection. Stomachs of H pylori-infected SPF male mice had significant reductions in Bacteroidetes and significant increases in Firmicutes.. Gastric lesions take 13 months longer to develop in germfree INS-GAS mice than male SPF INS-GAS mice. H pylori monoassociation accelerated gastritis and GIN but caused less severe gastric lesions and delayed onset of GIN compared with H pylori-infected INS-GAS mice with complex gastric microbiota. Changes in gastric microbiota composition might promote GIN in achlorhydric stomachs of SPF mice.

Topics: Adenocarcinoma; Animals; Bacteroidetes; Female; Gastrins; Gastritis; Gastrointestinal Neoplasms; Germ-Free Life; Helicobacter Infections; Helicobacter pylori; Inflammation Mediators; Insulin; Male; Mice; Mice, Transgenic; Precancerous Conditions; Sex Factors

Barrett's esophageal cancer is usually included in gastroesophageal (GE) junction adenocarcinoma in Japanese people. No study on the pathogenesis of Barrett's esophageal cancer in comparison with GE junction adenocarcinoma other than Barrett's esophageal cancer has been reported in Japan. The aim of this study was to evaluate the clinical and pathological characteristics and gastric acid secretion of Barrett's esophageal cancer and GE junction adenocarcinoma other than Barrett's esophageal cancer in Japanese subjects.. Twenty-three patients with Barrett's esophageal cancer and 23 patients with GE junction adenocarcinoma other than Barrett's esophageal cancer were enrolled in this study. We evaluated and compared them by assessing the Helicobactor pylori (HP) infection status and gastric acid secretion using the endoscopic gastrin test (EGT).. In the patients with Barrett's esophageal cancer, no significant difference was found in the mean EGT value between HP-positive and -negative patients, but in the patients with GE junction adenocarcinoma other than Barrett's esophageal cancer, the mean EGT value in HP-positive patients was significantly lower than that in HP-negative patients.. Two distinct types of cancer of different origin may be mixed in GE junction adenocarcinomas. One is Barrett's esophageal cancer associated with high gastric acid secretion and reflux of gastric acid into the esophagus, the other is cancer resembling distal gastric cancer associated with gastric atrophy and low gastric acid secretion.

Topics: Adenocarcinoma; Aged; Barrett Esophagus; Case-Control Studies; Endoscopy, Digestive System; Esophageal Neoplasms; Esophagogastric Junction; Female; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Japan; Male; Middle Aged; Prevalence; Severity of Illness Index

Parietal cell antibodies (PCA) are markers of autoimmune gastritis (AG). AG can lead to hypergastrinemia and iron-deficiency anaemia (IDA). Compared to healthy controls, adults with type 1 diabetes mellitus (T1DM) show a higher prevalence of PCA (1% vs 20%). The aim of the present study was to evaluate the frequency of PCA in children and adolescents with T1DM compared to healthy controls and the clinical and biochemical markers.. We studied 170 patients (87 boys) with T1DM (mean age 12.9 years) and 101 healthy controls (49 boys; mean age 13.0 years). PCA, free T4, free T3, thyroid-stimulating hormone (TSH), and thyroid antibodies were measured in all of the patients. In addition, gastrin, pepsinogen I, iron, ferritin, vitamin B12, and folate were measured in patients with T1DM only. Gastroscopy was carried out in patients with T1DM having high (>100 U/mL) PCA levels.. The frequency of PCA in patients with T1DM was 5.29% compared to 1.98% in healthy controls (not significant). PCA was strongly correlated to both thyroid peroxidase antibodies (TPOAb) and gastrin levels (P = 0.001). IDA was present in 4 of 9 patients from the PCA-positive group compared to 4 of 160 patients from the PCA-negative group. Hypergastrinemia was found in 2 PCA-positive patients. Histopathologically, 1 of 4 patients showed early symptoms of AG.. Children and adolescents with T1DM have a lower frequency of PCA than is reported for adults. Compared to healthy controls, they seem to be at increased risk for developing PCA, in particular if positive for TPOAb, but overt clinical disease is rare in children with T1DM.

Topics: Adolescent; Anemia, Iron-Deficiency; Autoantibodies; Biomarkers; Diabetes Mellitus, Type 1; Female; Gastrins; Gastritis; Humans; Iodide Peroxidase; Male; Parietal Cells, Gastric; Prevalence; Reference Values

To investigate if and how the proinflammatory cytokine interferon γ (IFNγ) affects ghrelin expression in mice.. The plasma concentration of ghrelin, and gastric ghrelin and somatostatin expression, were examined in wild-type mice and mice infected with Helicobacter pylori (H. pylori). Furthermore, ghrelin expression was examined in two achlorhydric mouse models with varying degrees of gastritis due to bacterial overgrowth. To study the effect of IFNγ alone, mice were given a subcutaneous infusion of IFNγ for 7 d. Finally, the influence of IFNγ and somatostatin on the ghrelin promoter was characterized.. H. pylori infection was associated with a 50% reduction in ghrelin expression and plasma concentration. Suppression of ghrelin expression was inversely correlated with gastric inflammation in achlorhdyric mouse models. Subcutaneous infusion of IFNγ suppressed fundic ghrelin mRNA expression and plasma ghrelin concentrations. Finally, we showed that the ghrelin promoter operates under the control of somatostatin but not under that of IFNγ.. Gastric infection and inflammation is associated with increased IFNγ expression and reduced ghrelin expression. IFNγ does not directly control ghrelin expression but inhibits it indirectly via somatostatin.

Topics: Animals; Cell Line; Female; Gastrins; Gastritis; Ghrelin; Helicobacter Infections; Helicobacter pylori; Histidine Decarboxylase; Humans; Interferon-gamma; Mice; Mice, Inbred C57BL; Mice, Knockout; Promoter Regions, Genetic; Somatostatin; Stomach

To establish optimal cutoff values for serologic diagnosis of fundic atrophy in a high-risk area for oesophageal squamous cell carcinoma and gastric cancer with high prevalence of Helicobacter pylori (H. pylori) in Northern Iran, we performed an endoscopy-room-based validation study.. We measured serum pepsinogens I (PGI) and II (PGII), gastrin 17 (G-17), and antibodies against whole H. pylori, or cytotoxin-associated gene A (CagA) antigen among 309 consecutive patients in two major endoscopy clinics in northeastern Iran. Updated Sydney System was used as histology gold standard. Areas under curves (AUCs), optimal cutoff and predictive values were calculated for serum biomarkers against the histology.. 309 persons were recruited (mean age: 63.5 years old, 59.5% female). 84.5% were H. pylori positive and 77.5% were CagA positive. 21 fundic atrophy and 101 nonatrophic pangastritis were diagnosed. The best cutoff values in fundic atrophy assessment were calculated at PGI<56 µg/l (sensitivity: 61.9%, specificity: 94.8%) and PGI/PGII ratio<5 (sensitivity: 75.0%, specificity: 91.0%). A serum G-17<2.6 pmol/l or G-17>40 pmol/l was 81% sensitive and 73.3% specific for diagnosing fundic atrophy. At cutoff concentration of 11.8 µg/l, PGII showed 84.2% sensitivity and 45.4% specificity to distinguish nonatrophic pangastritis. Exclusion of nonatrophic pangastritis enhanced diagnostic ability of PGI/PGII ratio (from AUC = 0.66 to 0.90) but did not affect AUC of PGI. After restricting study samples to those with PGII<11.8, the sensitivity of using PGI<56 to define fundic atrophy increased to 83.3% (95%CI 51.6-97.9) and its specificity decreased to 88.8% (95%CI 80.8-94.3).. Among endoscopy clinic patients, PGII is a sensitive marker for extension of nonatrophic gastritis toward the corpus. PGI is a stable biomarker in assessment of fundic atrophy and has similar accuracy to PGI/PGII ratio among populations with prevalent nonatrophic pangastritis.

Topics: Antigens, Bacterial; Area Under Curve; Bacterial Proteins; Female; Gastric Fundus; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter pylori; Humans; Male; Mass Screening; Middle Aged; Pepsinogen A; Pepsinogen C; Reference Values

Gastritis, an inflammation of gastric mucosa, may be due to many pathological factors and infection, such as with Helicobacter pylori. The use of experimental models of gastritis is important to evaluate the biochemical changes and study chemotherapeutic intervention. In a previous study we demonstrated an acute gastritis model induced by iodoacetamide.. Our objective in this study was to evaluate a new gastritis model induced by H. pylori infection in experimental rats in terms of certain biomarkers in serum and mucosal tissues in addition to histopathological examination.. Gastritis was induced in 20 albino Wistar rats by H. pylori isolated from antral biopsy taken from a 49-year-old male patient endoscopically diagnosed as having H. pylori infection. Another ten rats were used as controls. Serum gastrin, pepsinogen I activity, interleukin-6 (IL-6) and gastric mucosal myeloperoxidase (MPO) activity and prostaglandin E(2) (PGE(2)) were measured. Immunostaining for inducible nitric oxide synthase (iNOS), nitrotyrosine and DNA fragmentation were used to further evaluate H. pylori-induced gastritis.. Serum gastrin, IL-6, mucosal MPO activity, and PGE(2) demonstrated significant increases joined with a decreased serum pepsinogen I activity (P < 0.001). Immunohistochemistry demonstrated positive reaction for iNOS, nitrotyrosine and DNA fragmentation.. Helicobacter pylori-induced gastritis models demonstrated massive oxidative stress and pronounced injury in mucosal tissue. Since our model in rats reflected the clinical picture of H. pylori infection, it can be considered as a consistent model to study chemotherapeutic intervention for this type of gastritis.

Topics: Animals; Biomarkers; Biopsy; Dinoprostone; Disease Models, Animal; DNA Fragmentation; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-6; Male; Middle Aged; Nitric Oxide Synthase Type II; Pepsinogen A; Peroxidase; Pyloric Antrum; Rats; Rats, Wistar

to find out biomarker as diagnostic tool of H. pylori chronic gastritis.. the design of present study was a diagnostic test and there were 104 subjects with H. pylori chronic gastritis who fulfilled the inclusion and exclusion criteria. The diagnosis of H. pylori chronic gastritis was based on histopathological examination and PCR with ureC primer of the gastric biopsy specimen. In addition, we also performed the examination of serum gastrin, pepsinogen (PG) I and PG (pepsinogen) II level. By using analysis of receiver operating characteristic (ROC), an optimal cut off point of serum gastrin, PGI and PGII level as well as PGI/PGII ratio was determined. Analysis of bivariate logistic regression was used to determine the involved independent variables and possibilities as biomarkers. Significance level was determined by p value <0.05.. we found optimal cut off points on serum gastrin, PGI and PGII level as well as the PGI/PGII ratio at 5.89 pmol/L; 82.5 µg/L; 6.48 µg/L and 13.6 respectively. By using the analysis of bivariate logistic regression, we found gastrin level with p = 0.078 (OR 2.75;95%CI 0.89-8.45) and PGI/PGII ratio with p = 0.000 (OR 14.63;95%CI 3.55-60.63). The opportunity of gastrin level and PGI/PGII ratio as biomarkers was 0.8 with 47% sensitivity, 83% specificity, 74% PPV, 61% NPV, 65% accuracy, LR+ = 2.76 and LR- = 0.64.. gastrin level of >5.89 pmol/L and PGI/PGII ratio ≤13.6 can be utilized as biomarkers of H. pylori chronic gastritis.

Topics: Biopsy; Chronic Disease; Diagnosis, Differential; DNA, Bacterial; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Middle Aged; Pepsinogen A; Pepsinogen C; Polymerase Chain Reaction; ROC Curve

The combined evaluation of serum pepsinogens A (PGA) and C (PGC), gastrin-17 (G17) and anti-H. pylori antibodies (anti-H. pylori)(GastroPanel) has recently been proposed as a useful aid for investigating H. pylori-associated gastric mucosal inflammation. Our aim was to evaluate whether GastroPanel can correctly classify children who need or not endoscopy (EGD).. GastroPanel was performed in 554 consecutive children subjected to EGD.. PGC and anti-H. pylori were sensitive (82.5% and 73.1%) and specific (58.1% and 84.0%) indices of H. pylori infection. Antral H. pylori colonization density, inflammation and activity grades were correlated with PGC. PGC and G17 were significantly higher in children with celiac disease (14.9+/-0.88 microg/L and 5.6+/-0.79 pmol/L) than in controls (8.5+/-0.38 microg/L and 2.4+/-0.24 pmol/L). The best cut-offs to distinguish H. pylori infected children from controls were 7.45 microg/L for PGC, 4.2 pmol/L for G17, 18 U for anti-H. pylori and 25 microg/L for PGA. With these cut-offs, GastroPanel had a NPV of 89.6% and a PPV of 66.8%.. A negative GastroPanel result in children with upper abdominal non alarm symptoms, should allow the paediatrician to reasonably rule out the presence of major gastro-duodenal diseases and therefore avoid EGD.

Topics: Adolescent; Antibodies, Bacterial; Celiac Disease; Child; Child, Preschool; Endoscopy, Gastrointestinal; Female; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Diseases; Helicobacter Infections; Helicobacter pylori; Humans; Infant; Logistic Models; Male; Pepsinogen A; Pepsinogen C; Sensitivity and Specificity

To study the value of serum biomarker tests to differentiate between patients with healthy or diseased stomach mucosa: i.e. those with Helicobacter pylori (H pylori) gastritis or atrophic gastritis, who have a high risk of gastric cancer or peptic ulcer diseases.. Among 162 Japanese outpatients, pepsinogen I (Pg I) and II (Pg II) were measured using a conventional Japanese technique, and the European GastroPanel examination (Pg I and Pg II, gastrin-17 and H pylori antibodies). Gastroscopy with gastric biopsies was performed to classify the patients into those with healthy stomach mucosa, H pylori non-atrophic gastritis or atrophic gastritis.. Pg I and Pg II assays with the GastroPanel and the Japanese method showed a highly significant correlation. For methodological reasons, however, serum Pg I, but not Pg II, was twice as high with the GastroPanel test as with the Japanese test. The biomarker assays revealed that 5% of subjects had advanced atrophic corpus gastritis which was also verified by endoscopic biopsies. GastroPanel examination revealed an additional seven patients who had either advanced atrophic gastritis limited to the antrum or antrum-predominant H pylori gastritis. When compared to the endoscopic biopsy findings, the GastroPanel examination classified the patients into groups with "healthy" or "diseased" stomach mucosa with 94% accuracy, 95% sensitivity and 93% specificity.. Serum biomarker tests can be used to differentiate between subjects with healthy and diseased gastric mucosa with high accuracy.

Topics: Adult; Aged; Biopsy; Diagnosis, Differential; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Japan; Middle Aged; Outpatients; Pepsinogen A; Pepsinogen C; Peptic Ulcer; Prevalence; Reference Values; Risk Factors; Stomach; Stomach Neoplasms; Young Adult

Infection with Helicobacter pylori, carrying a functional cag type IV secretion system (cag-T4SS) to inject the Cytotoxin associated antigen (CagA) into gastric cells, is associated with an increased risk for severe gastric diseases in humans. Here we studied the pathomechanism of H. pylori and the role of the cag-pathogenicity island (cag-PAI) for the induction of gastric ulcer and precancerous conditions over time (2-64 weeks) using the Mongolian gerbil model. Animals were challenged with H. pylori B128 (WT), or an isogenic B128DeltacagY mutant-strain that produces CagA, but is unable to translocate it into gastric cells. H. pylori colonization density was quantified in antrum and corpus mucosa separately. Paraffin sections were graded for inflammation and histological changes verified by immunohistochemistry. Physiological and inflammatory markers were quantitated by RIA and RT-PCR, respectively. An early cag-T4SS-dependent inflammation of the corpus mucosa (4-8 weeks) occurred only in WT-infected animals, resulting in a severe active and chronic gastritis with a significant increase of proinflammatory cytokines, mucous gland metaplasia, and atrophy of the parietal cells. At late time points only WT-infected animals developed hypochlorhydria and hypergastrinemia in parallel to gastric ulcers, gastritis cystica profunda, and focal dysplasia. The early cag-PAI-dependent immunological response triggers later physiological and histopathological alterations towards gastric malignancies.

Topics: Achlorhydria; Animals; Antigens, Bacterial; Bacterial Proteins; Cytokines; Gastrins; Gastritis; Genomic Islands; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Hypertrophy; Immunoenzyme Techniques; Precancerous Conditions; Radioimmunoassay; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Somatostatin; Stomach Neoplasms; Stomach Ulcer

Upper gastrointestinal (GI) bleeding is a feared consequence of open heart surgery in children. Increased gastric acid secretion is a known key factor in the pathogenesis of gastritis and upper intestinal ulcerations. The aim of this study is to evaluate the serum kinetics of acid-stimulating factors and associated perioperative parameters after heart surgery in children.. Fifteen pediatric patients after open heart surgery and 15 children with cardiac catheterization were included in this study. Serum levels of gastrin, histidine, alanine, and tryptophan were analyzed before and up to 26 h after surgery.. In the postoperative period there was a significant elevation of gastrin with a peak at 4 h after surgery. Serum histidine was increased significantly immediately after surgery only in patients undergoing heart surgery with cardioplegia. No association of gastrin and histidine elevation with ischemia, perfusion time or lactate was observed.. Factors that are responsible for postoperative gastrin elevation still have to be determined. Circumstances of extracorporeal circulation (ECC) in low-risk patients most likely do not lead to relevant elevation of amino acids with acid-stimulatory effect in our study population.

Topics: Cardiac Surgical Procedures; Child; Child, Preschool; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Humans; Infant; Postoperative Complications

We have previously described a synergistic interaction between hypergastrinemia and Helicobacter felis infection on gastric corpus carcinogenesis in FVB/N mice housed under specific-pathogen-free conditions. However, gastrin-deficient (GAS-KO) mice on a mixed C57BL/6/129Sv genetic background maintained in conventional housing were reported to develop spontaneous gastric antral tumors. Therefore, we investigated the role of gastrin in Helicobacter-associated gastric carcinogenesis in H. felis-infected mice on a uniform C57BL/6 background housed in specific-pathogen-free conditions. Hypergastrinemic transgenic (INS-GAS) mice, GAS-KO mice, and C57BL/6 wild-type mice were infected with H. felis for either 12 or 18 months. At 12 months postinfection, INS-GAS mice had mild corpus dysplasia, while B6 wild-type mice had either severe gastritis or metaplasia, and GAS-KO mice had only mild to moderate gastritis. At 18 months postinfection, both INS-GAS and B6 wild-type mice had both severe atrophic gastritis and corpus dysplasia, while GAS-KO mice had severe gastritis with mild gastric atrophy, but no corpus dysplasia. In contrast, both GAS-KO and B6 wild-type mice had mild to moderate antral dysplasia, while INS-GAS mice did not. H. felis antral colonization remained stable over time among the three groups of mice. These results point to a distinct effect of gastrin on carcinogenesis of both the gastric corpus and antrum, suggesting that gastrin is an essential cofactor for gastric corpus carcinogenesis in C57BL/6 mice.

Topics: Animals; Cytokines; Female; Gastrins; Gastritis; Helicobacter felis; Helicobacter Infections; Immunohistochemistry; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Precancerous Conditions; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Stomach Neoplasms; T-Lymphocytes, Helper-Inducer

Matrix metalloproteinases (MMPs) have roles in inflammation and other processes relevant to the architectural disturbances seen in the gastric mucosa in response to Helicobacter pylori infection. Upregulation of MMPs has been reported in H pylori infection, but there are no detailed reports regarding altered production of their inhibitors, the tissue inhibitors of metalloproteinases (TIMPs).. To investigate changes in the abundance of TIMPs in human gastric corpus mucosa and murine stomach in Helicobacter infection, and to study cellular sources in man.. Gastric corpus biopsy samples were assessed for abundance of mRNA or protein for TIMP-1 to -4 by real-time quantitative PCR or western blotting, respectively. Antral and corpus biopsies were processed for histology, H pylori status and inflammatory scoring. Cellular sources of TIMP-1, -3 and -4 were examined by indirect immunohistochemistry. Circulating gastrin was measured by radioimmunoassay. Also, abundance of TIMP-1, -3 and -4 mRNA in the stomach of Helicobacter felis infected mice post-infection was compared with that of uninfected control animals.. Compared with uninfected patients, mRNA and protein for TIMP-1, -3 and -4 were significantly more abundant in the gastric corpus of H pylori infected subjects. Gastric TIMP expression did not differ significantly between hyper- and normogastrinaemic subjects within the H pylori negative and positive groups. There was no difference in mRNA abundance for MMP-3 or -8. Immunohistochemistry showed TIMP proteins localised to gastric epithelial, stromal cells and inflammatory cells. Murine H felis infection was associated with upregulation of TIMP-1 and -3 mRNA.. Helicobacter infection is associated with upregulation of specific TIMPs (TIMP-1 and -3) in glandular epithelium and stroma. It is suggested that increased expression of specific protease inhibitors in the corpus mucosa may exert important effects on extracellular matrix remodelling and influence the outcome of H pylori infection.

Topics: Animals; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Mice; Mice, Transgenic; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Severity of Illness Index; Tissue Inhibitor of Metalloproteinases; Up-Regulation

Elevated gastrin concentration leading to gastritis is explained as the effect of change in the density of D and G cells. The aim of the study was to determine and compare fasting serum gastrin concentrations, G and D cell densities in gastric antrum mucosa in children with chronic gastritis and in children with no gastritis or Helicobacter pylori infection.. A total of 184 patients aged 6-18 years, with chronic abdominal pain underwent endoscopic examination. We created three groups: I--patients with chronic gastritis and H. pylori infection; II--patients with chronic gastritis but no H. pylori infection; III--patients with neither gastric mucosal abnormalities nor H. pylori infection. G and D cell densities were determined in the biopsy specimens (using Rbalpha H Gastrin & Somatostatin antibodies). Fasting serum gastrin concentrations were measured using a Beckmann gamma-counter and a GASK-PR kit.. The mean serum gastrin concentration in group I was higher when compared with group II (p = 0.04) and group III (p = 0.019). No statistically significant differences were found between groups II and III (p = 0.91). There were no statistically significant differences in G and D cell densities between groups.. The mean G/D cell ratios in groups I and III were almost identical. The mean fasting serum gastrin concentration was higher in children with both chronic gastritis and H. pylori infection compared with patients without infection or without antral inflammation. No difference in the G cell density or D cell density in children was found, regardless of the presence or absence of gastritis or H. pylori infection.

Topics: Adolescent; Cell Count; Child; Child, Preschool; Chronic Disease; Female; Gastrin-Secreting Cells; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Pyloric Antrum; Somatostatin-Secreting Cells

Oxidative stress is linked to gastric carcinogenesis because of its ability to damage DNA. Here we examined antioxidative and anti-inflammatory effects of 4-vinyl-2,6-dimethoxyphenol (canolol), a recently identified potent antioxidative compound obtained from crude canola oil, on Helicobacter (H.) pylori-induced gastritis and gastric carcinogenesis using a Mongolian gerbil model. The animals were allocated to H. pylori-infection alone (12 weeks) or H.pylori + N-methyl-N-nitrosourea (MNU) administration (52 weeks). After oral inoculation of H. pylori, they were fed for 10 and 44 weeks with or without 0.1% canolol. H. pylori-induced gastritis, 5'-bromo-2'-deoxyuridine (BrdU) labeling and scores for cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) immunohistochemistry were attenuated in the canolol-treated groups. Expression of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), COX-2 and iNOS mRNA in the gastric mucosa, and serum 8-hydroxy-2'-deoxyguanosine (8-OHdG), anti-H. pylori IgG and gastrin levels were also significantly lower in canolol-treated groups. Furthermore, the incidence of gastric adenocarcinomas was markedly reduced in the H. pylori + MNU + canolol-treated group [15.0% (6/40)] compared to the control group [39.4% (13/33)] (p < 0.05). These data indicate canolol to be effective for suppressing inflammation, gastric epithelial cell proliferation and gastric carcinogenesis in H. pylori-infected Mongolian gerbils. Interestingly, the viable H. pylori count was not changed by the canolol containing diet. Thus, the data point to the level of inflammation because of H. pylori rather than the existence of the bacteria as the determining factor. Importantly, canolol appears to suppress induction of mRNAs for inflammatory cytokines.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Anti-Inflammatory Agents; Antibodies, Bacterial; Antioxidants; Biomarkers; Cell Proliferation; Cell Transformation, Neoplastic; Cyclooxygenase 2; Deoxyguanosine; Disease Models, Animal; Gastric Mucosa; Gastrins; Gastritis; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Immunoglobulin G; Immunohistochemistry; Interleukin-1beta; Nitric Oxide Synthase Type II; Oxidative Stress; Phenols; Polymerase Chain Reaction; RNA, Messenger; Stomach Neoplasms; Tumor Necrosis Factor-alpha; Vinyl Compounds

First-degree relatives of gastric cancer patients are at risk for developing precancerous conditions. The aim of this study was to investigate the potential of biomarkers pepsinogen I (PGI), pepsinogen II (PGII), their ratio (PG I:II), as well as gastrin 17 for screening of precancerous conditions and corpus predominant gastritis.. First-degree relatives of gastric cancer patients underwent endoscopy. Three biopsy specimens from the antrum and 3 from the corpus were evaluated according to the Sydney classification. Serum was taken for the measurement of fasting PGI, PGII, and gastrin 17 by enzyme-linked immunosorbent assay kits.. A total of 481 patients were examined (age, 47.8 +/- 6.7 y). With the extension of gastritis, PGII was increased up to 2.5 times (6.6 +/- 2.8 microg/mL in normal mucosa, 9.5 +/- 6.7 microg/mL in antral gastritis, and 16.9 +/- 12.4 microg/mL in corpus-predominant gastritis; P < .01), PGI increased slightly (88.3 +/- 29.4 microg/mL in normal mucosa and 111.2 +/- 71.4 microg/mL in corpus-predominant gastritis), and gastrin 17 was increased substantially in corpus-predominant gastritis (15.3 +/- 19.5 pmol/mL vs 3.8 +/- 5.7 pmol/mL in normal mucosa). By using a cut-off value of 7.5 microg/mL for PGII, any type of gastritis from normal mucosa can be diagnosed with a sensitivity and specificity of 80%. The sensitivity and specificity of the PG I:II ratio (< or =3) and gastrin 17 (>17 pmol/mL) together were 9.4% and 99% for screening corpus-predominant gastritis and 14.8% and 97.8%, respectively, for screening intestinal metaplasia in the corpus.. PGII is a suitable marker for screening any gastritis from normal mucosa, but neither PGI, the PG I:II ratio, gastrin 17, nor their combination were able to select those with precancerous conditions and corpus-predominant gastritis among the first-degree relatives of gastric cancer patients.

Topics: Adult; Biomarkers; Biopsy; Enzyme-Linked Immunosorbent Assay; Family; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Sensitivity and Specificity; Serum; Stomach Neoplasms

Gastritis, an inflammatory state in gastric mucosa, can be induced experimentally in various ways. The present study considered the iodoacetamide model (Iodo). Omega-3 fatty acids (fish oil), black seed oil, and curcuminoids (natural products) in addition to omeprazole (synthetic proton-pump inhibitor) were tested. Supplementation of 0.1% iodoacetamide to drinking water of experimental rats for two consecutive weeks resulted in: (i) increased serum nitric oxide (NO) and gastrin, and decreased pepsinogen, (ii) depletion of gastric mucosal glutathione (GSH), and (iii) increased gastric mucosal lipid peroxidation (MDA), but failed to affect gastric mucosal myeloperoxidase (MPO) activity. Histological examination showed marked neutrophilic infiltration after 1 week of iodoacetamide administration and shedding of apical cell layer with pale edematous vacuolated gastric gland cells and thickening of muscularis mucosa after 2 weeks of iodoacetamide intake. Individual administration of omega-3 fatty acids 12 mg/kg, black seed oil 50 mg/kg, and curcuminoids 50 mg/kg body weight orally daily for 3 weeks decreased MDA, gastrin, and NO, and normalized mucosal GSH but failed to affect serum pepsinogen level. Combined administration of these natural products for 3 weeks normalized MPO activity, and other effects were nearly the same as with individual use. Omeprazole administration 30 mg/kg body weight orally daily for 3 weeks induced a similar response except for an observed increase in serum gastrin and pepsinogen levels.

Topics: Administration, Oral; Analysis of Variance; Animals; Curcuma; Disease Models, Animal; Fatty Acids, Omega-3; Gastric Mucosa; Gastrins; Gastritis; Iodoacetamide; Lipid Peroxidation; Male; Malondialdehyde; Nitrites; Omeprazole; Pepsinogen A; Peroxidase; Plant Extracts; Plant Oils; Rats; Rats, Wistar

Helicobacter pylori gastritis may lead to impairment of the production of pepsinogen and acid, which are essential to cobalamin absorption. In turn, cobalamin deficiency leads to hyperhomocysteinaemia, a risk factor for cardio and cerebrovascular diseases.. To evaluate the effect of H pylori eradication on plasma homocysteine levels in elderly patients.. Sixty-two H pylori-positive elderly patients with cobalamin deficiency were prospectively studied.. Homocysteine and cobalamin concentrations were determined before, 6 and 12 months after H pylori eradication.. Corpus atrophy was observed in a few patients; otherwise, in most of them, the degree of corpus gastritis was moderate to severe. The initial homocysteine mean (SD) levels decreased from 41.0 (27.1) to 21.6 (10.1) micromol/l at the 6 month follow-up (p<0.001) and to 13.1 (3.8) micromol/l 12 months after H pylori eradication (p<0.001). Conversely, initial cobalamin mean levels increased from 145.5 (48.7) pmol/l to 209.8 (87.1) pmol/l and to 271.2 (140.8) pmol/l, 6 and 12 months after treatment, respectively (p<0.001 for both). Although the erythrocyte mean corpuscular volume was within reference intervals, it decreased significantly 6 (p = 0.002) and 12 (p<0.001) months after treatment.. The results of the current study demonstrated that the eradication of H pylori in elderly patients with cobalamin deficiency is followed by increasing of cobalamin and decreasing of homocysteine blood levels.

Topics: Aged; Aged, 80 and over; Autoantibodies; Female; Follow-Up Studies; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Homocysteine; Humans; Intrinsic Factor; Male; Middle Aged; Parietal Cells, Gastric; Pepsinogen A; Prospective Studies; Vitamin B 12 Deficiency

Helicobacter pylori infects over half the population worldwide and is a leading cause of chronic gastritis and gastric cancer. However, the mechanism by which this organism induces inflammation and carcinogenesis is not fully understood. In the present study we used insulin-gastrin (INS-GAS) transgenic mice that fully develop gastric adenocarcinoma after infection of H. pylori-related Helicobacter felis. Histological examination revealed that more than half of those mice developed invasive adenocarcinoma after 8 months of infection. These carcinomas were stained by NCC-ST-439 and HECA-452 that recognize 6-sulfated and non-sulfated sialyl Lewis X. Lymphocytic infiltration predominantly to submucosa was observed in most H. felis-infected mice, and this was associated with the formation of peripheral lymph node addressin (PNAd) on high endothelial venule (HEV)-like vessels detected by MECA-79. Time-course analysis of gene expression by using gene microarray revealed upregulation of several inflammation-associated genes including chemokines, adhesion molecules, surfactant protein D (SP-D), and CD74 in the infected stomach. Immunohistochemical analysis demonstrated that SP-D is expressed in hyperplasia and adenocarcinoma whereas CD74 is expressed in adenocarcinoma in situ and invasive carcinoma. These results as a whole indicate that H. felis induces HEV-like vessels and inflammation-associated chemokines and chemokine receptors, followed by adenocarcinoma formation.

Topics: Adenocarcinoma; Animals; Antigens, Differentiation, B-Lymphocyte; Female; Gastric Mucosa; Gastrins; Gastritis; Gene Expression Profiling; Glycosyltransferases; Helicobacter felis; Helicobacter Infections; Histocompatibility Antigens Class II; Hyperplasia; Immunohistochemistry; Insulin; Lymphocytes; Male; Mice; Mice, Transgenic; Oligonucleotide Array Sequence Analysis; Oligosaccharides; Pulmonary Surfactant-Associated Protein D; Sialyl Lewis X Antigen; Stomach; Stomach Neoplasms; Up-Regulation

Proper absorption of vitamin B12 requires gastric corpus mucosa that functions appropriately and secretes intrinsic factor needed as an essential cofactor for the absorption of dietary vitamin B12 in the small bowel. Here we describe the prevalence of vitamin B12 deficiency and atrophic corpus gastritis (ACG) in patients with coronary heart disease. Fasting serum was obtained from patients who were admitted for cardiovascular diseases at the Coronary Care Unit in Nijmegen, the Netherlands. The status of gastric mucosa was assessed by using the serum levels of pepsinogens I and II, gastrin-17, and Helicobacter pylori IgG antibodies and analyzed over vitamin B12 level subgroups. The study population consisted of 376 patients (mean age, 65 years [SD, 13 years], 227 [60%] males). Low vitamin B12 levels (<150 pM) were detected in 28 patients (7%). Of these 28 patients, 5 (18%) had ACG according to the biomarker assays. Altogether, another 140 patients (37%) had vitamin B12 levels between 150 and 250 pM, of whom 10 (7%) had ACG. Of the remaining patients, five (2%) had ACG. Deficiency of vitamin B12 is common among subjects with coronary heart disease. Up to 20% of these deficiencies are related to ACG.

Topics: Aged; Biomarkers; Coronary Disease; Enzyme-Linked Immunosorbent Assay; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Pepsinogens; Retrospective Studies; Vitamin B 12

Studies in 45 cryolite production workers (facing chronic gastritis and gastroduodenitis) demonstrated that the diseases in them have moderate inflammatory activity, atrophy of gastric lining contaminated with Helicobacter pylori, hypergastrine mia, hypopancreozymine mia and hyposecretine mia in half of the examinees.

Topics: Adult; Duodenitis; Female; Fluorine Compounds; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Occupational Diseases; Occupational Exposure

To investigate the influence of gender, age, site of lesion, disease type and Helicobacter pylori (H. pylori) infection on the human serum gastrin-17 level and to study the diagnostic value of serum gastrin-17 in gastric precancerous lesions and gastric cancer.. Serum gastrin-17 and serum H. pylori IgG antibody were detected by the ELISA method. The different gastric disease groups were confirmed by endoscopy and histopathology.. Among the 3906 serum samples according to the gender, age, site of lesion and the data of different gastric disease groups, the serum gastrin-17 level was markedly higher in people>or=60 years old than that in younger age groups. The serum gastrin-17 level increased progressively in the following order: healthy control group, nonatrophic gastritis group, gastric ulcer group, and the serum gastrin-17 level was higher in the atrophic gastritis with dysplasia group than that without it, the lowest level being in the gastric cancer group. Among the 2946 serum samples matched with the site of the lesion, the serum gastrin-17 level was higher in those with antral diseases than in those with gastric corpus diseases. Among the 3805 serum samples matched with the H. pylori infection data, the serum gastrin-17 level was higher in the H. pylori-positive group than in the H. pylori-negative group.. In people over 60 years of age, the serum gastrin-17 level tends to increase. In subjects with precancerous gastric lesions, it may increase significantly with the progression of gastric disease, and ultimately decrease in gastric cancer. Serum gastrin-17 is a good biomarker to differentiate benign from malignant gastric diseases. The site of the gastric lesions is an important factor affecting the serum gastrin-17 level, whereas H. pylori infection is usually associated with its increment.

Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; China; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Precancerous Conditions; Retrospective Studies; Stomach Neoplasms

Helicobacter pylori-induced gastritis is an important factor for gastric carcinogenesis. However, it is still controversial whether it is also applicable for cardiac cancer development. Recently, we reported that H. pylori is an important factor for the induction of cardiac inflammation. We examined the status of H. pylori-induced gastritis in patients with cardiac cancer.. Seventy-five Japanese patients (58 men; mean age, 64.2 years) with cardiac cancer were studied. Cardiac cancer was defined as that mainly located within 2 cm from the squamo-columnar junction (SCJ). Histological gastritis including the cardiac region was evaluated using the biopsy or surgically resected sections. Cardiac inflammation was evaluated at 1 cm distal from SCJ in lesser curvature. Sera were collected and several markers were evaluated. The status of H. pylori infection was evaluated by histology and serum antibodies. Expressions of cytokeratins were examined by immunohistochemical analysis.. Out of 75 patients with cardiac cancer, H. pylori was positive in 71 (95%) patients. The cardiac inflammation was examined in 30 patients (26 with H. pylori and four without H. pylori infection) and we found cardiac inflammation was present in all cases with H. pylori infection. Histologically, H. pylori-related gastritis was also found in the gastric corpus and antrum. Serological data were consistent with the presence of chronic atrophic gastritis. Intestinal metaplasia was found in 18 cases in the cardiac mucosa, and their cytokeratin 7/20 pattern was judged as a gastric pattern in all cases.. H. pylori infection is closely associated with cardiac cancer.

Topics: Adult; Aged; Aged, 80 and over; Autoantibodies; Cardia; Chronic Disease; Enzyme-Linked Immunosorbent Assay; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Male; Middle Aged; Parietal Cells, Gastric; Pepsinogen A; Stomach Neoplasms

Non-invasive methods are advisable for the detection of Helicobacter pylori-related chronic gastritis in pediatric patients. Serum pepsinogens I and II (sPGII and sPGII), gastrin-17 (G-17) and anti-H. pylori antibodies (IgG-Hp) have been proposed as a 'serological gastric biopsy'.. To assess H. pylori infection and to evaluate gastric mucosa status in a pediatric population by means of serological parameters such as sPGI, sPGII, G-17 and IgG-Hp.. 45 consecutively children evaluated for upper gastrointestinal symptoms were analyzed. All children were submitted to upper gastrointestinal endoscopy with biopsies. Serum samples were analyzed for IgG-Hp, sPGII, sPGI and G-17 (Biohit, Helsinki, Finland).. 18 children had H. pylori-related mild or moderate non-atrophic chronic gastritis. They presented significantly higher mean levels of sPGII and of IgG-Hp than negative ones, either under or up to 10 years. sPGI showed significantly increased levels in H. pylori-positive patients only over 10 years. G-17 levels were not different between H. pylori-positive and -negative ones. The best cut-offs of IgG-Hp, sPGII and of product IgG-Hp x sPGII, to identify H. pylori infection, were 30 IU/l, 9 microg/l, and 241 IU/l x microg/l, respectively. The product IgG-Hp x sPGII identified H. pylori infection with a 100% sensitivity, 92% specificity, 90% positive predictive value and 100% negative predictive value. IgG-Hp and IgG-Hp showed a correlation (r = 0.94; p < 0.001).. Combined analysis of sPGII and IgG-Hp antibody levels could be recommended as a non-invasive panel for the assessment of H. pylori-related histological alterations of gastric mucosa in childhood.

Topics: Adolescent; Biomarkers; Biopsy; Child; Child, Preschool; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Pepsinogens

Topics: Adult; Aged; Aged, 80 and over; Biomarkers, Tumor; Chronic Disease; Duodenal Ulcer; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Pyloric Antrum; Retrospective Studies; Stomach Neoplasms; Stomach Ulcer

Iron deficiency is a known complication of achlorhydria and may precede the development of pernicious anemia. Among 160 patients with autoimmune gastritis identified by hypergastrinemia and strongly positive antiparietal antibodies, we explored the overlap between 83 subjects presenting with iron deficiency anemia (IDA), 48 with normocytic indices, and 29 with macrocytic anemia. Compared with macrocytic patients, patients with IDA were 21 years younger (41 +/- 15 years versus 62 +/- 15 years) and mostly women. All groups had a high prevalence of thyroid disease (20%) and diabetes (8%) suggestive of the autoimmune polyendocrine syndrome. Stratification by age cohorts from younger than 20 years to older than 60 years showed a regular and progressive increase in mean corpuscular volume (MCV) from 68 +/- 9 to 95 +/- 16 fl, serum ferritin levels from 4 +/- 2 to 37 +/- 41 microg/L, gastrin level from 166 +/- 118 to 382 +/- 299 pM/L (349 +/- 247 to 800 +/- 627 pg/mL), and a decrease in cobalamin level from 392 +/- 179 to 108 +/- 65 pg/mL. The prevalence of Helicobacter pylori infection was 87.5% at age younger than 20 years, 47% at age 20 to 40 years, 37.5% at 41 to 60 years, and 12.5% at age older than 60 years. These findings challenge the common notion that pernicious anemia is a disease of the elderly and imply a disease starting many years before the establishment of clinical cobalamin deficiency, by an autoimmune process likely triggered by H pylori.

Topics: Adult; Aged; Anemia, Iron-Deficiency; Anemia, Pernicious; Autoantibodies; Autoimmune Diseases; Disease Progression; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Reference Values; Vitamin B 12

The stimulation of gastric acid secretion from parietal cells involves both intracellular calcium and cAMP signaling. To understand the effect of increased cAMP on parietal cell function, we engineered transgenic mice expressing cholera toxin (Ctox), an irreversible stimulator of adenylate cyclase. The parietal cell-specific H(+),K(+)-ATPase beta-subunit promoter was used to drive expression of the cholera toxin A1 subunit (CtoxA1). Transgenic lines were established and tested for Ctox expression, acid content, plasma gastrin, tissue morphology, and cellular composition of the gastric mucosa. Four lines were generated, with Ctox-7 expressing approximately 50-fold higher Ctox than the other lines. Enhanced cAMP signaling in parietal cells was confirmed by observation of hyperphosphorylation of the protein kinase A-regulated proteins LASP-1 and CREB. Basal acid content was elevated and circulating gastrin was reduced in Ctox transgenic lines. Analysis of gastric morphology revealed a progressive cellular transformation in Ctox-7. Expanded patches of mucous neck cells were observed as early as 3 mo of age, and by 15 mo, extensive mucous cell metaplasia was observed in parallel with almost complete loss of parietal and chief cells. Detection of anti-parietal cell antibodies, inflammatory cell infiltrates, and increased expression of the Th1 cytokine IFN-gamma in Ctox-7 mice suggested that autoimmune destruction of the tissue caused atrophic gastritis. Thus constitutively high parietal cell cAMP results in high acid secretion and a compensatory reduction in circulating gastrin. High Ctox in parietal cells can also induce progressive changes in the cellular architecture of the gastric glands, corresponding to the development of anti-parietal cell antibodies and autoimmune gastritis.

Topics: Aging; Animals; Animals, Genetically Modified; Antibodies; Autoimmune Diseases; Cholera Toxin; Cyclic AMP; Disease Models, Animal; Gastric Acid; Gastrins; Gastritis; Gastritis, Atrophic; H(+)-K(+)-Exchanging ATPase; Mice; Mice, Inbred C57BL; Parietal Cells, Gastric; Promoter Regions, Genetic

Corpus gastritis is a common diagnosis. Studies have shown that about 25% of patients that undergo gastroscopy receive this diagnosis. This study was undertaken to investigate etiological associations in patients with corpus gastritis in our northern Icelandic population.. Patients who had had a histological diagnosis of chronic corpus gastritis between the years of 1994 to 1998 were retrieved from the computer files of the department of pathology. In all 172 patients fulfilled the Sydney pathological criteria. Pathology review was performed by the same pathologist. Blood samples were also taken for variable serology and a urea breath test for Helicobacter pylori (H. pylori) was performed.. Mean age 71 year old (24-99 year). Males were 57%. H. pylori infection was diagnosed in 39%. There appears to be a relationship between active gastritis and H. pylori positivity, especially if there was only chronic gastritis without atrophy or metaplasia. Atrophy was significantly greater if anti-parietal antibody was present. No connections were found between anti-parietal antibody and anti-microsomal antibody. There was significantly higher mean gastrin levels in patients with atrophy or metaplasia compared with only chronic gastritis (p<0.05), present also in patients with chronic gastritis vs active gastritis (p<0.01). There was no difference in mean gastrin levels between H. pylori positive and H. pylori negative patients. Significantly higher mean gastrin levels were seen in patients with anti-parietal antibody (p<0.001). No difference was found in mean gastrin levels between patients with or with out antimicrosomal antibody.. There is a high probability that corpus gastritis and related complications are related to H. pylori infection in a large proportion of our population. Serum gastrin may well be a predictor of the histological grading of the chronic gastritis. We did not see a relationship with antimicrosomal activity.

Topics: Adult; Aged; Aged, 80 and over; Atrophy; Biomarkers; Chronic Disease; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Medical Records Systems, Computerized; Middle Aged; Predictive Value of Tests; Retrospective Studies; Stomach

Gender differences have been shown regarding the changes in the inflammatory response, gastrin secretion, and gastric acidity during Helicobacter pylori infection.. To investigate the role of estradiol and progesterone in the changes of the gastric mucosa induced by H. pylori during the early stage of infection in female gerbils.. Thirty-three adult ovariectomized female gerbils were infected with H. pylori (SS1); 7 days after infection they were treated with low and high doses of estradiol (50 and 250 microg/60 days pellet), progesterone (15 and 50 mg/60 days pellet) and vehicle. Non-ovariectomized infected gerbils were used as control. Gerbils were euthanized after 6 weeks of infection. Histologic evaluation, immunohistochemical detection of proliferation cell nuclear antigen (PCNA), gastrin, and apoptosis by terminal deoxynucleotide nick end labeling (TUNEL) assay were performed. Positive cells for PCNA, TUNEL, and gastrin were counted in 10 oriented glands per animal. Two-sided p = .05 was considered significant.. Estradiol-treated groups showed more intense and extended acute and follicular gastritis compared to the vehicle group, whereas progesterone-treated groups presented less gastritis than the other groups. Proliferation and apoptosis indexes were significantly lower in the vehicle group when compared with those of the control; both indexes were increased in the high-dose estradiol and progesterone groups as compared with those of the vehicle. Grade I nonmetaplastic atrophy was observed in the vehicle and progesterone groups. The high-dose progesterone group showed a significant reduction in the number of gastrin cells.. Estradiol and progesterone participate in the gastric mucosal response to early H. pylori infection in gerbils.

Topics: Animals; Apoptosis; Cell Proliferation; Disease Models, Animal; Estradiol; Female; Gastric Mucosa; Gastrins; Gastritis; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Immunohistochemistry; In Situ Nick-End Labeling; Progesterone; Proliferating Cell Nuclear Antigen

We attempted to clarify the pathogenesis of gastric inflammation in the cardia. Eighty Japanese participated in this study. Biopsy specimens of the gastric antrum, corpus, and cardia (1 cm from the squamocolumnar junction) were obtained, and histological gastritis was evaluated. Cardiac inflammation was also evaluated using magnifying gastroscopy. We examined Helicobacter pylori infection, gastric juice pH/bile acid (BA), serum pepsinogen and gastrin levels, gastroesophageal reflux disease (GERD), and habitual smoking and assessed the relations between these factors and cardiac inflammation. The prevalence of H. pylori infection was statistically higher in patients with cardiac inflammation than in those without inflammation (P < 0.05). The relationship was also demonstrated by magnifying gastroscopy. Cardiac inflammation was linked to low acid output but not linked to the BA concentration or habitual smoking. Cardiac inflammation was more pronounced in patients without GERD. These results suggest that H. pylori is a major risk factor for cardiac inflammation in the Japanese.

Topics: Adult; Aged; Aged, 80 and over; Biopsy; Cardia; Female; Gastric Acid; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Risk Factors

To study the expressions of gastrin (GAS) and somatostatin (SS) in gastric antrum tissues of children with chronic gastritis and duodenal ulcer and their role in pathogenic mechanism.. Specimens of gastric antrum mucosa from 83 children were retrospectively analyzed. Expressions of GAS and SS in gastric antrum tissues were assayed by the immunohistochemical En Vision method.. The expressions of GAS in chronic gastritis Hp+ group (group A), chronic gastritis Hp-group (group B), the duodenal ulcer Hp+group (group C), duodenal ulcer Hp-group (group D), and normal control group (group E) were 28.50+4.55, 19.60+2.49, 22.69+2.71, 25.33+4.76, and 18.80+2.36, respectively. The value in groups A-D was higher than that in group E. The difference was not statistically significant. The expressions of SS in groups A-E were 15.47+1.44, 17.29+2.04, 15.30+1.38, 13.11+0.93 and 12.14+1.68, respectively. The value in groups A-D was higher than that in group E. The difference was also not statistically significant.. The expressions of GAS and SS are increased in children with chronic gastritis and duodenal ulcer.

Topics: Child; Chronic Disease; Duodenal Ulcer; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Pyloric Antrum; Retrospective Studies; Somatostatin

Acid secretion is intimately associated with most upper gastrointestinal diseases. Helicobacter pylori infection is a major environmental factor modifying acid secretion.. To study the association between the pattern of H pylori gastritis and gastric secretory function in a large number of subjects without specific upper gastrointestinal disease.. Maximal acid output (MAO) was measured in 255 patients with dyspepsia showing normal endoscopy. Activity and severity of gastritis, atrophy and H pylori infection were assessed in body and antral biopsies. The correlations of histological parameters as well as age, sex, height, weight, smoking, serum gastrin, pepsinogen I and II, and their ratio with MAO were determined. Multiple linear regression was used to show the best possible predictors of MAO.. Negative relationships: Body atrophy and body-combined (active and chronic) inflammatory scores showed a potent inverse correlation with MAO (correlation coefficients (CC) 0.59 and 0.50, respectively). Body:antral chronic gastritis ratio and body:antral combined inflammation ratio (both with CC = 0.49) and age (CC = 0.44) were also inversely correlated with MAO. Intestinal metaplasia at both antral and body sites had negative relationships with acid output with CC = 0.23 and 0.20, respectively. Positive relationships: Serum pepsinogen I, body H pylori density:combined inflammation ratio and pepsinogen I:II ratio with CC of 0.38, 0.38 and 0.30, respectively, correlated with MAO. The H pylori density: combined inflammation of both antrum and body positively correlated with MAO (CC = 0.29 and 0.38, respectively). Male sex and patient height also positively correlated with acid output. Modelling showed that body combined inflammatory score, body atrophy, age and serum pepsinogen I are independent predictors of acid output (R(2) = 0.62).. Combination of body gastritis, body atrophy, age and serum pepsinogen I can be used as predictors of acid-secretory state in populations infected with H pylori.

Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Antigens, Bacterial; Bacterial Proteins; Biomarkers; Biopsy; Chronic Disease; Female; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Linear Models; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Pyloric Antrum

Gastrin deficiency and proton pump inhibitor treatment cause achlorhydria, which predisposes to disease. To elucidate the underlying molecular biology, we examined the changes in gastric gene expression in both types of achlorhydria. We also explored the associated changes in the gastric microflora and the long-term consequences of gastrin-deficient achlorhydria.. Expression profiles were generated from gastric RNA from wild-type mice, gastrin knockout (KO) mice, gastrin KO mice after 1 week of gastrin infusion, and wild-type mice treated for 1 month with a proton pump inhibitor. The results were confirmed using real-time polymerase chain reaction and immunohistochemistry. Selective media were used to characterize the gastric microflora.. The number of gastric bacteria was increased in both gastrin KO and PPI-treated mice. The expression profiles revealed activation of immune defense genes, interferon-regulated response genes, and intestinal metaplasia of the gastric mucosa. In young gastrin-deficient mice, gastrin infusions reversed the changes. Over time, the changes accumulated, became irreversible, and progressed into metaplasia and polyp development. Finally, the study showed that gastrin regulated the expression of genes encoding extracellular matrix proteins.. Independently of gastrin, achlorhydria is associated with gastric bacterial overgrowth and intestinal gene expression patterns and is associated with predisposition to disease. Gastrin is therefore essential for prevention of gastric disease, mainly through control of acid secretion but to a lesser extent also through control of gastric gene expression. The gastrin-deficient mouse serves as a useful new model for gastric metaplasia and neoplasia.

Topics: Animals; CDX2 Transcription Factor; Disease Models, Animal; DNA, Neoplasm; Female; Gastric Mucosa; Gastrins; Gastritis; Gene Expression; Homeodomain Proteins; Hormones; Immunohistochemistry; Male; Metaplasia; Mice; Mice, Inbred C57BL; Mice, Knockout; Polymerase Chain Reaction; Stomach Neoplasms; Transcription Factors

The gp130(757F/F) mouse is a well-characterized and robust model of distal gastric tumorigenesis displaying many of the characteristics of human intestinal type gastric cancer. Key to the development of tumors in this model, and in many examples of human tumor development, is hyperactivation of the transcription factor STAT3. This study addressed the requirement for STAT3 activation in tumor initiation and characterized some of the genes downstream of STAT3 required for tumor development. Furthermore, the interaction among STAT3, the microbial environment, and tumorigenesis was evaluated.. The role of STAT3 in gastric tumor development was assessed in detail in gp130(757F/Y757F):STAT3(+/-) mice displaying reduced STAT3 activity. Tumor size was quantified morphologically, and the effects on endocrine cell populations, neovascularization, and inflammatory cell infiltration as well as the outcome of STAT3 activation on transcription of a number of genes relevant in growth and inflammation were quantified.. Loss of one STAT3 allele in gp130(757F/F) mice reduced the frequency and rate of tumor development because of inhibition of proliferation-induced glandular hyperplasia. There was also a concomitant reduction in the degree of inflammatory infiltration and cytokine and chemokine expression, angiogenesis, and expression of metalloproteinases and growth factors. Antimicrobial treatment of gp130(757F/F) mice slowed tumor growth coincident with reduced macrophage and neutrophil infiltration.. Activation of STAT3 and the microbial environment are pivotal for gastric tumor initiation and development in the gp130(757F/F) mouse, thus supporting the notion that STAT3 activation may play a role in human gastric cancer development.

Topics: Animals; Cell Division; Cell Movement; Cytokine Receptor gp130; Disease Models, Animal; Extracellular Matrix; Gastric Mucosa; Gastrins; Gastritis; Gene Expression Regulation, Neoplastic; Leptin; Macrophages, Peritoneal; Mice; Mice, Inbred C57BL; Mice, Mutant Strains; Neovascularization, Pathologic; Neutrophils; Phosphorylation; Pyloric Antrum; Somatostatin; STAT3 Transcription Factor; Stomach Neoplasms

We reviewed the clinicopathologic profile of a series of recently diagnosed sporadic duodenal gastrin-cell (G-cell) tumors. All cases were discovered incidentally and had a unique clinicopathologic profile: all 18 cases were gastrin-positive tumors located in the duodenal bulb, were small in size (mean size 5.4 mm), demonstrated an insular architectural pattern, and were localized to the lamina propria and submucosa. None of the patients had Zollinger-Ellison or carcinoid syndrome. The behavior was indolent and there was no evidence of metastasis at diagnosis or during follow-up. In our sampled population, the presence of Helicobacter pylori gastritis and the use of proton pump inhibitors (PPIs) were significantly associated with the presence of G-cell tumors. Both the presence of H. pylori gastritis and use of PPI remained significant in a logistic regression model adjusted for age, race/ethnicity, and sex with P values of 0.0016 (odds ratio=10.1, 95% confidence interval: 2.3 to 42.4) and 0.008 (odds ratio=8.9, 95% confidence interval: 1.76 to 45.4), respectively. Most patients with tumors showed G-cell hyperplasia in the nontumorous regions of the duodenum. The high incidence of sporadic duodenal G-cell tumors in patients with H. pylori gastritis and long-term PPI use suggests an association that needs to be further explored. Presence of G-cell hyperplasia in the nontumorous duodenal mucosa suggests that these may originate from a proliferative phase, similar to the hyperplasia-dysplasia-neoplasia sequence seen in other endocrine tumors.

Topics: Aged; Aged, 80 and over; Anti-Ulcer Agents; Carcinoid Tumor; Duodenal Neoplasms; Duodenum; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Histamine H2 Antagonists; Humans; Male; Middle Aged; Proton Pump Inhibitors

Since application of pediatric gastroscopy in the mid-nineteen nineties, there has been a trend that the prevalence rates of pediatric gastritis and duodenal ulcer (DU) are increasing. The diagnosed rate of pediatric gastritis has accounted for 85% - 95% of the total number of children who received gastroscopy, and the rate of DU accounted for 8% - 22%. Such a high rates of the diseases may influence the development of the children severely. However, the etiology and pathogenesis of pediatric chronic gastritis and DU have not been completely elucidated. The disordered gastrointestinal hormones play a crucial role in the pediatric chronic gastritis and DU. This study focused on the expression of gastrin (GAS), somatostatin (SS) in the mucosa of gastric antrum and PCNA and Fas-L in the sinus ventriculi and their possible roles in the pathogenesis of pediatric chronic gastritis and DU.. The sinus ventriculi mucosal samples of 83 cases were collected via gastroscopic biopsy from the hospital during the recent two years and the cases were divided into five groups: group A, chronic superficial gastritis, Helicobacter pylori (Hp)(+); group B, chronic superficial gastritis, Hp(-); group C, DU, Hp(+); Group D, DU, Hp(-); Group E, normal sinus ventriculi mucosa, Hp(-). Immunohistochemical staining (En Vision) was carried out for GAS, SS, PCNA and Fas-L, and positive cells of each slide were counted (x 400). Statistically significant differences among groups for continuous data were assessed with the software SPSS10.0.. The expressions of GAS and SS in the groups A through E had no significant difference. The expression of PCNA in group A was significantly higher than that in group B (P < 0.05), and no significant differences were found among the other groups. There were no significant differences in expressions of Fas-L among the five groups.. There seems to be an increasing tendency in the expressions of GAS and SS in children with chronic gastritis and duodenal ulcer. Hp infection promotes the multiplication of the sinus ventriculi mucosal epithelium cells in the pediatric chronic gastritis.

Topics: Adolescent; Biopsy; Child; Child, Preschool; Duodenal Ulcer; Fas Ligand Protein; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Intestinal Mucosa; Male; Proliferating Cell Nuclear Antigen; Pyloric Antrum; Somatostatin

The conventional view of gastric acid secretion is that a negative feedback mechanism arises in response to high acidity, such that somatostatin keeps G-cells and parietal cells from producing more gastrin and acid, respectively. When the stomach becomes infected, for example with Helicobacter pylori (H. pylori), the feedback mechanism is impaired. In animal models, our laboratory has demonstrated that other types of bacteria besides H. pylori can cause gastritis. For example, under conditions of low acidity, gastritis is secondary to bacterial overgrowth, not production of excessive acid, thus suggesting a new paradigm for the regulation of gastric acid secretion under inflammatory conditions. Cytokines, released during the gastric inflammatory response, including IFN gamma, TNF alpha and IL-1 beta stimulate the G-cell to produce gastrin. Gastrin in turn triggers the release of acid, and hypergastrinemia suppresses somatostatin, the inhibitor of acid. The overall response results in maximal gastric acid output that acts as the stomach's most important anti-microbial agent. The increased acid secretion by the stomach in the presence of H. pylori seems to be part of the innate immune response, in that gastrin and somatostatin are reciprocally regulated by Th1 or Th2 cytokines, respectively. In a mouse model, we showed that octreotide, a somatostatin, analog, is an efficacious treatment for Helicobacter gastritis. In humans, octreotide might accelerate recovery from H. pylori infection, reducing the duration of antibiotic therapy.

Topics: Cytokines; Feedback; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Humans; Stomach Neoplasms

This is our final report on the clinical effectiveness and safety of long-term pantoprazole in patients with severe peptic ulcer or reflux disease during continuous treatment for up to 5 years.. Patients (n= 150) with peptic ulcer or reflux erosive oesophagitis running an aggressive course or with complications, and refractory to H2-receptor antagonists, were entered into this 5-year programme. Assessment was by serial endoscopy, clinical examination, serum gastrin estimation, gastric mucosal histology and mucosal endocrine cell quantification.. Healing results were presented earlier. The estimated rates of remission on maintenance treatment with pantoprazole (n = 115) were 82% at 1 year, 75% at 2 years, 72% at 3 years, 70% at 4 years and 68% at 5 years. Helicobacter pylori infection appeared not to influence the outcome in reflux patients, with roughly two-thirds continuing in remission irrespective of infection. Only four patients had adverse events considered to be definitely related to pantoprazole. Median gastrin levels rose by 1.5-2-fold and were higher in those with H. pylori infection; 13 patients had levels >500 ng/L on at least one occasion, but these high levels were not sustained. Histological changes were more marked in patients infected with H. pylori: chronic gastritis decreased in the antrum and increased in the corpus, which also showed atrophic changes. The total number of endocrine cells in the antrum showed little variation over 60 months but fell by around one-third in the corpus.. Long-term treatment with pantoprazole is effective and safe.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Anti-Ulcer Agents; Benzimidazoles; Cell Count; Enteroendocrine Cells; Female; Gastric Mucosa; Gastrin-Secreting Cells; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole; Pantoprazole; Peptic Ulcer; Sulfoxides

The current study tests the hypothesis that chronic atrophic gastritis from hypochlorhydria in the gastrin-deficient mouse predisposes the stomach to gastric cancer. Gross morphology and histology of 12-month-old wild-type (WT), gastrin-deficient (G-/-) and somatostatin-deficient (SOM-/-) mice were examined. Parietal and G cells, Ki67, TUNEL, villin and MUC2 expression were analysed by immunohistochemistry. RUNX3 and STAT3 expression was analysed by Western blot. Anchorage-independent growth was determined by cell cluster formation in soft agar. Compared to the WT and SOM-/- mice, hypochlorhydric G-/- mice developed parietal cell atrophy, significant antral inflammation and intestinal metaplasia. Areas of metaplasia within the G-/- mouse stomach showed decreased RUNX3 expression with elevated MUC2 and villin expression. Cells isolated from the tumor grew in soft agar. However, the cells isolated from WT, nontransformed G-/- and SOM-/- gastric tissue did not form colonies in soft agar. Consistent with elevated antral proliferation, tumor tissue isolated from the G-/- mice showed elevated phosphorylated STAT3 expression. We then examined the mechanism by which STAT3 was constitutively expressed in the tumor tissue of the G-/- mice. We found that IFNgamma expression was also significantly higher in the tumor tissue of G-/- mice compared to WT and SOM-/- animals. To determine whether STAT3 was regulated by IFNgamma, MKN45 cells were cocultured with IFNgamma or gastrin. IFNgamma significantly stimulated phosphorylation of STAT3 in the MKN45 cell line, but not gastrin. Therefore, we show here that in the hypochlorhydric mouse stomach, the chronic gastritis, atrophy, metaplasia, dysplasia paradigm can be recapitulated in mice. Moreover, neoplastic transformation of the antral gastric mucosa does not require gastrin.

Topics: Adenocarcinoma; Animals; Base Sequence; Blotting, Western; Chronic Disease; Disease Progression; DNA Primers; Gastrins; Gastritis; Immunohistochemistry; Mice; Radioimmunoassay; Reverse Transcriptase Polymerase Chain Reaction; Stomach Neoplasms

Little is known about the natural course of multiple gastric carcinoids associated with type A gastritis. Between 1993 and 2003, we enrolled eight patients, diagnosed as having multiple gastric carcinoids associated with type A gastritis, in a follow-up program without surgical resection. In these patients, endoscopy showed multiple small polyps on the gastric body, with nonantral atrophic gastritis. Histologically, biopsy specimens obtained from the polyps revealed carcinoid tumors. The serum gastrin level was found to be very high in all patients, and testing for anti-parietal cell antibody was positive in seven. The mean follow-up was 5.8 years (range, 1.5-10.8 years). The levels of serum gastrin increased in all patients, but, endoscopically, the carcinoid tumors did not change in size. Neither hepatic nor lymphatic metastasis was detected on abdominal computed tomography (CT). These patients were free of the development or metastasis of carcinoids, in spite of their continuous hypergastrinemia. It was concluded that multiple gastric carcinoids associated with type A gastritis may be indolent.

Topics: Aged; Biopsy; Carcinoid Tumor; Endoscopy, Gastrointestinal; Female; Follow-Up Studies; Gastrins; Gastritis; Humans; Male; Middle Aged; Neoplasm Metastasis; Prognosis; Stomach Neoplasms

Epidemiological studies suggest that atrophic corpus-dominant gastritis is an increased risk factor for gastric carcinogenesis. The role of the Helicobacter pylori type IV secretion system (T4SS) for pathogenesis in the Mongolian gerbil model was explored.. Mongolian gerbils were infected for 32 weeks either with H. pylori type I strain B128 or with isogenic mutant strain B128delta cytotoxin-associated gene (cagY) or B128delta cagA , defective in T4SS or in the production of its effector protein CagA, respectively. Quantitative H. pylori reisolation was performed from the gastric antrum and corpus separately, cytokines were measured by quantitative reverse-transcription polymerase chain reaction, and gastric pH and hormones were determined.. B128-infected gerbils harbored high numbers of bacteria in the gastric antrum and corpus, whereas B128delta cagY and B128delta cagA colonized the antrum more densely than the corpus. All infected animals showed a strong antral inflammation and epithelial cell proliferation. B128-infected, rather than mutant-infected, gerbils presented a severe transmural inflammation with huge lymph aggregates, increased proliferation, significant atrophy, and mucous gland metaplasia in the corpus. Plasma gastrin levels and gastric pH values were significantly increased only in B128-infected gerbils. In all infected animals, the expression of the proinflammatory cytokines interleukin 1beta, interferon gamma, and growth-regulated protein was considerably increased in the antrum, but only in wild type-infected animals was an increase seen in the corpus mucosa.. The presence of an intact T4SS allows H. pylori to colonize the gastric corpus. This results in atrophic corpus-dominant gastritis, a severe precancerous condition, thus highlighting T4SS and CagA as major risk factors for gastric cancer development.

Topics: Achlorhydria; Animals; Antigens, Bacterial; Atrophy; Bacterial Proteins; Cytokines; Female; Gastric Mucosa; Gastrins; Gastritis; Gerbillinae; H(+)-K(+)-Exchanging ATPase; Helicobacter Infections; Helicobacter pylori; Hypertrophy; Mutation; Precancerous Conditions; Promoter Regions, Genetic; Pyloric Antrum; Reproducibility of Results; Reverse Transcriptase Polymerase Chain Reaction; Virulence

Follicular gastritis is thought to be caused by Helicobacter pylori infection. However, the pathophysiology of it remains unclear.. We assessed gastric acidity in 15 patients with follicular gastritis, aged 20-37 years, using a 24-hour intragastric pH-metry, as well as by histologic and serologic evaluations; and compared it with that in other age-matched groups: 18 cases of H. pylori-positive antrum-predominant gastritis, 12 of pangastritis, and 24 H. pylori-negative normals. In eight cases with follicular gastritis, it was re-assessed 6 months after the eradication therapy for H. pylori.. During nighttime, the percentage of time with intragastric pH above 3.0 in follicular gastritis was significantly higher than that in normals (p<.0001), and in antrum-predominant gastritis (p<.001), but was comparable with that in pangastritis. In the daytime period, this parameter in follicular gastritis was significantly higher than that in normal (p<.001), in antrum-predominant gastritis (p<.001), and in pangastritis (p<.05). Marked mononuclear cell and neutrophil infiltration but no apparent glandular atrophy were observed in both the antrum and corpus. Serum pepsinogen I/II ratio was significantly lower in follicular gastritis than that in normals (p<.0001) and in antrum-predominant gastritis (p<.001), whereas serum gastrin was significantly higher than that in normals (p<.0001), in antrum-predominant gastritis (p<.01) and in pangastritis (p<.05). After eradication for H. pylori, all of the parameters in follicular gastritis were altered to the same ranges as those in normals.. In follicular gastritis, gastric acidity is significantly reduced, but can be normalized by eradication of H. pylori. It can thus be speculated that inflammatory cytokines or H. pylori-infection-induced prostaglandins might strongly inhibit gastric acid secretion in follicular gastritis.

Topics: Adult; Female; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Pepsinogens; Pyloric Antrum

Conventional endoscopic and radiographic methods fail to identify a probable source of gastrointestinal blood loss in about one third of males and post-menopausal females and in most women of reproductive age with iron deficiency anemia (IDA). Such patients, as well as subjects refractory to oral iron treatment, are often referred for hematologic evaluation.. Patient clinic, screened for non-bleeding gastrointestinal conditions including celiac disease (antiendomysial antibodies), autoimmune atrophic gastritis (hypergastrinemia with strongly positive antiparietal cell antibodies) and H. pylori infection (IgG antibodies confirmed by urease breath test).. The mean age of all subjects was 39+/-18 years, and 119 of 150 were females. We identified 8 new cases of adult celiac disease (5%). Forty IDA patients (27%) had autoimmune atrophic gastritis of whom 22 had low serum vitamin B12 levels. H. pylori infection was the only finding in 29 patients (19%), but was a common co-existing finding in 77 (51%) of the entire group. Refractoriness to oral iron treatment was found in 100% of patients with celiac disease, 71% with autoimmune atrophic gastritis, 68% with H. pylori infection, but only 11% of subjects with no detected underlying abnormality. H. pylori eradication in previously refractory IDA patients in combination with continued oral iron therapy resulted in a significant increase in hemoglobin from 9.4+/-1.5 (mean +/- 1SD) before, to 13.5+/-1.2 g/ dL (p<0.001 by paired t test) within 3 to 6 months.. The recognition that autoimmune atrophic gastritis and H. pylori infection may have a significant role in the development of unexplained or refractory IDA in a high proportion of patients should have a strong impact on our daily practice of diagnosing and managing IDA.

Topics: Adolescent; Adult; Aged; Amoxicillin; Anemia, Iron-Deficiency; Antibodies, Bacterial; Autoantibodies; Autoimmune Diseases; Bacterial Proteins; Breath Tests; Celiac Disease; Child; Clarithromycin; Comorbidity; Drug Therapy, Combination; Female; Ferrous Compounds; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Omeprazole; Parietal Cells, Gastric; Prospective Studies; Urease; Vitamin B 12 Deficiency

The role of Helicobacter pylori (H pylori) infection in gastric acid secretion of patients with chronic gastritis remains controversial. This study was designed to elucidate the effect of H pylori on H+/K+-ATPase activities in gastric biopsy specimens.. Eighty-two patients with chronic gastritis who had undergone upper endoscopy were included in this study. H pylori infection was confirmed by rapid urease test and histology. Gastric H+/K+-ATPase activities and serum gastrin concentrations were measured by an enzymatic method and radioimmunoassay, respectively. For those patients who received triple therapy for eradicating H pylori, changes in the activity of gastric H+/K+-ATPase and serum gastrin levels were also measured.. The mean gastric H+/K+-ATPase activity in H pylori-positive group (42 patients) was slightly higher than that in H pylori-negative group (29 patients) (169.65+/-52.9 and 161.38+/-43.85 nmol Pi/(mg.h), respectively, P=0.301). After eradication of H pylori, the gastric H+/K+-ATPase activities slightly decreased compared to prior therapy (165.03+/-59.50 and 158.42+/-38.93 nmol Pi/(mg.h), respectively, P=0.805). The mean basal gastrin concentration was slightly higher in H pylori-positive patients than in H pylori-negative patients (87.92+/-39.65 pg/mL vs 75.04+/-42.57 pg/mL, P=0.228). The gastrin levels fell significantly after the eradication of H pylori. (Before treatment 87.00+/-30.78 pg/mL, after treatment 64.73+/-18.96 pg/mL, P=0.015).. Gastric H+/K+-ATPase activities are not associated with H pylori status in patients with chronic gastritis.

Topics: Chronic Disease; Gastric Mucosa; Gastrins; Gastritis; H(+)-K(+)-Exchanging ATPase; Helicobacter Infections; Helicobacter pylori; Humans; Reference Values

Several tests have been proposed for evaluating dyspeptic symptoms and their relationship to the underlying gastric disease. Serum pepsinogens and gastrin-17 are known to be useful biomarkers for the detection of gastric pathologies.. To evaluate the capability of screening dyspeptic patients in the primary care by analyses of serum pepsinogens I (sPGI) and II (sPGII), gastrin-17 (sG-17) and the IgG anti-Helicobacter pylori antibodies (IgG-Hp).. Three hundred and sixty-two consecutive patients with dyspeptic symptoms (208 females, mean age 50.6 +/- 16 years, range 18-88 years) referred by general practitioners for upper gastrointestinal endoscopy were enrolled. A blood sample was taken from each subject for IgG-Hp, sPGI, sPGII and sG-17 analyses.. Two hundred and eighty-seven patients had a complete screening; of these, 132 resulted positive for Hp infection. Patients with atrophic chronic gastritis showed significantly lower serum pepsinogen I levels and sPGI/sPGII ratio than patients with non-atrophic chronic gastritis. Moreover, by calculating the values of sPGI by sG-17 and sG-17 by sPGII/sPGI, subjects with atrophic chronic gastritis could be distinguished from those with non-atrophic chronic gastritis and from those with normal mucosa, respectively. sG-17 levels were found to be a useful biomarker for the detection of antral atrophic gastritis, while the combination of sPGI, the sPGI/sPGII ratio and sG-17 was found effective in identifying corpus atrophy.. A panel composed of PGI, PGII, G-17 and IgG-Hp could be used as a first approach in the 'test and scope' and/or 'test and treat' strategy in the primary care management of dyspeptic patients.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Chronic Disease; Dyspepsia; Female; Gastrins; Gastritis; Gastroscopy; Helicobacter pylori; Humans; Immunoglobulin G; Male; Mass Screening; Middle Aged; Pepsinogen A; Pepsinogen C; Primary Health Care

H+/K+-ATPase beta-subunit-deficient mice (129/Sv background) display numerous pathologies in the stomach. Expression of the mutation in BALB/cCrSlc mice results in the development of an aberrant 'mucus-rich' cell population. 'Mucus-rich' cells have been described in stomachs of mice with autoimmune gastritis, a disease mediated by CD4+ T cells. Other pathological features of autoimmune gastritis are similar to those in H+/K+ beta-deficient mice and include a mononuclear cell infiltrate in the gastric mucosa, non-functional or absent parietal cells, depletion of zymogenic cells, hypergastrinaemia, and gastric unit hypertrophy caused by immature cell hyperplasia. The present study investigates further the aberrant gastric 'mucus-rich' cell lineage and analyses the mRNA expression of mucus cell products TFF1 and TFF2. 'Mucus-rich' cells stained for both acidic and neutral mucins, and with a TFF2-specific antibody. Stomachs from both models expressed decreased TFF1 mRNA and reciprocally increased TFF2 mRNA. The involvement of gastrin in regulating trefoil mRNA expression was also investigated using gastrin-deficient mice. In contrast to previous findings, gastrin did not positively regulate TFF1 mRNA expression, but there was possible augmentation of TFF2. Additionally, a clear role for inflammation was established involving both polymorphonuclear and mononuclear cells in these models, and a link was found between mucosal hypertrophy and increased interleukin-11 (IL-11) expression.

Topics: Animals; Autoimmune Diseases; Cytokines; Disease Models, Animal; Gastric Mucosa; Gastrins; Gastritis; Gene Expression Regulation; H(+)-K(+)-Exchanging ATPase; Hyperplasia; Hypertrophy; Interleukin-11; Mice; Mice, Inbred BALB C; Mice, Mutant Strains; Mucins; Muscle Proteins; Peptides; RNA, Messenger; Species Specificity; Trefoil Factor-1; Trefoil Factor-2

In development of chronic gastritis of elderly persons there has been increased the functional activity of diffuse neuroendocrine systems, especially EC-cells. It results in decreasing of the indexes of proliferationand increasing of apoptosis index. At patients with chronic gastritis in elderly, we found diffuse lesion of gastric mucous, combination with intestinal methaplasy and atrophy of stomach mucous more often. The further studying of processes of cellular updating and mechanisms of regulation of apoptosis and proliferation will allow stopping the development of chronic gastritis and occurrence of its irreversible complications at early stage.

Topics: Aged; Apoptosis; Chronic Disease; Disease Progression; Enterochromaffin Cells; Gastric Mucosa; Gastrins; Gastritis; Humans; Melatonin; Serotonin

Gastrin G cells and somatostatin D cells are important regulators of gastric acid secretion and alterations in their relative numbers may play a key role in gastroduodenal disease.. To investigate the effect of Helicobacter pylori infection on the density of immunoreactive G and D cells in gastric antral and corpus biopsies from patients with dyspeptic complaints.. One hundred and twenty two patients with dyspeptic complaints had two antrum and two corpus biopsies taken during upper endoscopy. The severity of inflammation and the density of H pylori were evaluated semiquantitatively. In addition, the density and distribution of neuroendocrine cells, especially G and D cells, were examined using immunohistochemistry. Patients were divided into three groups, those with H pylori positive gastritis, H pylori negative gastritis, and histologically normal gastric mucosa.. The number of immunoreactive G cells was significantly higher and the number of immunoreactive D cells lower in patients with H pylori positive gastritis compared with H pylori negative gastritis or histological normal gastric mucosa. The percentage of G cells as a percentage of mucosal endocrine cells was also raised and that of D cells was decreased.. Helicobacter pylori infection produces alterations in the number of endocrine cells responsible for regulating acid secretion in relation to intragastric pH and feeding. The alterations correlate best with the severity of inflammation and not with H pylori density.

Topics: Adolescent; Adult; Aged; Chromogranins; Dyspepsia; Female; Gastrin-Secreting Cells; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Male; Middle Aged; Pyloric Antrum; Severity of Illness Index; Somatostatin; Somatostatin-Secreting Cells

Topics: Carcinoid Tumor; Female; Gastrins; Gastritis; Humans; Middle Aged; Multiple Endocrine Neoplasia Type 1; Proto-Oncogene Proteins; Stomach Neoplasms

Epidemiological studies have shown that Helicobacter pylori infection with associated chronic gastritis is the main risk factor for development of gastric cancer. The aim of this study was to investigate the long-term development of H. pylori-induced gastritis in Mongolian gerbils in terms of morphology, gastrin secretion, epithelial proliferation and gene expression of pro-inflammatory cytokines.. A total of 133 gerbils were inoculated with H. pylori and 62 served as controls. The gerbils were killed at different time-points between 6 and 94 weeks after inoculation. Serum concentrations of anti-H. pylori IgG and gastrin were determined by enzyme-linked immunoabsorbent assay (ELISA) and radioimmunoassay (RIA), respectively. Epithelial proliferation was evaluated immunohistochemically after labeling with 5-bromo-2'-deoxy-uridine. Gene expression of beta-actin, interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) were measured by real-time reverse transcriptase-polymerase chain reaction (RT-PCR). Histological parameters of gastritis were assessed semiquantitatively and expressed as a "gastritis score".. Serum concentrations of anti-H. pylori IgG and gastrin increased over time. Epithelial proliferation in the antrum was increased 6 weeks after inoculation, followed by increased proliferation in the corpus 32 weeks after inoculation. Gene expression of IL-1beta and TNF-alpha were increased in H. pylori-infected gerbils. Beta-actin was not a reliable endogenous control for RT-PCR. With time, gastritis expanded from the antrum to the corpus and the gastritis score increased to reach a peak 32 weeks after inoculation. Pseudopyloric metaplasia (loss of specialized cells) was a characteristic feature in the corpus mucosa. Gastric ulcers, but neither dysplasia nor carcinoma, were observed during 94 weeks of infection.. Long-term H. pylori infection in Mongolian gerbils led to progressive gastritis, glandular atrophy, hypergastrinemia, increased epithelial proliferation and elevated gene expression of pro-inflammatory cytokines.

Topics: Actins; Animals; Biomarkers; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Gastric Mucosa; Gastrins; Gastritis; Gene Expression Regulation, Bacterial; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Immunoglobulin G; Immunohistochemistry; Interleukin-1; Male; Pyloric Antrum; Radioimmunoassay; Reverse Transcriptase Polymerase Chain Reaction; Time Factors; Tumor Necrosis Factor-alpha

Determining how Helicobacter pylori promotes gastric cancer and whether H pylori eradication decreases cancer risk would be helped by suitable murine models. Mice lacking the cyclin-dependent kinase inhibitor p27kip1 are susceptible to carcinogen-induced tumors. Furthermore, p27 stimulates gastric epithelial apoptosis and inhibits proliferation, expression is decreased by H pylori, and low levels are associated with a poor prognosis in gastric cancer. We therefore evaluated p27-deficient mice as a model for H pylori-associated gastric cancer.. Wild-type and p27-/- C57BL/6 mice were infected with H pylori mouse-adapted Sydney strain at 6-8 weeks of age and 6-10 mice of each type were euthanized 15, 30, 45, 60, and 75 weeks later.. Uninfected p27-/- mice developed gastric hyperplasia. H pylori-infected p27-/- mice frequently developed intestinal metaplasia (40% at 30 weeks, 67% at 45 weeks), and after 60 weeks 7 of 12 mice developed significant dysplasia and gastric cancer, recapitulating human intestinal-type gastric carcinogenesis. Wild-type mice developed intestinal metaplasia only after 75 weeks of infection; significant gastric dysplasia was observed in 1 animal (P < .05 for each comparison with p27-/- mice). No disease developed in uninfected mice. H pylori infection in p27-/- mice was associated with significantly decreased apoptosis and increased epithelial proliferation, inflammation, and H pylori density compared with infection in wild-type mice.. p27 loss and H pylori colonization cooperate to produce gastric cancer. The p27-deficient mouse affords opportunities to examine the pathogenesis of H pylori in gastric carcinogenesis and to test eradication and chemopreventive strategies.

Topics: Animals; Apoptosis; Cell Division; Cyclin-Dependent Kinase Inhibitor p27; Female; Gastrins; Gastritis; Genetic Predisposition to Disease; Helicobacter Infections; Helicobacter pylori; Hyperplasia; Male; Metaplasia; Mice; Mice, Inbred C57BL; Mice, Mutant Strains; Stomach Neoplasms

Helicobacter pylori has been established as a major cause of gastritis and peptic ulcer disease in adults and children. H. pylori infection may also have a role in the development of some extra-gastrointestinal diseases, including iron deficiency anemia. The aim of this study is to investigate H. pylori-related changes in gastric physiology and histology and the relationship of these changes to iron deficiency anemia in children.. Fifty-two patients with gastrointestinal complaints were studied. Hematologic parameters, 3-day vitamin C and iron consumption, serum gastrin levels, and gastric juice ascorbic acid levels were compared in patients with and without H. pylori infection. Dietary intake of vitamin C and iron, serum gastrin, gastric juice ascorbic acid content, and gastric histology were compared in patients with H. pylori infection and anemia and in patients with H pylori infection and no anemia. The CagA status of the H. pylori organisms was evaluated.. Twenty-eight of 52 patients had H. pylori. Thirty-one patients had iron deficiency anemia. H. pylori infection was associated with low serum iron levels. H. pylori gastritis was associated with a decrease in the gastric juice ascorbic acid level. Infection with CagA-positive strains was associated with a greater decrease in gastric juice ascorbic acid than infection with CagA-negative strains. However, the gastric juice ascorbic acid levels of patients with H. pylori and anemia were not different from those of non-anemic patients with H. pylori. Among patients with H. pylori infection, pangastritis was twice as common in those with anemia than in those without anemia.. H. pylori infection was associated with a decrease in gastric juice ascorbic acid concentration, and this effect was more pronounced in patients with the CagA-positive strain. Pangastritis was more common in patients whose H. pylori.infection was accompanied by anemia.

Topics: Anemia, Iron-Deficiency; Antigens, Bacterial; Ascorbic Acid; Bacterial Proteins; Child; Female; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Absorption; Iron; Iron, Dietary; Male; Stomach; Virulence

Rebound increased acid secretion has been observed at 2 weeks after discontinuing omeprazole treatment in Helicobacter pylori -negative, but not H. pylori -positive, subjects. It is unknown whether this is a prolonged phenomenon or whether a similar phenomenon appears later in H. pylori positives or is released by eradication therapy. The aims of this study were to answer these 3 questions.. Twelve H. pylori -negative and 20 H. pylori -positive subjects were studied. Each had a basal, submaximal, and maximal pentagastrin-stimulated acid secretion study before, during, and at 7, 14, 28, 42, and 56 days after a 56-day course of omeprazole 40 mg/day. Ten of the H. pylori -positive subjects had their infection eradicated during the last week of treatment.. In the H. pylori -negative subjects, there was rebound secretion of submaximal (P < 0.003) and maximal (P < 0.003) acid output, which persisted until at least 56 days after discontinuing omeprazole. The H. pylori -uneradicated subjects had no rebound increased secretion other than in maximal acid output at 28 (P < 0.01) and at 42 days after treatment (P < 0.02). In those eradicated of H. pylori close to the end of omeprazole, there was rebound increased secretion of submaximal acid output (P < 0.04) lasting until 56 days and of maximal acid output (P < 0.01) lasting until 28 days after treatment.. Rebound increased acid secretion following omeprazole is a prolonged phenomenon in H. pylori -negative subjects. There is little evidence of it in H. pylori -infected subjects, but eradicating the infection releases the phenomenon. The accentuated H. pylori -related oxyntic gastritis induced by omeprazole is likely to protect against the rebound phenomenon.

Topics: Adult; Anti-Bacterial Agents; Anti-Ulcer Agents; Fasting; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Omeprazole

Comparative studies of gastric acid secretion in children related to Helicobacter pylori infection are lacking. The purpose of this study was to compare acid secretion and meal-stimulated gastrin in relation to H. pylori infection among pediatric patients.. Thirty-six children aged 10-17 years (17 with H. pylori infection) undergoing diagnostic endoscopy participated in the study. Diagnoses included gastritis only (n = 23), duodenal ulcer (n = 5) and normal histology (n = 8). Gastric acid output was studied using the endoscopic gastric secretion test before and 2-3 months after H. pylori eradication. Meal-stimulated serum gastrin response was assessed before and 12 months after eradication.. H. pylori gastritis was typically antrum-predominant. Acid secretion was greater in H. pylori-positive patients with duodenal ulcer than in gastritis-only patients or controls [mean +/- standard error (SE): 6.56 +/- 1.4, 3.11 +/- 0.4 and 2.65 +/- 0.2 mEq/10 minutes, respectively; p <.001]. Stimulated acid secretion was higher in H. pylori-positive boys than girls (5.0 +/- 0.8 vs. 2.51 +/- 0.4 mEq/10 minutes, respectively; p <.05). Stimulated acid secretion pre- and post-H. pylori eradication was similar (5.47 +/- 0.8 vs. 4.67 +/- 0.9 mEq/10 minutes, respectively; p =.21). Increased basal and meal-stimulated gastrin release reversed following H. pylori eradication (e.g. basal from 134 to 46 pg/ml, p <.001 and peak from 544 to 133 pg/ml, p <.05).. H. pylori infection in children is associated with a marked but reversible increase in meal-stimulated serum gastrin release. Gastric acid hypersecretion in duodenal ulcer remains after H. pylori eradication, suggesting that the host factor plays a critical role in outcome of the infection.

Topics: Adolescent; Biopsy; Breath Tests; Child; Duodenal Ulcer; Eating; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Urea; Urease

High levels of inducible nitric oxide synthase and nitrotyrosine in Helicobacter pylori-infected gastric mucosa may contribute to development of gastric cancer. We investigated the relation between expression of inducible nitric oxide synthase and proinflammatory cytokines in gastric mucosa and serum markers of gastritis.. The study included 103 patients with H. pylori infection. We examined levels of interleukin-1beta, interleukin-6 and interleukin-8 by enzyme-linked immunosorbent assay and evaluated expression of inducible nitric oxide synthase and nitrotyrosine by immunohistochemical staining. Furthermore, we assessed serum levels of pepsinogens, gastrin, anti-parietal cell antibody, nitrite and nitrate, as markers of gastritis.. Thirty-seven of 103 (35.6%) gastric mucosa specimens showed simultaneous expression of inducible nitric oxide synthase and nitrotyrosine. In these patients (inducible nitric oxide synthase-positive group), the serum level of gastrin was significantly higher than that of the inducible nitric oxide synthase-negative group (509.5 +/- 141.5 pg/mL vs. 210.0 +/- 227.2 pg/mL; P < 0.01), whereas there were no significant differences in serum levels of pepsinogen, anti-parietal cell antibody, and nitrate and nitrite or in scores of histological gastritis. Interleukin-6 levels were significantly higher in the inducible nitric oxide synthase-positive group than in the inducible nitric oxide synthase-negative group (25.9 +/- 7.0 pg/mg protein vs. 10.6 +/- 4.9 pg/mg protein; P < 0.05).. Inducible nitric oxide synthase-producing gastritis was correlated with high levels of interleukin-6. Patients with hypergastrinaemia should be carefully followed on a long-term basis to ensure that the development of any malignancy is detected early.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Chronic Disease; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-6; Male; Middle Aged; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; Tyrosine

A prominent pathological feature of murine autoimmune gastritis is a pronounced mucosal hypertrophy. Here, we examined factors that may be responsible for inducing this hypertrophy. Because gastrin is known to be both an inducer of gastric mucosal cell proliferation and is elevated in autoimmune gastritis, mice deficient in gastrin were thymectomised at day 3 and assessed for autoimmune gastritis. Gastrin-deficient mice showed all the characteristic features of murine autoimmune gastritis, including gastric unit hypertrophy due to hyperproliferation and accumulation of immature epithelial cells, decreases in the number of zymogenic and parietal cells, and autoantibodies to the gastric H+/K+-ATPase. Hence, gastrin is not required for either the establishment of chronic gastritis or development of the typical pathological features of this disease. We also examined mRNA levels of a number of gastric mucosal growth factors in RNA samples from mice with hypertrophic autoimmune gastritis. Members of the Reg family, RegIIIbeta and RegIIIgamma, were greatly elevated in mice with hypertrophic gastritis, whereas RegI and amphiregulin (an EGF receptor ligand) were more modestly and/or inconsistently induced. These data demonstrate that induction of gastric mitogenic factors, such as members of the Reg family, can be achieved in inflammatory situations by gastrin-independent pathways. Members of the Reg family, in particular RegIIIbeta and RegIIIgamma, are good candidates to be involved in inducing the mucosal hyperproliferation in autoimmune gastritis. These findings are likely to be of relevance to other gastric inflammatory conditions.

Topics: Amphiregulin; Animals; Autoantibodies; Autoimmune Diseases; Chronic Disease; EGF Family of Proteins; Epidermal Growth Factor; ErbB Receptors; Gastric Mucosa; Gastrins; Gastritis; Gene Expression; Glycoproteins; Growth Substances; H(+)-K(+)-Exchanging ATPase; Heparin-binding EGF-like Growth Factor; Hypertrophy; Intercellular Signaling Peptides and Proteins; Mice; Mice, Inbred BALB C; Mice, Mutant Strains; Proteins; RNA, Messenger; Transforming Growth Factor alpha

This study was conducted to explore whether cholecystokinin-B/gastrin receptor (CCKBRwt) gene and its alternative splicing variant (CCKBRi4sv) are expressed in human gastric carcinomas cell line and tissues, and to find out their relationship with the development and progression of human gastric carcinoma. The mRNA expression levels of CCKBRwt and CCKBRi4sv were detected in 30 human gastric carcinomas and normal tissues adjacent to cancer, 10 gastritis specimens, 2 autopsied normal stomach specimens as well as in a gastric carcinoma cell line SGC-7901 cells. The results revealed that the transcripts of CCKBRwt and CCKBRi4sv were observed in all of the human gastric specimens tested, but only CCKBRwt was expressed in gastric cancer cell line SGC-7901 cells. The expression levels of the two receptors were not correlated with the differentiation and metastases of gastric cancers. From the results, we infer that human gastric tissues simultaneously express CCKBRwt and CCKBRi4sv, and CCKBRi4sv may have unknown physiological functions in gastric epithelial cells.

Topics: Base Sequence; Epithelial Cells; Gastric Mucosa; Gastrins; Gastritis; Humans; Molecular Sequence Data; Receptor, Cholecystokinin B; RNA, Messenger; Stomach Neoplasms; Tumor Cells, Cultured

Helicobacter pylori infection causes hypergastrinemia. This study aimed to determine the association between serum gastrin and the severity of H. pylori-related gastric histology.. A total of 458 dyspeptic patients were included in this study after the absence of gastric malignancy was confirmed using endoscopy. The gastric specimens of each patient were collected from the antrum and corpus for the analysis of H. pylori-related histology changes by updated Sydney's system. Before endoscopy, the fasting blood samples were collected for gastrin analysis.. The H. pylori-infected patients had higher gastrin levels than those without infection (P = 0.01). Gastrin levels were related to H. pylori density and acute and chronic inflammation scores in the corpus mucosa (P < 0.05), but not in the antral mucosa (P = NS). Gastrin levels were also not related to the presence of gastric atrophy. Multivariate regression showed that the gastrin level was only related to acute corpus inflammation. However, in the patients without infection, the gastrin level was also associated with acute corpus inflammation. Nevertheless, the patients with denser H. pylori infection were more likely to have acute corpus gastritis than those with lighter H. pylori infection, and thus presented with higher gastrin levels (P < 0.05).. The increased level of gastrin of serum after H. pylori infection was associated with acute inflammation in the gastric corpus mucosa, but not in the antral mucosa. Denser H. pylori infection causes more severe corpus gastritis and thus may lead to a higher fasting level of gastrin of serum.

Topics: Adult; Analysis of Variance; Biomarkers; Chi-Square Distribution; Endoscopy, Gastrointestinal; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation; Male; Middle Aged; Regression Analysis

Juvenile patients affected with autoimmune thyroid disorders showed a 14-21% prevalence of parietal cell antibodies (PCA) reacting against the H+/K+-ATPase of the gastric parietal cells. PCA are the principal immunological markers of atrophic body gastritis (ABG).ABG is characterized by loss of oxyntic glands, achlorhydria, and hypergastrinemia. The aim of this study was to determine whether PCA positivity could be associated with biochemical and histological manifestations of gastric autoimmunity in juvenile patients with autoimmune thyroid disease (AITD). We studied 129 children (96 females and 33 males) with chronic lymphocytic thyroiditis (n = 115) or Graves' disease (n = 14). Mean age at diagnosis of AITD was 9.7 +/- 3.3 yr, and mean age at sampling was 12.3 +/- 3.7 yr. We determined PCA and Helicobacter pylori antibodies, gastrin, and pepsinogen I plasma levels. Gastroscopy with multiple biopsies was carried out in a subgroup of patients with PCA positivity. We found that 30% of children had detectable PCA. Hypergastrinemia was found in 45% of the PCA-positive children (range, 40-675 pg/ml) vs. 12% of PCA-negative children (range, 35-65 pg/ml; P < 0.001). Eighteen patients with PCA positivity underwent gastroscopy; eight of these children had normogastrinemia, which showed no signs of ABG, and 10 children had hypergastrinemia, of whom five had mild to severe ABG. Our study shows that autoimmune gastritis is an early event in juvenile AITD with detectable PCA. Gastrin plasma level is a reliable marker of gastric atrophy.

Topics: Adolescent; Atrophy; Autoantibodies; Biomarkers; Biopsy; Child; Female; Gastrins; Gastritis; Humans; Male; Parietal Cells, Gastric; Pepsinogen A; Seroepidemiologic Studies; Thyroiditis, Autoimmune

In Japan, where the incidence of gastric cancer is high, Helicobacter pylori infection could affect gastric acid secretion differently from that in Western countries. The aim of this study was to investigate the relationship between H. pylori infection, acid secretion, aging, and gender in normal Japanese subjects.. The study comprised 193 Japanese subjects who had undergone routine endoscopy. Gastrin-stimulated acid output was performed during the routine endoscopic examination using the endoscopic method of gastric acid secretory testing (EGT: endoscopic gastrin test), which has been reported previously. H. pylori status was determined by histology, rapid urease test, and serology.. Mean EGT values were 3.9 +/- 1.5 mEq/10 min in H. pylori-negative men, 1.6 +/- 2.5 in H. pylori-positive men, 2.2 +/- 0.9 in H. pylori-negative women, and 1.5 +/- 1.2 in H. pylori-positive women. Although acid secretion was lower in H. pylori-positive subjects compared with H. pylori-negative subjects in both men and women, the decrease was more marked in men with H. pylori infection. Multiple linear regression analysis showed that aging is positively associated with gastric acid secretion in the H. pylori-negative subjects, whereas a negative association was found between them in the H. pylori-positive subjects.. In Japanese subjects, aging affects gastric acid secretion differently depending on the status of H. pylori infection. H. pylori infection showed a stronger inhibitory effect on the acid secretion in men than in women. This gender-related difference in the susceptibility of acid secretion to H. pylori infection may explain the higher rates of gastric cancer in men in Japan.

Topics: Adult; Aged; Aging; Antibodies, Bacterial; Endoscopy, Gastrointestinal; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Japan; Male; Middle Aged; Reference Values; Sex Characteristics; Stomach Neoplasms

This observation recalls that gastric phytobezoar should lead to a search for an underlying disease and that a iron deficiency can be associated and hide macrocytosis related to a vitamin B12 deficiency.. A 19 year-old woman consulted for asthenia. Microcyte anaemia associated with iron deficiency was diagnosed. Upper digestive endoscopy revealed severe, totally asymptomatic phytobezoar. Biological investigations revealed a vitamin B12 deficiency, high serum gastrin level and strong positivity for gastric antiparietal anti-cell antibodies, suggestive of an autoimmune gastritis. Total immunoglobulin A deficiency was also noted.. Autoimmune gastritis is responsible for megaloblastic anaemia (vitamin B12 deficiency) but can also provoke microcytic (iron-deficiency) anaemia due to insufficient absorption of the latter and related to gastric achlorhydria. Phytobezoar might also be related to achlorhydria and/or gastroparesia associated with autoimmune gastritis. Hence, autoimmune gastritis should be searched for when confronted with unexplained gastric bezoar or iron-deficiency anaemia.

Topics: Adult; Anemia, Iron-Deficiency; Autoimmune Diseases; Bezoars; Female; Gastrins; Gastritis; Humans; Plants; Vitamin B 12 Deficiency

As a result of a complex survey of 120 patients with erosive gastroduodenal affections, significant abnormalities of the aggressive-protective balance of the mucous coat of the stomach were discovered. In addition to affections of local protection factors, the change of the hormonal status characterized by hypercortisolemia, hyperinsulinemia, hypergastrinemia and increased level of such cyclic nucleotides as cAMP and cGMP was revealed. The dependence of the mucus-producing function, lysozyme activity and acid production on the level of blood hormones was discovered. Alternate dependencies of cortisol, insulin and gastrin levels on cAMP and cGMP levels as well as alternate impact of cAMP and cGMP on acid-producing gastric cells were established.

Topics: Adenylyl Cyclases; Adolescent; Adult; Aged; Cyclic AMP; Cyclic GMP; Duodenitis; Duodenum; Female; Gastrins; Gastritis; Guanylate Cyclase; Hormones; Humans; Hydrocortisone; Insulin; Male; Middle Aged; Stomach

Disturbances of gastric motor, secretory and/or sensory functions are frequently associated with gastritis. The aim of this study was to characterize motor and secretory alterations associated to chemically-induced gastritis in mice. Mild gastritis was induced with 0.1% iodoacetamide administered intragastrically and added to the drinking water for a 6 days period. A significant loss of body weight and a reduction in food and water intake was observed in iodoacetamide-treated animals compared with those receiving vehicle. At the end of the treatment period, no macroscopic alterations were observed in the gastric mucosa of iodoacetamide-treated mice. However, histological sections revealed a mixed inflammatory infiltrate, with a predominance of mast cells in the submucosa; suggesting a mild gastritis. Gastric emptying rate of a nutrient solid meal was not modified in mice with gastritis compared with normal controls. In animals with gastritis, basal gastric acid secretion was increased compared with normal controls. Basal gastric acid secretion was not modified by either indomethacin or compound 48/80. Secretory response to secretagogues (pentagastrin and histamine) was enhanced during gastritis. Hypersecretory responses to both gastrin and histamine in iodoacetamide-treated mice were blocked by the mast cell stabilizer sodium cromoglycate, and enhanced by indomethacin, without affecting the secretory response in normal mice. These results suggest that mild gastritis alters gastric acid secretory responses through a mechanism related, at least partially, to mast cells activation. Moreover, prostaglandins also modulate secretory responses during mild inflammation. This animal model of gastritis might be useful to characterize pathophysiological changes and potential therapeutic targets in secretory-related gastric pathologies.

Topics: Animals; Anti-Inflammatory Agents; Body Weight; Cromolyn Sodium; Drinking; Eating; Gastric Acid; Gastric Emptying; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Agents; Histamine; Indomethacin; Iodoacetamide; Irritants; Male; Mice; Pentagastrin; Pharmaceutical Vehicles

Serum levels of pepsinogen and gastrin are parameters that can be used as biomarkers for gastric mucosa. The aim of this study was to validate these serum biomarkers, that is pepsinogen A (PGA), pepsinogen C (PGC), PGA/PGC ratio, and gastrin, as screening tests for precancerous lesions: atrophic chronic gastritis (ACG) or Helicobacter pylori-related corpus-predominant or multifocal atrophy. The study population was comprised of a subsample of 284 patients from the 451 included in the Eurohepygast cohort, between 1995 and 1997. The concentrations of PGA, PGC, and gastrin were measured by radioimmunoassays. Histological diagnosis was the gold standard. Cut-off points were calculated using receiving operator characteristics (ROC) curves. Factors linked to variation of biomarkers were identified using multivariate linear regression. The mean of each biomarker in the sample was: PGA, 77.4 microg x l(-1); PGC, 13.2 microg x l(-1); PGA/PGC, 6.7; and gastrin, 62.4 ng x l(-1). For ACG patients, the areas under the PGA, PGC, PGA/PGC, and gastrin ROC curves were 0.55, 0.62, 0.73, and 0.58, respectively. The best cut-off point for PGA/PGC was 5.6, with sensitivity 65% and specificity 77.9%. For H. pylori-related corpus-predominant or multifocal atrophy, the areas under the respective ROC curves were 0.57, 0.67, 0.84, and 0.69. The best cut-off point for PGA/PGC was 4.7, with sensitivity 77.1% and specificity 87.4%. The results suggested that only the PGA/PGC ratio can be considered as a biomarker for precancerous lesions of the stomach, and may be useful as a screening test.

Topics: Antigens, Bacterial; Bacterial Proteins; Biomarkers; Biopsy; Dyspepsia; Europe; Gastrins; Gastritis; Helicobacter pylori; Humans; Pepsinogen A; Pepsinogen C; Radioimmunoassay

Helicobacter pylori is a human gastric carcinogen. Sterigmatocystin (ST), a fungus toxin, is a risk factor of gastric cancer. Cytotoxin-vacuolation toxin A (VacA) present in supernatants of H. pylori suspensions can cause gastritis and ulcer. The aim of this study was to examine the effects of H. pylori, ST and VacA in Mongolian gerbils.. Male Mongolian gerbils (n = 196) were treated with H. pylori supernatants (10 ml/1000 mg) mixed with diet or inoculated intragastrically with H. pylori alone or with ST (100 or 1000 ppb), and then killed 27 months later. Gastric tissue sections were stained with haematoxylin and eosin (H&E), periodic acid-Schiff (PAS), Alcian blue (AB, pH 2.5) and with immunostaining for PCNA and p53 expression.. In H. pylori-infected gerbils, the normal mucosa was replaced by hyperplastic epithelium. Severe gastritis, cystic dilatation of gastric glands, hyperplastic polyps and intestinal metaplasia were observed. In H. pylori + ST (1000 ppb) gerbils, intestinal metaplasia was significantly more frequent than in H. pylori alone animals. No pathological changes were observed in the H. pylori supernatant group. Osseous metaplasia was observed in the H. pylori + ST (100 ppb) group. Serum gastrin levels of the H. pylori + ST (1000 ppb) group were significantly higher than those of the other groups. PCNA labelling index and p53 index of infected gerbils were significantly higher than those of uninfected groups.. H. pylori causes gastritis, ulcer and intestinal metaplasia. ST enhances the development of intestinal metaplasia and increases gastrin levels in H. pylori-infected Mongolian gerbils.

Topics: Animals; Bacterial Proteins; Disease Models, Animal; Gastric Mucosa; Gastrins; Gastritis; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Male; Metaplasia; Sterigmatocystin; Tumor Suppressor Protein p53

Topics: Atrophy; Biopsy; Carcinoid Tumor; Endoscopy, Digestive System; Fatal Outcome; Female; Gastrins; Gastritis; Humans; Immunohistochemistry; Middle Aged; Pulmonary Emphysema; Stomach Neoplasms; Tomography, X-Ray Computed

Helicobacter pylori infection of Mongolian gerbils is an established model of gastric carcinogenesis, but gastric secretory aspects of this carcinogenesis have not been studied.. The effects of single intragastric inoculation of gerbils with H. pylori strain (cagA+ vacA+, 5 x 10(6) CFU/ml) or vehicle (saline) were examined at 1, 2, 4, 6, 9, 12 and 30 weeks from inoculation. Gastric morphology, the presence of H. pylori using the rapid urease test, the density of H. pylori and 16S rRNA and the plasma gastrin and somatostatin were determined.. H. pylori was detected in gastric mucosa in all infected animals. Basal gastric acid in gerbils was reduced by about 50% after H. pylori inoculation. Early lesions seen at 4 weeks after H. pylori inoculation consisted of chronic gastritis with thickened mucosal folds, oedema, congestion and mucosal lymphocytic infiltration. Adenomatous hyperplasia with cellular atypia with increased mitotic activity and the formation of apoptotic bodies and visible erosions and ulcerations were observed at 12-30 weeks after inoculation. The atypical gastric glands were situated 'back-to-back', suggesting gastric pre-cancer. The gastric blood flow in H. pylori-infected gerbils was significantly lower than that in the controls. Six- to seven-fold increase in plasma gastrin levels combined with significant fall in gastric somatostatin contents and the intraepithelial neoplasia were noticed in gerbils at all tested periods.. H. pylori-infection in gerbils resulted in gastric pre-cancer associated with functional changes, such as suppression of gastric secretion and impairment of both gastric mucosal microcirculation and the gastrin-somatostatin link.

Topics: Animals; Cell Transformation, Neoplastic; Disease Models, Animal; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Male; Microcirculation; Precancerous Conditions; Somatostatin; Stomach Neoplasms

Hypochlorhydria, hypergastrinaemia, inflammation and Helicobacter pylori infection, dose and duration of omeprazole treatment may separately, or in combination, influence the proliferation of enterochromaffin-like (ECL) cells and parietal cell changes in gastric mucosa. To assess the effects of these variables comparisons were carried out in patients with the acid related Zollinger-Ellison syndrome (ZES) versus patients with progressive systemic sclerosis (PSS) and gastro-oesophageal reflux disease.. Twenty-five patients with PSS and 16 patients with ZES were included and received continuous omeprazole treatment for a mean of 7.5 and 9 years. The patients were investigated every 6-12 months with endoscopy, biopsies and histology, and plasma gastrin measurements. PSS patients were titrated by 24 h pH-metry to oesophageal pH>4, and all ZES patients were titrated to a basal acid output of zero H+.. Changes towards diffuse and linear ECL cell hyperplasia were observed in 41% of the PSS patients. Micronodular hyperplasia and neoplasia were not seen. In the ZES patients changes towards linear and micronodular hyperplasia were observed in all patients. Two patients developed ECL cell carcinoids; one of these had MEN-1 syndrome. Also parietal cell changes were more pronounced in the ZES group than in the PSS group.. In patients without intrinsic acid hypersecretion and hypergastrinaemia significant proliferation of ECL cells is not an issue irrespective of gastric mucosal inflammation, omeprazole dose, duration of treatment and acid inhibition. The level of gastrin secretion and high plasma gastrin appear to accelerate ECL cell proliferation and parietal cell changes possibly influenced by chronic gastritis and H. pylori infection.

Topics: Achlorhydria; Aged; Aged, 80 and over; Anti-Ulcer Agents; Cell Division; Drug Administration Schedule; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Neurosecretory Systems; Omeprazole; Parietal Cells, Gastric; Scleroderma, Systemic; Zollinger-Ellison Syndrome

To determine the frequency and significance of pancreatic acinar cells in the gastric oxyntic mucosa.. One hundred gastric oxyntic mucosal biopsy specimens from patients with chronic active gastritis (n = 30), multifocal atrophic gastritis (n = 15), autoimmune gastritis (n = 18), and normal gastric oxyntic mucosa (n = 37) were evaluated for the presence of pancreatic acinar cells. Formalin-fixed, paraffin-embedded tissues were stained with hematoxylin-eosin, and those positive for pancreatic acinar cells were immunostained with antibodies against trypsin and pancreatic amylase.. Eleven (11%) of 100 oxyntic mucosal tissue samples contained pancreatic acinar cells. These samples came from 9 of the 18 (50%) specimens of autoimmune gastritis, 1 of the 15 (6.6%) specimens of multifocal atrophic gastritis, and 1 of the 37 (2.7%) specimens of normal oxyntic mucosa. None of the samples with chronic active gastritis contained pancreatic acinar cells.. Pancreatic acinar cells were found in the oxyntic mucosa of patients with autoimmune gastritis significantly more frequently (P <.001) than in individuals with multifocal atrophic gastritis, normal oxyntic mucosa, or chronic active gastritis. Our study supports a metaplastic origin for pancreatic acinar cells in the oxyntic mucosa. Furthermore, detection of pancreatic acinar cells in the oxyntic mucosa of patients with gastritis strongly suggests an autoimmune pathogenesis.

Topics: Autoimmune Diseases; Carrier Proteins; Formaldehyde; Gastrectomy; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Glycoproteins; Helicobacter Infections; Helicobacter pylori; Humans; Lipase; Metaplasia; Pancreas; Paraffin Embedding; Parietal Cells, Gastric; Tissue Fixation

Gastric cancer remains the second biggest cause of cancer death worldwide. The most common type of gastric cancer, the intestinal type, is usually preceded by chronic atrophic gastritis. Gastritis serology is therefore of crucial importance for population-based screening and prevention studies. Helicobacter pylori serum antibodies can adequately diagnose inflammation of the gastric mucosa, but the serological diagnosis of atrophic gastritis is more hazardous. Many tests have been used for this purpose, either alone or in various combinations. Depending on the population, pepsinogens and gastrin often have a high specificity but low sensitivity for the diagnosis of atrophic gastritis, whereas antibodies against H. pylori or CagA have a high sensitivity but low specificity. A combination of two tests, e.g. H. pylori antibodies and pepsinogen I, may balance this issue and provide adequate screening tools, although there is a clear need for further improvement and simplification of serological testing for atrophic gastritis.

Topics: Antibodies, Bacterial; Antigens, Bacterial; Atrophy; Bacterial Proteins; Biomarkers; Gastric Mucosa; Gastrins; Gastritis; Helicobacter pylori; Humans; Immunoglobulin G; Pepsinogen A; Sensitivity and Specificity; Stomach Neoplasms

Serum levels of gastrin-17 (S-G-17) and pepsinogen I (S-PGI) are biomarkers of gastric antral and corpus mucosa, respectively. In a prospective multicentre investigation, we determined whether these tests, together with the assay of Helicobacter pylori antibodies, are a non-endoscopic tool for the diagnosis of atrophic gastritis.. The series comprised 404 consecutive adult outpatients undergoing diagnostic upper-gastrointestinal endoscopy for various dyspeptic symptoms in five outpatient clinics. Gastric biopsies from the antrum and corpus (at least two biopsies from both sites) were available from all patients, and they were evaluated according to the guidelines of the updated Sydney system. S-PGI and S-G-17 were assayed with ELISA methods using monoclonal antibodies to pepsinogen I and amidated gastrin-17. In addition to the fasting level (S-G-17(fast)), a postprandial S-G-17 (S-G-17(prand)) level was measured 20 min after ingestion of a protein-rich drink. H. pylori antibodies were determined using a polyclonal EIA method.. S-G-17(prand) (and S-G-17(fast)) and S-PGI levels decreased with increasing grade of atrophy of the antrum or corpus, respectively. S-G-17(prand) levels were significantly lower in patients with advanced (moderate or severe) atrophic antral H. pylori gastritis than in those with non-atrophic H. pylori gastritis. All patients with a resected antrum demonstrated S-G-17(prand) levels that were almost undetectable. Of the nine patients with an H. pylori-positive moderate or severe atrophic antral gastritis, six had S-G-17(prand) levels below 5 pmol/l. Similarly, S-PGI levels were significantly lower in patients with advanced corpus atrophy than in those without. Of the 45 patients with moderate or severe corpus atrophy in endoscopic biopsies, 35 patients had S-PGI levels < 25 microg/l. By using the cut-off levels for S-G-17(prand) and S-PGI with the best discrimination, the sensitivity and specificity of the blood test panel in delineation of patients with advanced atrophic gastritis (either in the antrum or the corpus, or both) were 83% and 95%, respectively. The predictive values of the positive and negative test results were 75% and 97%, respectively. In the diagnosis of atrophic gastritis, the application of S-G-17(fast) showed a slightly lower sensitivity and specificity than the application of S-G-17(prand) as a biomarker for antral atrophy.. The diagnosis of atrophic gastritis obtained with the blood test panel of S-G-17, S-PGI and H. pylori antibodies is in good agreement with the endoscopic and biopsy findings. The panel is a tool for non-endoscopic diagnosis and screening of atrophic gastritis.

Topics: Adult; Aged; Antibodies, Bacterial; Atrophy; Biomarkers; Enzyme-Linked Immunosorbent Assay; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter pylori; Hematologic Tests; Humans; Immunoglobulin G; Male; Middle Aged; Pepsinogen A; Prospective Studies; Pyloric Antrum

The effects of rebamipide on chronic gastritis associated with Helicobacter pylori have not been well-defined. We compared these effects of rebamipide with those of cimetidine in Mongolian gerbils infected with H. pylori.. Mongolian gerbils with or without H. pylori were divided into 10 groups 6 weeks after inoculation and fed diets containing a drug (rebamipide or cimetidine) or control diet. All animals were sacrificed 4 weeks after grouping. Their stomachs were examined for histology, colonization by H. pylori, myeloperoxidase activity (myeloperoxidase), production of neutrophil chemokine (CINC/KC) and tumour necrosis factor-alpha (TNF-alpha), and serum gastrin levels.. H. pylori colonized all of the inoculated animals. Neither rebamipide nor cimetidine decreased myeloperoxidase activity, but each reduced wet stomach weight in H. pylori-infected animals. The amount of increase in CINC/KC and TNF-alpha in gastric tissue caused by H. pylori infection was decreased by treatment with rebamipide or cimetidine. H. pylori infection increased serum gastrin levels, and this increase was significantly enhanced by cimetidine but not rebamipide.. Rebamipide may improve H. pylori-infected chronic gastritis by preventing the production of inflammatory cytokines and chemokines, as does cimetidine, but may be preferable to cimetidine for long-term administration for treatment of H. pylori-infected chronic gastritis due to its effect on serum gastrin levels.

Topics: Alanine; Animals; Anti-Ulcer Agents; Chemokines; Cimetidine; Gastrins; Gastritis; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Male; Neutrophils; Peroxidase; Quinolones; Tumor Necrosis Factor-alpha

Although regenerating gene (Reg) protein is reported to have a trophic effect on gastric epithelial cells, its involvement in human gastric diseases is not clear. We have recently shown that both gastrin and gastric mucosal inflammation enhance Reg gene expression in the fundic mucosa in rats. This study was designed to clarify whether Reg protein is involved in Helicobacter pylori-induced gastritis and whether Reg gene expression is linked to serum gastrin levels in this condition. Mongolian gerbils were inoculated with an H. pylori strain isolated from a gastric cancer patient. Four weeks later, some of the gerbils with H. pylori infection were eradicated by lansoprazole, amoxicillin, and clarithromycin. The time courses of changes in Reg gene expression, serum gastrin levels, gastric acidity, and histopathologic factors were examined. Four weeks after H. pylori infection, gastritis started spreading to the fundic mucosa, and gastric acidity started reducing. Serum gastrin levels and Reg mRNA expression in the fundus were significantly increased 6 weeks after infection. Reg mRNA expression in the fundus correlated significantly with both serum gastrin levels and the severity of fundic mucosal inflammation. After H. pylori eradication, serum gastrin levels and fundic mucosal inflammation were normalized, and the increase in Reg mRNA expression was abolished. The Reg gene is associated with hypergastrinemia and fundic mucosal inflammation and may be involved in H. pylori-induced gastritis.

Topics: Animals; Anti-Bacterial Agents; Apoptosis; Base Sequence; Calcium-Binding Proteins; Cell Division; Disease Models, Animal; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Lithostathine; Male; Molecular Sequence Data; Nerve Tissue Proteins; RNA, Messenger; Sequence Alignment; Up-Regulation

Topics: Acinetobacter Infections; Animals; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Mice; Stomach Neoplasms

H. pylori is a major cause of primary chronic gastritis and peptic ulcer disease in children. The authors give an account of H. pylori infection (cagA+, vacA+) in a 15-year-old girl where the initial clinical features included fatigue, collapses, and anorexia, elevated serum gastrin level (> 1000 mIU/l) raised the suspicion of gastrinoma. H. pylori gastric infection was also associated with iron-deficiency anemia. After treatment for H. pylori infection (omeprazole, clarithromycin, amoxycillin), clinical symptoms improved consistently, the serum gastrin level was repeteadly quite normal and hematologic and iron profiles were within the normal range. There is compelling evidence that H. pylori must be taken into account as a cause of hypergastrinemia other than gastrinoma in childhood.

Topics: Adolescent; Anemia, Iron-Deficiency; Diagnosis, Differential; Female; Gastrinoma; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Pancreatic Neoplasms

Helicobacter pylori (H. pylori) infection in patients with chronic renal failure plays an important role in the pathogenesis of upper gastrointestinal tract diseases. In our earlier study we did not find significant relationship between parathormone (PTH) concentration abnormalities and H. pylori infection in hemodialysis patients (HD pts). The aim of our present study was to examine other parameters and interrelationships between them, connected with H. pylori infection in HD pts. The serum concentration of the following substances were measured: gastrin (G), parathormone (PTH), and IgG antibodies against H. pylori. The study was conducted in 65 (36 M, 29 F) stable HD pts: age 49 +/- 12 years, dialysed from 6 to 288 months. The control group (CG) consisted of 15 healthy people, mean age 38 +/- 8 years. The mean concentration of serum PTH serum was significantly higher in HD pts than in CG (538 +/- 520 vs 35 +/- 9.3 pg/ml, p < 0.001). The mean concentration of gastrin in serum was significantly higher in HD pts than in CG (155.37 +/- 235.4 vs 87.97 +/- 9.5 pg/ml, p < 0.01). The mean concentrations of IgG antibodies against IgG H. pylori was similar in HD pts and CG (88.1 +/- 80.0 vs 91.34 +/- 66.8 U/ml). We found significant positive correlation between IgG antibodies against H. pylori infection and gastrin level in serum of HD pts (r = 0.315, p < 0.001). We did not find significant correlation between concentrations: PTH vs G and PTH vs IgG against H. pylori.. Helicobacter pylori infection contributes to hypergastrinaemia in hemodialysed patients. There is no relationships between PTH abnormalities and H. pylori infection.

Topics: Adult; Case-Control Studies; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Renal Dialysis; Risk Factors

Hypergastrinemia and a reduction in tissue somatostatin occur in Helicobacter pylori-infected patients. We investigated whether the D cell may be a direct target of gastric inflammation and hypergastrinemia. D cells were quantified by morphometry and flow cytometry in 16-wk-old wild-type (G+/+) and gastrin-deficient (G-/-) mice. Hypochlorhydric G-/- mice were treated with either antibiotics for 20 days or infused with gastrin (G-17) for 14 days. G+/+ mice were made hypochlorhydric by treating them with omeprazole for 2 mo. G-/- mice showed significant inflammation compared with the G+/+ mice, which resolved after 20 days of antibiotic treatment. D cell numbers were not significantly different between G-/- and G+/+ mice. After G-17 was infused, fundic and antral D cell numbers decreased in the G-/- mice. G+/+ animals made hypergastrinemic with omeprazole exhibited decreased D cell numbers. When omeprazole-treated mice were treated with antibiotics alone, elevated plasma gastrin levels returned to baseline and D cell numbers returned to resting levels despite persistent hypochlorhydria. Hypergastrinemia, induced by inflammation, results in decreased D cell numbers. Thus the stomach responds to the presence of inflammation by reducing somatostatin levels, thereby releasing the inhibition on the G and parietal cells to maximize gastric acid output.

Topics: Animals; Anti-Ulcer Agents; Female; Gastric Acid; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Lymphocytes; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Omeprazole; Parietal Cells, Gastric; Pyloric Antrum; Somatostatin

Reduced gastric acid predisposes the stomach to colonization by bacteria and inflammation. Therefore, we investigated how the chronic gastritis in mice made hypochlorhydric by either gastrin deficiency or omeprazole treatment modulates epithelial cell function.. The gastric pathology of 16-week-old wild-type gastrin-expressing (G+/+) and gastrin-deficient (G-/-) mice maintained in conventional housing was compared. G-/- mice were then treated with antibiotics for 20 days. In a separate experiment, G+/+ mice were treated with omeprazole for 2 months or treated with omeprazole and antibiotics.. Compared with the G+/+ animals, the hypochlorhydric G-/- mice showed significant inflammation that resolved after 20 days of antibiotic treatment and correlated with a decrease in bacterial overgrowth. Elevated G- and parietal-cell numbers in the G-/- mice, quantified by flow cytometry, normalized after antibiotic treatment. G+/+ mice treated with omeprazole had increased bacteria and mucosal lymphocytes that resolved after antibiotic therapy. Quantitation of the gastric cells in these omeprazole-treated mice revealed a significant increase in G- and parietal-cell numbers. On resolution of the gastritis, a decrease in parietal and gastrin-expressing (G) cells was observed despite sustained hypochlorhydria in the presence of omeprazole.. Genetic or chemical hypochlorhydria predisposes the stomach to bacterial overgrowth resulting in inflammation. The specific changes in parietal and G cells correlate with the presence of inflammation and not directly with gastric acid. Thus, the normal stomach responds to inflammation by increasing the number and function of cell types that are able to maximize gastric acid output.

Topics: Achlorhydria; Animals; Anti-Bacterial Agents; Anti-Ulcer Agents; B-Lymphocytes; Bacteriological Techniques; Campylobacter; Campylobacter Infections; Female; Flow Cytometry; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Male; Mice; Omeprazole; Parietal Cells, Gastric; T-Lymphocytes

Gastrin/CCK-B receptors (CCKB-Rs) are present on parietal and enterochromaffin-like cells in the gastric mucosa but not on pit cells in the proliferative zone. Because serum gastrin levels are well correlated with the growth of the gastric pit, we examined whether pit precursor cells express CCKB-Rs using hypergastrinemic transgenic mice and a mouse pit precursor cell line, GSM06. In situ hybridization indicated that CCKB-R mRNA was limited to the lower one-third of the mucosa in control mice, whereas it was faintly distributed along the mid- to low glandular region in the hypergastrinemic transgenic mouse mucosa. CCKB-R-positive midglandular cells appear to have a pit cell lineage; therefore, GSM06 cells were used for an [(125)I]gastrin binding study. [(125)I]gastrin bound to the membrane fraction of the GSM06 cells when precultured with gastrin. Gastrin dose dependently induced CCKB-R expression in GSM06 cells and stimulated their growth. Thus these findings suggest that gastrin directly stimulates the growth of the pit cell lineage by inducing its own receptor in pit cell precursors.

Topics: Amino Acid Sequence; Animals; Cell Division; Gastric Mucosa; Gastrins; Gastritis; Gene Expression; Hypertrophy; In Situ Hybridization; Iodine Radioisotopes; Mice; Mice, Inbred ICR; Mice, Transgenic; Molecular Sequence Data; Receptor, Cholecystokinin B; Receptors, Cholecystokinin; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Sincalide; Stem Cells

Autoimmune gastritis (AG) can be easily recognized when the histological features are fully developed, but recognizing AG before the complete loss of the oxyntic mucosa is more challenging. One feature of fully developed AG is enterochromaffin cell-like (ECL) hyperplasia, but its presence or absence in earlier stages of AG has not been fully evaluated. A retrospective study of biopsy specimens from 40 patients was performed; all of the patients were originally diagnosed with possible AG based on the presence of lymphocytic infiltration and damage to oxyntic glands and/or the presence of metaplastic epithelium that disproportionately involved the body mucosa. Nineteen cases had follow-up serological studies for anti-parietal cells and/or anti-intrinsic factor antibodies: 13 were positive and 6 negative. The remaining 21 cases were indeterminate because of incomplete testing. The histological findings were similar in the patients who were serologically positive and those who were indeterminate for AG. In all of these cases, the oxyntic mucosa showed lymphoplasmacytic infiltrates within the lamina propria with focal gland infiltration and damage. Sixty-five percent (22/34) of the cases showed intestinal and/or pyloric metaplasia, and 85% (29/34) showed parietal cell pseudohypertrophy. Chromogranin stains were performed in 11 of 13 cases with positive serological markers for AG, and all showed at least linear ECL cell hyperplasia. In contrast, none of the six cases with negative serological studies had linear ECL cell hyperplasia, P <.001. In conclusion, the following constellation of findings supports a diagnosis of AG before the complete loss of oxyntic mucosa: deep or diffuse lymphoplasmacytic infiltrates within the lamina propria with foci of gland infiltration and damage, epithelial metaplasia, parietal cell pseudohypertrophy, and ECL cell hyperplasia at the linear or greater level.

Topics: Adult; Aged; Aged, 80 and over; Autoimmune Diseases; Female; Gastrins; Gastritis; Humans; Immunohistochemistry; Male; Middle Aged; Parietal Cells, Gastric

Helicobacter pylori may increase or inhibit gastric acid. We studied acid variations and plasma gastrin in cats harboring Helicobacter felis, harboring H. pylori, or free of gastric pathogens with reference to thioperamide (H(3) receptor antagonist) and SR-27417A (PAF receptor antagonist). In cats harboring H. felis, gastric mucosa were histologically normal. After H. felis eradication, pentagastrin-stimulated acid secretion was increased (40%) compared with the situation before eradication. Thioperamide abolished this inhibitory effect of H. felis, whereas SR-27417A did not. Basal and meal-stimulated plasma gastrin levels were not affected by eradication therapy. Acid secretion was inhibited (-80%) in week 3, increased from weeks 5 to 9, and remained constant for up to 42 weeks after H. pylori infection. SR-27417A had no effect on acid secretion before week 8 but inhibited it thereafter, and thioperamide increased it (20%) only before week 7 in those cats. Helicobacter inhibits gastric acid via an H(3) receptor pathway. Inflammatory mediators are thus involved in adaptation to the inhibitory effects of H. pylori on acid secretion.

Topics: Animals; Anti-Bacterial Agents; Cats; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Helicobacter; Helicobacter Infections; Helicobacter pylori; Histamine Antagonists; Kinetics; Pentagastrin; Piperidines; Platelet Membrane Glycoproteins; Receptors, Cell Surface; Receptors, G-Protein-Coupled; Receptors, Histamine H3; Thiazoles; Urease

In Japan, most cases of gastric carcinoid tumor (GCT) are unassociated with either autoimmune gastritis (AIG) showing type-A chronic atrophic gastritis (CAG-A) or Zollinger-Ellison syndrome (ZES). However, the pathogenesis of this tumor remains unknown. Recent studies have determined that Helicobacter pylori infection induces gastric carcinoid in Mongolian gerbils and that H. pylori lipopolysaccharide exerts a mitogenic effect on ECL cells. We examined five patients with histologically diagnosed GCT, 40 patients with H. pylori-positive gastric ulcer (Hp+GU), 24 patients with H. pylori-positive duodenal ulcer (Hp+DU), and 12 patients with AIG showing CAG-A topographically. We compared the prevalence of H. pylori infection, and the levels of gastrin and pepsinogen (PG) in the serum of patients with GCT with those of patients with Hp+GU, or Hp+DU, and AIG. We also investigated the histological characteristics of the tumor and the gastric corpus mucosa in the GCT patients. The levels of serum gastrin and PG I and II were measured using an RIA kit. In all five (100%) patients with GCT, H. pylori infection was present, without any evidence of AIG or ZES. The serum levels of gastrin in the GCT patients were higher than those in either Hp+GU or Hp+DU patients and lower than those in the AIG patients. In contrast, serum PG I levels and the PG I/II ratio were lower in the GCT group than in the Hp+GU or Hp+DU groups. Histologically, all GCTs were ECL cell tumors and peritumoral corporal mucosal atrophy was observed in four of the five patients with GCT. In conclusions, H. pylori infection and hypergastrinemia were found in the patients with GCT without AIG. This finding suggests that H. pylori infection may induce corporal mucosal atrophy and hypergastrinemia that can produce a GCT with time.

Topics: Adult; Aged; Aged, 80 and over; Autoimmune Diseases; Carcinoid Tumor; Duodenal Ulcer; Female; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Peptic Ulcer; Stomach Neoplasms

The relationship between serum parameters of gastric function and Helicobacter pylori infection in human immunodeficiency virus (HIV)-positive patients is almost unknown.. To investigate in HIV-infected patients: (i) the relationship between serum gastrin and serum pepsinogens over the progressive phases of HIV-related disease; (ii) the impact of H. pylori infection on gastrin and pepsinogen serum levels and its relation to antral histology; (iii) the prevalence of parietal cell autoantibodies.. Fifty-nine HIV-positive patients were studied by upper endoscopy plus gastric antral biopsy. Serum samples were tested for gastrin, pepsinogen A, pepsinogen C and parietal cell autoantibodies.. In patients without overt acquired immunodeficiency syndrome (AIDS), or with a CD4+ count of > 100 x 10(6) cells/L, mean serum levels of gastrin and pepsinogen C were higher than in subjects with AIDS or with a CD4+ count of < 100 x 10(6) cells/L (P < 0.01). Only one patient was found to be positive for parietal cell autoantibodies. H. pylori infection was associated with increased values of gastrin and pepsinogen C only in HIV-positive patients without AIDS or with a CD4+ count of > 100 x 10(6) cells/L. Atrophy was more frequent in patients with overt AIDS than in those without overt AIDS (57% vs. 33%, P=N.S.), and/or in patients with a CD4+ count of < 100 x 10(6) cells/L than in those with a CD4+ count of > 100 x 10(6) cells/L (62% vs. 26%, P < 0.05).. HIV-positive patients without overt AIDS have increased serum levels of gastrin and pepsinogen C compared with HIV-positive patients with overt AIDS.

Topics: Acquired Immunodeficiency Syndrome; Adult; AIDS-Related Opportunistic Infections; Autoantibodies; CD4 Lymphocyte Count; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Parietal Cells, Gastric; Pepsinogen C

In mouse models and humans, Helicobacter pylori is associated with an increase in serum gastrin and gastrin-expressing (G) cells with a concomitant decrease in somatostatin-expressing D cells. Inflammation of the gastric mucosa can progress to metaplastic changes in the stomach and to decreased colonization by H. pylori and increased colonization by non-H. pylori organisms. In addition, about 20% of individuals with chronic gastritis are H. pylori negative, suggesting that other organisms may induce gastritis. Consistent with this hypothesis, we report here that Acinetobacter lwoffii causes the same histologic changes as does H. pylori. Gastric epithelial cells were isolated from the entire stomach by an enzymatic method for quantitation by both flow cytometry and morphometric analysis. Two months after mice were inoculated with H. pylori or A. lwoffii, the mucosal T- and B-cell numbers significantly increased. After 4 months of infection, there was a threefold increase in the number of G cells and a doubling in the number of parietal cells. A threefold decrease in the number of D cells occurred in H. pylori- and A. lwoffii-infected mice. Plasma gastrin levels increased after both H. pylori and A. lwoffii infection. Histology revealed the presence of inflammation in the gastric mucosa with both A. lwoffii and H. pylori infection. A periodic acid-Schiff stain-alcian blue stain revealed mucous gland metaplasia of the corpus. Collectively, the results demonstrate that gastritis and hypergastrinemia are not specific for H. pylori but can be induced by other gram-negative bacteria capable of infecting the mouse stomach.

Topics: Acinetobacter Infections; Animals; DNA, Bacterial; ErbB Receptors; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Ki-67 Antigen; Mice; Mice, Inbred C57BL; T-Lymphocytes

In patients with the chronic gastritis in a combination with opisthorchiasis and with duodenogastric reflux it was marked the more expressed endoscopic and histological changes of stomach mucosa in comparison with the patients without reflux. In the patients with chronic gastritis and DGR the small colonization degree of mucosa by H. pylori was marked. The combination of endoscopic and histological changes in stomach mucosa at DGR allows to recommend the endoscopy as the basic method in clinical practice.

Topics: Adolescent; Adult; Chronic Disease; Duodenogastric Reflux; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter pylori; Humans; Male; Opisthorchiasis

The association between gastroesophageal reflux disease and end-stage renal disease remains unclear. We aimed to assess the prevalence of gastroesophageal reflux disease and also to identify possible pathogenetic factors in the development of reflux in symptomatic end-stage renal disease patients.. The study involved 42 end-stage renal disease patients with upper GI symptoms (group I) and 46 age- and sex-matched controls who did not have renal disease but had the same symptoms (group II). Endoscopy, endoscopic biopsies, and 24-h esophageal pH studies were used to diagnose gastroesophageal reflux disease. Subjects were also investigated for Helicobacter pylori gastritis and GI amyloidosis.. The prevalences of gastroesophageal reflux disease in the two groups were similar (81% vs 84.8%, p = 0.423). The prevalence of H. pylori infection was significantly lower in group I than in group II (38.1% vs 67.4%, p = 0.01). There were II cases of GI amyloidosis in group I. Multivariate logistic regression analysis in group I showed that GI amyloidosis (OR = 7.28, 95% CI = 1.13-46.93), chronic ambulatory peritoneal dialysis treatment (OR = 5.54, 95% CI = 1.01-30.43), and absence of H. pylori infection (OR = 3.75, 95% CI = 1.01-13.9) were significantly associated with reflux esophagitis.. Upper GI symptoms are important in predicting gastroesophageal reflux disease in end-stage renal disease patients. Chronic ambulatory peritoneal dialysis, GI amyloidosis, and absence of H. pylori infection seem to be risk factors for the development of gastroesophageal reflux disease in end-stage renal disease patients.

Topics: Adult; Amyloidosis; Esophagitis; Esophagus; Female; Gastrins; Gastritis; Gastroesophageal Reflux; Gastrointestinal Diseases; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Male; Middle Aged; Monitoring, Physiologic; Multivariate Analysis; Prevalence; Risk Factors

To investigate the effect of Hewei capsule (HWC) on gastric dynamics.. Sixty-two patients with dysmotility-like functional dyspepsia (DFD) were included in the study. The principal symptoms, electrogastrogram (EGG), plasma motilin (MTL), serum gastrin (Gas) and nitric oxide (NO) of the patients were the chief parameters observed before and after treatment.. There were arrhythmia of EGG, deficiency of MTL, Gas and NO in the patients with DFD, and these abnormal changes could be improved significantly by treating with HWC.. The abnormal gastric dynamics of the patients with DFD could be improved by HWC through multiple pathways.

Topics: Adolescent; Adult; Aged; Drugs, Chinese Herbal; Dyspepsia; Gastrins; Gastritis; Gastritis, Atrophic; Gastrointestinal Motility; Humans; Middle Aged; Motilin; Phytotherapy

Helicobacter pylori is said to cause atrophy of the gastric corpus and enterochromaffin-like cell proliferation in gastro-oesophageal reflux disease (GERD) patients treated long-term with a proton pump inhibitor.. To determine the effect of H. pylori infection on gastritis, enterochromaffin-like cell density and hyperplasia, mucosal atrophy and serum gastrin in patients with gastric hypersecretion (basal acid output gt; 15 mmol/h) with either hypergastrinemia (Zollinger-Ellison syndrome) or normal gastrin (non-Zollinger-Ellison syndrome) before and during long-term treatment with lansoprazole.. Lansoprazole was individually titrated to reduce basal acid output to < 5 mmol/h (< 1 mmol/h in post-surgical Zollinger-Ellison syndrome). Gastric corpus biopsies were obtained every 6 months before treatment and up to 8 years later.. H. pylori was present in corpus biopsies in approximately 50%, causing active gastritis which resolved rapidly in 15 subjects after elimination of H. pylori. Patchy mild/moderate corpus atrophy was present at entry in two and at the end in four out of 60 patients, one being H. pylori-positive. Intestinal metaplasia (< 10%) was seen in six isolated biopsies (1% of total). H. pylori did not affect serum gastrin, enterochromaffin-like cell density or hyperplasia. Enterochromaffin-like cell density was twice as high in Zollinger-Ellison syndrome as in non-Zollinger-Ellison syndrome patients (241 vs. 126 cells/mm2, P < 0.001). Enterochromaffin-like cells remained normal in the non-Zollinger-Ellison syndrome hypersecretors regardless of H. pylori status.. Corpus enterochromaffin-like cell increases were related to serum gastrin elevation, but neither H. pylori nor long-term treatment with lansoprazole alone or together had any effect on enterochromaffin-like cell density or hyperplasia. Corpus acute gastritis resulted from H. pylori infection, but did not result in mucosal atrophy despite long-term proton pump inhibitor treatment and promptly resolved with loss of H. pylori.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Enterochromaffin-like Cells; Enzyme Inhibitors; Female; Gastric Acid; Gastrins; Gastritis; Helicobacter pylori; Humans; Hyperplasia; Intestinal Mucosa; Lansoprazole; Male; Metaplasia; Middle Aged; Omeprazole; Zollinger-Ellison Syndrome

Gastric infection with Helicobacter pylori is associated with hypergastrinemia. Platelet activating factor (PAF) is produced in H. pylori-infected mucosa. The effects of PAF on gastrin release from cultured antral rabbit G cells were examined. Rabbit antral G-cells were obtained by collagenase-EDTA digestion and enriched by centrifugal elutriation. After 40 hr in culture, gastrin release in response to PAF was assessed. PAF stimulated gastrin release in a dose-dependent manner. A maximal release of 67% above basal was seen with PAF at 100 nM. PAF also enhanced the gastrin release stimulated by forskolin and bombesin. PAF-stimulated gastrin release was abolished by a PAF-receptor antagonist. Gastrin release stimulated by PAF was abolished by chelation of intra- or extracellular calcium or the L-type calcium channel inhibitor verapamil as well as by the protein kinase C inhibitor chelerythrine. Platelet-activating factor may contribute to the hypergastrinemia of H. pylori infection by stimulating gastrin release from G cells. PAF-stimulated gastrin release involves influx of extracellular calcium via L-type channels and activation of protein kinase C.

Topics: Animals; Bombesin; Calcium Channels, L-Type; Cells, Cultured; Colforsin; Disease Models, Animal; Gastrin-Secreting Cells; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Platelet Activating Factor; Protein Kinase C; Rabbits

Further elucidation of the consequences of Helicobacter pylori infection on gastric mucosal inflammation and gastric secretory function would be facilitated by an animal model that is susceptible to infection with H. pylori, is broadly similar in gastric physiology and pathology to people, and is amenable to repeated non-invasive evaluation. The goal of this study was to examine the interrelationship of bacterial colonization, mucosal inflammation and gastric secretory function in cats with naturally acquired H. pylori infection.. Twenty clinically healthy cats with naturally acquired H. pylori infection (cagA-, picB) and 19 Helicobacter-free cats were evaluated. Gastric colonization was determined by tissue urease activity, light microscopy, culture and PCR. The mucosal inflammatory response was evaluated by light microscopy, and by RT-PCR of the pro-inflammatory cytokines IL-1alpha, IL-1beta, IL-8 and TNF-alpha in gastric mucosa. Gastric secretory function was assessed by measuring pentagastrin-stimulated acid secretion, fasting plasma gastrin, and antral mucosal gastrin and somatostatin immunoreactivity.. H. pylori colonized the pylorus, fundus and cardia in similar density. Bacteria were observed free in the lumen of gastric glands and were also tightly adherent to epithelial cells where they were associated with microvillus effacement. Mononuclear inflammation, lymphoid follicle hyperplasia, atrophy and fibrosis were observed primarily in H. pylori-infected cats, with the pylorus most severely affected. Neutrophilic and eosinophilic infiltrates, epithelial dysplasia, and up-regulation of mucosal IL-1beta and IL-8 were observed solely in infected cats. Fasting plasma gastrin concentrations and pentagastrin-stimulated acid output were similar in both infected and uninfected cats. There was no relationship of bacterial colonization density or gastric inflammation to plasma gastrin concentrations or gastric acid output.. The pattern of colonization and the mucosal inflammatory response in cats with naturally acquired H. pylori are broadly similar to those in infected people, particularly children, and non-human primates. The upregulation of IL-8 in infected cats was independent of cagA and picB. Our findings argue against a direct acid-suppressing effect of H. pylori on the gastric secretory-axis in chronically infected cats.

Topics: Animals; Antigens, Bacterial; Bacterial Proteins; Cardia; Cat Diseases; Cats; Disease Models, Animal; Female; Gastric Acidity Determination; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Interleukin-1; Interleukin-8; Male; Pyloric Antrum; Reverse Transcriptase Polymerase Chain Reaction; Somatostatin; Tumor Necrosis Factor-alpha

Atrophic gastritis can develop in patients with Helicobacter pylori infection leading to a reduction in basal acid output. Whether the atrophy that develops is reversible is controversial.. To investigate the effect of H. pylori eradication in infected subjects who had developed atrophy of the corpus mucosa.. Ten H. pylori positive patients with corpus atrophy were identified at oesophagogastroduodenoscopy (OGD). They received eradication therapy with amoxicillin, clarithromycin and omeprazole. Repeat OGD with biopsy was performed at least 3 months later. Fasting plasma gastrin was measured at baseline and at re-endoscopy. H. pylori eradication was confirmed by 13C urea breath testing.. Median time to re-endoscopy was 5 months. There was improvement in corpus atrophy in 50% of patients after H. pylori eradication, and a significant reduction in plasma gastrin (P = 0.03). The index patients had a significant diminution of basal acid output compared to controls.. Corpus atrophy as defined by the Sydney System is reversible in some patients after H. pylori eradication. Improvement in atrophy is associated with a fall in fasting plasma gastrin levels. This may have implications in the prevention of gastric carcinoma.

Topics: Adult; Aged; Atrophy; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged

Body gastritis caused by Helicobacter pylori infection appears to inhibit gastric acid secretion. The aim of this study was to determine the effects of H pylori infection on gastric acid secretion and clarify its mechanisms with reference to interleukin 1beta (IL-1beta).. (1) Mongolian gerbils were inoculated orally with H pylori. Before, six, and 12 weeks after inoculation, serum gastrin levels, gastric acid output, and IL-1beta mRNA levels in the gastric mucosa were determined. Pathological changes were also determined according to the updated Sydney system. (2) Effects of recombinant human IL-1 receptor antagonist (rhIL-1ra) on gastric acid output and serum gastrin levels were also determined.. (1) Scores for activity and inflammation of gastritis and serum gastrin levels were significantly increased, and gastric acid output was significantly decreased six and 12 weeks after inoculation with H pylori. IL-1beta mRNA levels in the gastric mucosa were also elevated six and 12 weeks after inoculation with H pylori. (2) Acid output and serum gastrin levels in the infected groups returned to control levels after rhIL-1ra injection.. Gastric acid secretion is decreased and serum gastrin levels are increased in Mongolian gerbils infected with H pylori. This change in gastric acid secretion appears to be mediated by IL-1beta induced by H pylori infection.

Topics: Analysis of Variance; Animals; Electrophoresis, Agar Gel; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Interleukin-1; Male; Neutrophil Infiltration; Receptors, Interleukin-1; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Sequence Analysis, DNA; Specific Pathogen-Free Organisms; Statistics, Nonparametric

Serum chromogranin A (CgA), a marker of neuroendocrine neoplasia, increases during profound gastric acid inhibition, possibly reflecting the trophic effect of gastrin on the enterochromaffin-like (ECL) cells.. This study investigated the clinical value of serum CgA as a screening test for gastric fundic enterochromaffin-like (ECL) cell hyperplasia during acid-suppressive therapy.. A consecutive series of 230 dyspeptic patients referred for upper gastrointestinal endoscopy was investigated in a cross-sectional design. They were 154 patients on continuous medium-term (6 weeks to one year) or long-term (longer than one year) acid inhibition with either proton pump inhibitors (PPIs, n = 117) or histamine2-receptor antagonists (H2RAs, n = 37) for gastro-oesophageal reflux disease, and 76 nontreated subjects, with normal endoscopic findings (control group). Fasting blood samples were analysed for gastrin and CgA. Gastric biopsy specimens (oxyntic mucosa) were examined for histological evaluation of gastritis (Sydney classification) and of ECL cell hyperplasia (Solcia classification).. Serum CgA levels correlated positively with serum gastrin, following a quadratic function (r = 0.78, P < 0.0001). Elevated serum CgA values during long-term acid inhibition correlated with the presence and severity of fundic ECL cell hyperplasia. Multivariate analysis identified hypergastrinaemia (P < 0.0001), duration of acid inhibition (P < 0.0001), H. pylori infection (P = 0.008), ECL cell hyperplasia (P = 0.012), and body gland atrophy (P = 0.043) as independent predictors of elevated serum CgA. In subjects on long-term acid inhibition (n = 123), serum CgA was equally sensitive but more specific than serum gastrin for the detection of ECL cell hyperplasia (sensitivity, 91.3% for both; specificity, 73% vs. 43%, P < 0.0001).. During long-term gastric acid inhibition, serum CgA levels reflect the presence and severity of fundic ECL cell hyperplasia. Serum CgA is therefore a useful screening test for gastric ECL cell proliferative changes within this context.

Topics: Adult; Aged; Anti-Ulcer Agents; Chromogranin A; Chromogranins; Cross-Sectional Studies; Enterochromaffin-like Cells; Female; Gastric Acid; Gastric Fundus; Gastrins; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Hyperplasia; Male; Mass Screening; Middle Aged; Multivariate Analysis; Sensitivity and Specificity

Recent studies have reported an association between iron deficiency anaemia and Helicobacter pylori. Helicobacter pylori could cause iron deficiency anaemia by altering iron absorption. We observed that most patients with Helicobacter pylori infection and iron deficiency anaemia present a chronic superficial pangastritis.. To investigate whether Helicobacter pylori-positive patients with iron deficiency anaemia have peculiar histological and functional features when compared with non-anaemic Helicobacter pylori-positive subjects.. Fifty-one patients with iron deficiency anaemia, in whom chronic superficial Helicobacter pylori gastritis was the only gastrointestinal finding, and 103 non-anaemic Helicobacter pylori-positive controls were included in the study. Thirty-seven patients were randomly matched with 37 controls of the same sex and age.. Gastroscopy, with antral (n=3) and body (n=3) biopsies, was performed. Gastrin and pepsinogen I levels and antiparietal cell antibodies were evaluated. Intragastric pH was also measured.. Gastritis involved the corporal mucosa in 90% of patients compared to 42.7% of controls (P < 0.0001). The mean inflammatory score in the gastric body was significantly higher among patients than in controls (2.2 vs. 0.6; P=0.012). Gastrin was significantly higher in patients than in controls (mean 60.2 vs. 29 pg/mL; P=0.0069). Intragastric pH was higher in patients than in controls (median 5.7 vs. 2; P=0.0026).. These data suggest that patients with iron deficiency anaemia and Helicobacter pylori infection have a peculiar pattern of gastritis with corporal involvement and related changes in intragastric pH.

Topics: Adolescent; Adult; Aged; Anemia, Iron-Deficiency; Case-Control Studies; Chronic Disease; Female; Gastric Acid; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Inflammation; Male; Middle Aged

Gastric dilatation (GD) has been observed in Tac:(SW)fBR surveillance mice, with mean age of 10 months, that are exposed to high levels of environmental antigens during routine exposure to dirty bedding. The aim of the study reported here was to determine whether GD was associated with other systemic conditions affecting mice. Three groups of nine animals including-surveillance mice not exposed to dirty bedding (control), surveillance mice with out GD (NGD), and surveillance mice with GD (group GD)-had mean stomach weight with ingesta of 0.5 +/- 0.02 g, 1.09 +/- 0.07 g (P < 0.0001), and 2.54 +/- 0.4 g (P < 0.0001), respectively. Mean serum creatinine concentration was significantly higher in GD (1.6 +/- 0.25 mg/dl), compared with NGD (0.17 +/- 0.22 mg/dl, P < 0.0001) and control (0.2 +/- 0.16 mg/ dl, P < 0.0001) mice. In addition, lesions consistent with severe chronic nephropathy and mild gastritis were common in GD, compared with NGD and control mice. Finally, serum amidated gastrin concentration was significantly high in GD (179.37 +/- 53.86 pM, P < 0.03) and NGD (264.89 +/- 115.89 pM, P < 0.009), compared with control (60.77 +/- 8.39 pM) mice. Gastric dilatation syndrome is associated with chronic nephropathy, hypergastrinemia, and gastritis in surveillance mice exposed to high levels of environmental antigens.

Topics: Animals; Antigens; Dilatation, Pathologic; Environmental Monitoring; Gastrins; Gastritis; Kidney Diseases; Mice; Stomach; Syndrome

It remains controversial whether or not Helicobacter pylori infection causes altered gastric acid secretion. A novel test for evaluating gastric acid secretion (endoscopic gastrin test; EGT) has recently been developed.. To investigate by EGT the effects of H pylori eradication on the state of gastric acid secretion in patients with peptic ulcer.. Twenty six patients with duodenal ulcer and 33 with gastric ulcer, for all of whom H pylori infection had been documented, were studied by EGT, histological examination of gastric mucosa, and measurement of plasma gastrin levels before and one and seven months after H pylori eradication.. In patients with duodenal ulcer, the mean EGT value before H pylori eradication was higher than that in H pylori negative controls, but it had decreased significantly seven months after the treatment. In contrast, the mean EGT value of patients with gastric ulcer before H pylori eradication was lower than that in H pylori negative controls, but it had increased one month after the treatment; this was followed by a slight decrease at seven months. In both groups, mean EGT values seven months after the treatment were not significantly different from the mean control value.. The reduced acid secretion in gastric ulcer patients and gastric acid hypersecretion in duodenal ulcer patients were both normalised after the clearance of H pylori.

Topics: Adult; Aged; Atrophy; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Stomach Ulcer; Tetragastrin

Human colonization with Helicobacter pylori increases the risk for distal gastric adenocarcinoma, possibly by altering gastric epithelial cell cycle events and/or gastrin secretion. This study aimed to determine whether H. pylori virulence-related characteristics affect apoptosis, proliferation, and gastrin levels in a rodent model of gastric adenocarcinoma.. Mongolian gerbils were challenged with H. pylori wild-type or isogenic cagA(-) and vacA(-) mutants, and apoptotic and proliferating cells were identified by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling and proliferating cell nuclear antigen immunohistochemistry, respectively. Serum gastrin levels were determined by radioimmunoassay.. Gastric epithelial cell turnover was no different after infection with the wild-type, cagA(-), or vacA(-) strains. H. pylori infection significantly increased antral apoptosis 2-4 weeks after challenge, before apoptotic indices decreased to baseline. In contrast, antral proliferation rates were significantly higher 16-20 weeks after inoculation, but then decreased by 40 weeks. Antral proliferation was significantly related to serum gastrin levels, whereas antral apoptosis was inversely related to acute inflammation and lymphoid follicles.. In H. pylori-infected gerbils, enhanced antral apoptosis is an early and transient cell cycle event. Epithelial cell proliferation peaks later and is significantly related to increased gastrin levels, suggesting that epithelial cell growth in H. pylori-colonized mucosa may be mediated by gastrin-dependent mechanisms.

Topics: Animals; Apoptosis; Cell Division; Epithelial Cells; Gastrins; Gastritis; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Mutation; Statistics, Nonparametric; Stomach; Virulence

The relationship of Helicobacter felis, a bacterium observed in the stomachs of cats, to gastric disease is unclear. The objective of this study was to determine if H. felis infection alters gastric histopathology, proinflammatory cytokine expression, and secretory function and evokes a humoral immune response in cats. Five specific-pathogen-free (SPF) Helicobacter-free cats were studied before and for 1 year after oral inoculation with H. felis (ATCC 49179). Four SPF H. felis-uninfected cats served as controls. The stomachs of all five H. felis-inoculated cats became colonized, as determined by urease activity, histopathology, PCR, culture, and transmission electron microscopy of serial gastric biopsies at 0, 3, 5, 8, and 12 months. Uninoculated cats remained Helicobacter free. Lymphoid follicular hyperplasia, atrophy, and fibrosis were observed primarily in the pylorus of infected cats. Mild mononuclear inflammation was detected in both infected and uninfected cats, but was more extensive in infected cats, with pangastric inflammation, eosinophilic infiltrates, and cardia gastritis observed only in infected cats. No upregulation of antral mucosal interleukin 1alpha (IL-1alpha), IL-1beta, or tumor necrosis factor alpha was detected by reverse transcription-PCR in any cat. The gastric secretory axes, assessed by fasting plasma gastrin, antral mucosal gastrin and somatostatin immunoreactivity, and pentagastrin-stimulated gastric acid secretion, were similar in both infected and uninfected cats. Gradual seroconversion (immunoglobulin G) was observed in four of five infected cats, with enzyme-linked immunosorbent assay values reaching 4x to 12x baseline 12 months postinfection. These findings indicate that H. felis infection in cats induces lymphoid follicular hyperplasia, mild gastritis, and seroconversion, but is associated with normal gastric secretory function.

Topics: Animals; Antibodies, Bacterial; Cats; Cytokines; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Hyperplasia; Immunohistochemistry; Lymphoid Tissue; Male; Polymerase Chain Reaction; Somatostatin; Urease

Recent studies have clarified a close association between H. pylori infection and gastritis, peptic ulcer disease, and gastric cancer, but there is little information concerning the relationship between H. pylori infection and reflux esophagitis (RE). We investigated the relationship between H. pylori, RE, and corpus gastritis.. Ninety-five patients with RE and 190 sex- and age-matched asymptomatic healthy controls demonstrating no localized lesions in the upper GI tract were studied and evaluated for H. pylori infection, histologic gastritis, serum gastrin, and pepsinogens (PGs).. H. pylori infection was significantly lower in RE patients than in asymptomatic controls (41% vs. 76%, p <.01). Histologic gastritis of both the antrum and corpus was significantly less frequent (antrum; p <.01, corpus; p <. 01), and serum levels of PGI and the PG I/II ratio were significantly higher in RE patients than in controls (PGI; p <.05, PG I/II ratio; p <.01). When the subjects were divided into two age groups (59 years of age and younger and 60 years of age and older), a significant difference was found only among patients over 60 years of age (29% vs. 85%, p <.01). Among subjects in this age group, gastritis in both the antrum and corpus were significantly milder in RE patients than in controls. Although the prevalence of H. pylori infection was similar between the two groups of patients under 59 years of age, corpus gastritis was significantly milder in patients than in controls (p <.05).. A significantly low prevalence of H. pylori infection was found in RE patients over 60 years of age but not in those under 59 in comparison with sex- and age-matched controls. The relative lack of corpus gastritis might play a role in the pathogenesis of RE in our population through preservation of the acid secretion area.

Topics: Age Factors; Aged; Case-Control Studies; Endoscopy, Gastrointestinal; Esophagitis, Peptic; Female; Gastrins; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Japan; Male; Middle Aged; Pepsinogens; Prevalence; Pyloric Antrum; Stomach

The efficacy and safety of long-term acid suppression remains a subject for debate. We report data from patients with refractory reflux esophagitis who were undergoing maintenance therapy with >/=20 mg omeprazole daily for a mean period of 6.5 years (range, 1.4-11.2 years).. Patients with severe reflux esophagitis resistant to long-term therapy with H(2)-receptor antagonists and who were not eligible for surgery were evaluated at least annually for endoscopic relapse and histological changes in the gastric corpus.. In 230 patients (mean age, 63 years at entry; 36% were >/=70 years), there were 158 relapses of esophagitis during 1490 treatment years (1 per 9.4 years), with no significant difference in relapse rates between Helicobacter pylori-positive and -negative patients. All patients rehealed during continued therapy with omeprazole at the same or higher dose. The annual incidence of gastric corpus mucosal atrophy was 4.7% and 0.7% in H. pylori-positive and -negative patients, respectively, which was mainly observed in elderly patients who had moderate/severe gastritis at entry. In patients with baseline moderate/severe gastritis, the incidences were similar: 7.9% and 8.4%, respectively. Corpus intestinal metaplasia was rare, and no dysplasia or neoplasms were observed. The adverse event profile was as might be expected from this elderly group of patients.. Long-term omeprazole therapy (up to 11 years) is highly effective and safe for control of reflux esophagitis.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Anti-Ulcer Agents; Barrett Esophagus; Child; Drug Resistance; Esophagitis; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Humans; Hyperplasia; Male; Middle Aged; Omeprazole; Time Factors; Treatment Outcome

Bacterial overgrowth in the stomach may occur under conditions of diminished or absent acid secretion. Under these conditions, secretion of the hormone gastrin is elevated. Alternatively, bacterial factors may directly stimulate gastrin. Consistent with this hypothesis, we found that mice colonized for 2 months with a mixed bacterial culture of opportunistic pathogens showed an increase in serum gastrin. To examine regulation of gene expression by bacterial proteins, stable transformants of AGS cells expressing gastrin or interleukin-8 (IL-8) promoters were cocultured with live organisms. Both whole-cell sonicates and a heat-stable fraction were also coincubated with the cells. A level of 10(8) organisms per ml stimulated both the gastrin and IL-8 promoters. Heat-stable proteins prepared from these bacterial sonicates stimulated the promoter significantly more than the live organism or unheated sonicates. A 38-kDa heat-stable protein stimulating the gastrin and IL-8 promoters was cloned and found to be an OmpA-related protein. Immunoblotting using antibody to the OmpA-like protein identified an Acinetobacter sp. as the bacterial species that expressed this protein and colonized the mouse stomach. Moreover, reintubation of mice with a pure culture of the Acinetobacter sp. caused gastritis. We conclude that bacterial colonization of the stomach may increase serum gastrin levels in part through the ability of the bacteria to produce OmpA-like proteins that directly stimulate gastrin and IL-8 gene expression. These results implicate OmpA-secreting bacteria in the activation of gastrin gene expression and raise the possibility that a variety of organisms may contribute to the increase in serum gastrin and subsequent epithelial cell proliferation in the hypochlorhydric stomach.

Topics: Acinetobacter; Amino Acid Sequence; Animals; Bacterial Outer Membrane Proteins; Base Sequence; Cloning, Molecular; Coculture Techniques; Gastrins; Gastritis; Genes, Bacterial; Humans; Interleukin-8; Mice; Mice, Inbred C57BL; Molecular Sequence Data; Moraxella catarrhalis; Promoter Regions, Genetic; Recombinant Proteins; Sequence Homology, Amino Acid; Stomach

Oxyntic atrophy is the hallmark of chronic gastritis. Many studies have sought to develop animal models for oxyntic atrophy, but none of them are reversible. We now report that rats administered high doses of DMP 777 demonstrate reversible oxyntic atrophy.. DMP 777 was administered to CD-1 rats by oral gavage (200 mg. kg(-1). day(-1)). Serum gastrin level, in vivo acid secretion, and gastric histological changes were evaluated in DMP 777-dosed animals. Direct effects of DMP 777 on parietal cells were evaluated by assessment of aminopyrine accumulation into isolated rabbit parietal cells, as well as by assessment of DMP 777 effects on acridine orange fluorescence and H(+),K(+)-adenosine triphosphatase (ATPase) activity in isolated tubulovesicles.. Oral dosing with DMP 777 caused a rapid increase in serum gastrin levels and severe hypochlorhydria. DMP 777 inhibited aminopyrine accumulation into rabbit parietal cells stimulated with either histamine or forskolin. DMP 777 reversed a stimulated proton gradient in isolated parietal cell tubulovesicles. Oral dosing with DMP 777 led to rapid loss of parietal cells from the gastric mucosa. In response to the acute loss of parietal cells, there was an increase in the activity of the progenitor zone along with rapid expansion of the foveolar cell compartment. DMP 777 treatment also led to the emergence of bromodeoxyuridine-labeled cells and cells positive for periodic acid-Schiff in the basal region of fundic glands. With extended dosing over 3-6 months, foveolar hyperplasia and oxyntic atrophy were sustained while chief cell, enterochromaffin-like cell, and somatostatin cell populations were decreased. No histological evidence of neoplastic transformation was observed with dosing up to 6 months. Withdrawal of the drug after 3 or 6 months of dosing led to complete restitution of the normal mucosal lineages within 3 months.. DMP 777 acts as a protonophore with specificity for parietal cell acid-secretory membranes. DMP 777 in high doses leads to the specific loss of parietal cells. Foveolar hyperplasia, loss of normal gland lineages, and the emergence of basal mucous cells appear as sequelae of the absence of parietal cells. The results suggest that parietal cells are critical for the maintenance of the normal mucosal lineage repertoire.

Topics: Acridine Orange; Aminopyrine; Animals; Anti-Inflammatory Agents, Non-Steroidal; Atrophy; Azetidines; Carbon Radioisotopes; Disease Models, Animal; Enzyme Inhibitors; Fluorescent Dyes; Gastric Acid; Gastrins; Gastritis; H(+)-K(+)-Exchanging ATPase; Ionophores; Leukocyte Elastase; Male; Necrosis; Nigericin; Parietal Cells, Gastric; Piperazines; Rabbits; Rats; Rats, Sprague-Dawley; Regeneration; Stomach

We report a case of pseudo-Zollinger-Ellison syndrome in a 17-year-old man presenting with gastrin levels exceeding 2000 pmol/l and BAO 24 mEq/hr. Histologically, apart from hypertrophic gastritis with the thickening of mucosal folds and diffuse G-cell hyperplasia, gastric mucosa was found to contain foci of pancreatic metaplasia.

Topics: Adolescent; Gastric Acidity Determination; Gastric Mucosa; Gastrin-Secreting Cells; Gastrins; Gastritis; Humans; Hyperplasia; Male; Metaplasia; Pancreas; Stomach; Zollinger-Ellison Syndrome

The association between Helicobacter pylori infection and gastric motility abnormalities is still controversial, partly because of the lack of an appropriate animal model. H. heilmannii type 1 (Hh1), a spiral bacterium that infects the stomach of both man and pigs, easily colonises and induces an inflammatory response in the gastric mucosa of rodents. For these reasons, the present study investigated the relationship between gastric motility in rats experimentally infected with Hh1 and correlated the results with serum gastrin and gastric somatostatin concentrations, as these hormones seem to be involved in gastric motility. Ten rats were inoculated with gastric mucus from an Hh1-positive pig and 10 animals with gastric mucus from an Hh1-negative pig (control group). After 56 days, gastric emptying was studied in vivo by scintigraphy. The animals were then killed, blood samples were collected for serum gastrin measurement, strips of the gastric wall were obtained for an in-vitro motor study and fragments of the gastric antrum were obtained for somatostatin content evaluation, Hh1 diagnosis and histological study. There was a significant increase in gastric emptying in the test group compared with the controls as demonstrated by the in-vivo and in-vitro studies. Serum gastrin levels were significantly higher and somatostatin levels were lower in the test group than in the controls. In addition, infected animals showed evidence of gastritis on histological examination. Gastric motility is altered in rats infected with Hh1, a fact possibly related to concurrent abnormalities of gastrin and somatostatin secretion.

Topics: Animals; Female; Gastric Emptying; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Pyloric Antrum; Rats; Rats, Wistar; Somatostatin

Topics: Anti-Ulcer Agents; Barrett Esophagus; Drug Administration Schedule; Esophageal Neoplasms; Esophagitis, Peptic; Fundoplication; Gastric Mucosa; Gastrins; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Humans; Omeprazole; Proton Pump Inhibitors; Time

Topics: Abomasum; Animals; Appetite; Cattle; Cattle Diseases; Gastrins; Gastritis; Host-Parasite Interactions; Leptin; Neuropeptide Y; Sheep; Sheep Diseases

We have experienced a case of the stomach with hypergastrinemia and type A gastritis with multiple carcinoids in a 37-year-old woman. An upper gastrointestinal series revealed multiple minute polyps in the upper body of the stomach. All polyps were diagnosed as carcinoid using endoscopic biopsies. She had neither symptom or signs of typical carcinoid disease. The serum gastrin level was as high as 725 pg/ml. Total gastrectomy was performed, and the diagnosis of multiple gastric carcinoids (sm, no) with type A gastritis was histologically confirmed. After the operation, the serum gastrin level returned to normal, and the patient has been doing well and is disease-free to date at 7 years after the operation. This case suggested that multiple gastric carcinoid lesions may be precipitated by chronic atrophic gastritis accompanying hypergastrinemia. In the treatment of multiple gastric carcinoids with type A gastritis, total gastrectomy with lymph node dissection should be standard operative procedure, in order to resect the fundic gland area completely which could be the origin of carcinoids and endocrine cell micronest.

Topics: Adult; Carcinoid Tumor; Female; Gastrins; Gastritis; Humans; Stomach Neoplasms

A 4-yr-old cheetah (Acinonyx jubatus) with a 2-yr history of chronic intermittent vomiting and spiral bacteria-associated gastritis presented with dramatically increased vomiting frequency and marked intermittent abdominal distention. Physical examination revealed loss of muscle mass and poor fur coat quality. Contrast radiography was consistent with delayed gastric emptying due to presumed gastric outlet obstruction. Both Y-U pyloroplasty and incisional gastropexy were performed, and no subsequent vomiting has been observed for 3 yr with the exception of three episodes during the immediate postoperative period. The cause of delayed gastric emptying was not determined, although a gastric motility disorder associated with gastric bacterial infection and elevated gastrin levels was suspected.

Topics: Acinonyx; Animals; Female; Gastric Emptying; Gastrins; Gastritis; Gastrointestinal Motility; Pylorus; Stomach Diseases; Vomiting

Helicobacter pylori infection induces selective reduction of the number of antral D-cells and results in abnormal regulation of serum gastrin secretion. The purpose of this study was to investigate the relationship between H. pylori infection and the numbers of G-cells and D-cells.. The numbers of antral G-cells and D-cells, the ratio of G-cells to D-cells and fasting serum gastrin concentrations were compared between 37 patients with (29 with duodenal ulcers and 8 with gastric ulcers) and 33 without H. pylori infection (22 with duodenal ulcers and 11 with gastric ulcers). Serum gastrin concentrations were measured using the radioimmunoassay technique. Antral mucosal biopsy specimens were examined using immunohistochemical staining with antibodies specific for gastrin and somatostatin and the numbers of G-cells and D-cells per gastric gland were counted.. Fasting serum gastrin concentrations were significantly higher in patients with H. pylori infection compared to patients without infection (80.3 +/- 23.5 vs 47.6 +/- 14.1 pg/ml, p < 0.001). The number of G-cells per gastric gland was similar in infected and uninfected patients (7.1 +/- 3.1 vs 7.3 +/- 3.9, respectively, p > 0.5). The number of D-cells was significantly lower in patients with H. pylori infection than in uninfected patients in both duodenal and gastric ulcer patients (1.3 +/- 0.4 vs 2.5 +/- 1.6, respectively, p < 0.001). The ratio of G-cells to D-cells was also significantly higher in infected patients compared with uninfected patients for both gastric and duodenal ulcers (5.7 +/- 2.7 vs 3.5 +/- 1.9, respectively, p < 0.001).. These results strongly suggest that Helicobacter pylori infection induces reduction of the number of antral D-cells. The resulting relative hypofunction of the inhibitory action of D-cells against G-cells may be responsible for increased serum gastrin secretion.

Topics: Case-Control Studies; Gastrin-Secreting Cells; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Somatostatin; Somatostatin-Secreting Cells

Helicobacter pylori infections are associated with hypochlorhydria in patients with pangastritis. It has previously been shown that eradication of H pylori leads to an increase in acid secretion in H pylori associated enlarged fold gastritis, suggesting that H pylori infection affects parietal cell function in the gastric body. The aim of this study was to evaluate the effects of H pylori infection on parietal cell morphology and function in hypochlorhydric patients.. The presence of H pylori infection, mucosal length, and inflammatory infiltration were investigated in six patients with enlarged fold gastritis and 12 patients without enlarged folds. Parietal cell morphology was examined by immunohistochemistry using an antibody against the alpha subunit of H(+),K(+)-ATPase and electron microscopy. In addition, gastric acid secretion and fasting serum gastrin concentration were determined before and after the eradication of H pylori.. In the H pylori positive patients with enlarged fold gastritis, fold width, foveolar length, and inflammatory infiltration were increased. In addition, the immunostaining pattern of H(+), K(+)-ATPase was less uniform, and the percentage of altered parietal cells showing dilated canaliculi with vacuole-like structures and few short microvilli was greatly increased compared with that in H pylori positive patients without enlarged folds. After eradication, fold width, foveolar length, and inflammatory infiltrates decreased and nearly all parietal cells were restored to normal morphology. On the other hand, altered parietal cells were negligible in H pylori negative patients. In addition, the basal acid output and tetragastrin stimulated maximal acid output increased significantly from 0.5 (0.5) to 4.1 (1.5) mmol/h and from 2.5 (1.2) to 13.8 (0.7) mmol/h (p<0.01), and fasting serum gastrin concentrations decreased significantly from 213.5 (31.6) to 70.2 (7.5) pg/ml (p<0.01) after eradication in patients with enlarged fold gastritis.. The morphological changes in parietal cells associated with H pylori infection may be functionally associated with the inhibition of acid secretion seen in patients with enlarged fold gastritis.

Topics: Adult; Dyspepsia; Female; Gastric Acid; Gastrins; Gastritis; H(+)-K(+)-Exchanging ATPase; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Male; Microscopy, Electron; Middle Aged; Parietal Cells, Gastric

Helicobacter pylori infection is associated with increased gastrin release in patients with normal renal function. Hypergastrinaemia is a common finding in haemodialysis patients and, in many cases, may be linked to H. pylori infection. The aim of this study was to examine the effect of H. pylori infection, and its eradication, on elevated gastrin levels in haemodialysis patients.. Eighty-nine dyspeptic patients were included in the study. While 44 patients had normal renal function, the remaining 45 were end-stage renal failure patients. Patients were assigned to one of four groups according to their H. pylori and renal function status. Infected patients were re-evaluated after 2 months following eradication treatment. Serum gastrin levels were measured in these groups both before and after eradication treatment.. Haemodialysis patients with H. pylori infection had higher serum gastrin levels than did H. pylori negative haemodialysis patients (321+/-131 pg/ml vs 154+/-25 pg/ml) (P<0.05). Mean serum gastrin concentration was 152+/-21 pg/ml in the non-uraemic H. pylori-positive group. This value was 58+/-17 pg/ml in the non-uraemic H. pylori-negative group (P<0.05). There were significant decreases in serum gastrin levels from pre- to post-eradication of H. pylori in the infected haemodialysis and non-uraemic patient groups (312+/-131 pg/ml to 179+/-85 pg/ml and 152+/-21 pg/ml to 72+/-2.4 pg/ml respectively, P<0.05). Four patients in group Ib and 5 patients in group IIb who had persistent infection did not have a decrease in serum gastrin level. All patients with successful eradication had a decrease in serum gastrin concentration.. Our findings suggest that H. pylori infection contributes to hypergastrinaemia in haemodialysis patients. More research is needed regarding the clinical consequences of hypergastrinaemia in these individuals.

Topics: Adult; Anti-Bacterial Agents; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Kidney Failure, Chronic; Male; Renal Dialysis

Gastrin levels have been reported to be often increased in patients with primary hyperparathyroidism (PHPT) considered to be caused by hypercalcemia. To determine the prevalence of increased basal gastrin and to investigate its causes, 52 consecutive patients with PHPT were studied prospectively, undergoing a clinical, biochemical, and gastric morphofunctional assessment before any parathyroid surgical procedure. This included evaluation of basal and secretin-stimulated gastrin, basal and pentagastrin-stimulated gastric acid secretion, upper gastrointestinal endoscopy, with histological evaluation for gastritis and Helicobacter pylori infection. Twenty of the 52 PHPT patients (38.5%) had increased fasting gastrin. Further investigation allowed us to clearly demonstrate the causes of hypergastrinemia in 16 of these 20 patients. In 7 of 20 (35%), hypergastrinemia was caused by gastric fundus atrophy; in 3 patients (15%), Zollinger-Ellison syndrome with Multiple Endocrine Neoplasia type I was diagnosed; whereas in another 20% of patients, mild hypergastrinemia was ascribed to Helicobacter pylori gastritis. Finally, in 2 patients, additional clinical history revealed an occasional use of the gastric antisecretory drug omeprazole a few days before the serum gastrin determination. This study shows that the hypercalcemic status per se is not sufficient to produce an increase in fasting gastrin levels. Furthermore, gastric fundus atrophy, and not gastrinoma, is the major cause of relevant (>160 pg/mL) hypergastrinemia.

Topics: Adult; Aged; Atrophy; Female; Gastric Acid; Gastric Fundus; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hyperparathyroidism; Male; Middle Aged; Multiple Endocrine Neoplasia Type 1; Pentagastrin; Prospective Studies; Secretin

Hypergastrinaemia-associated changes of non-antral argyrophil cells in man are of increasing interest, because of the development of potent inhibitors of gastric acid secretion. Using an antibody against chromogranin A, we identified micronodular endocrine cell hyperplasia of the oxyntic mucosa in gastric biopsy specimens of patients with hypergastrinaemia of different backgrounds. Consecutive ultrathin sections were examined at the electron-microscopical level. Endocrine cell types within the (extraepithelial) micronodules closely resembled those in the adjacent mucosa. Micronodules were classified into two groups. The first group was composed of endocrine cells only and predominated in patients with drug-induced hypergastrinaemia and/or chronic gastritis, and in a gastrinoma/MEN I patient. The second group represented "neuroendocrine complexes", showing a close intermingling of non-myelinated nerve fibres with endocrine cells, and was found predominantly in pernicious anaemia. Micronodular argyrophil cell growth in man is therefore heterogeneous and depends on the background of the hypergastrinaemia.

Topics: Anemia, Pernicious; Cell Division; Cell Size; Gastric Mucosa; Gastrinoma; Gastrins; Gastritis; Humans; Microscopy, Electron; Neurosecretory Systems; Parietal Cells, Gastric

Epidermal growth (EGF) and transforming growth factor alpha (TGFalpha) are potent gastric secretory inhibitors, mitogens, and mucosal protectors, but the impact of Helicobacter pylori infection on their mucosal expression and luminal release has not been clarified.. In this study, gene and immunoreactive and immunohistochemical expressions of EGF and TGFalpha were assessed in the gastric mucosa of 15 H. pylori-negative healthy normals, in 22 H. pylori-positive duodenal ulcer patients (DU) and in 24 H. pylori-positive non-ulcer dyspepsia patients (NUD). All studies in DU and NUD patients were repeated after 2 weeks of triple therapy (amoxicillin + clarithromycin + omeprazole) and 4 weeks and 2 years later.. Immunohistochemical expression of EGF and TGFalpha in H. pylori-positive DU and NUD was significantly higher than in H. pylori-negative normals, and this increase persisted at 2 and 4 weeks after therapy but normalized 2 years later. EGF mRNA was detected in the gastric mucosa of H. pylori-positive DU before and at 2 and 4 weeks after H. pylori eradication, but it was not found 2 years after the eradication of H. pylori or in gastric mucosa of H. pylori-negative control subjects. TGFalpha mRNA was detected in the gastric mucosa independently of H. pylori status, with the stronger expression observed in the gastric mucosa of H. pylori-positive DU and NUD before eradication than after this procedure. Plasma gastrin, which was significantly increased in H. pylori-positive DU, normalized already after 2 weeks of triple therapy. The eradication rate as determined by histology after triple therapy reached 86.3% in DU patients and 90.5% in NUD patients. Two years after the eradication the H. pylori reinfection rate was 4.5% among DU patients and 4.2% among NUD. Treatment of DU patients with triple therapy resulted in complete ulcer healing.. 1) Chronic H. pylori infection and resulting antral gastritis are associated with increased plasma gastrin and increased mucosal cell proliferation, probably due to enhanced expression of EGF and TGFalpha, and 2) the H. pylori eradication results in a decrease in plasma gastrin, but the increase in gastric TGFalpha and EGF content is sustained, suggesting that they may be involved in ulcer healing.

Topics: Adult; Cell Division; Duodenal Ulcer; Dyspepsia; Epidermal Growth Factor; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Male; Middle Aged; Polymerase Chain Reaction; Proliferating Cell Nuclear Antigen; Radioimmunoassay; Transforming Growth Factor alpha

This study aimed to investigate the cause of persistently increased serum gastrin concentration seen in some Graves' disease patients even when euthyroid during antithyroid drug treatment. The subjects studied consisted of three groups: 33 patients with a common-type of Graves' disease, 14 with triiodothyronine (T3)-predominant Graves' disease (characterized from previous studies as having potent immunologic abnormalities including greater concentrations of thyroid-stimulating antibodies together with larger goiter size), and a group of 20 normal subjects. Fasting serum gastrin concentrations in common Graves' disease patients were significantly higher than those of normal subjects (58.4 +/- 38.9 pmol/L vs. 37.8 +/- 18.9 pmol/L [mean +/- SD], p < 0.05). The serum gastrin concentrations were even greater in T3-predominant Graves' disease patients than common Graves' disease patients (162.9 +/- 224.0 pmol/L vs. 58.4 +/- 38.9 pmol/L, p < .05). Serum pepsinogen I (PGI) concentrations were significantly lower in the T3-predominant patient group than the common Graves' group (24.0 +/- 12.9 ng/mL vs. 39.7 +/- 19.6 ng/mL, p < .05). Serum ratios of PG I to PG II were significantly lower in the T3-predominant Graves' disease patients than normal subjects (3.59 +/- 2.66 vs. 5.97 +/- 1.56, p < .01). The ratios also had a significant (p < .05) inverse correlation with serum gastrin concentrations in T3-predominant Graves' disease patients. The results suggest that autoimmune gastritis is associated with Graves' disease, particularly in patients with potent thyroid-autoimmunity.

Topics: Adolescent; Adult; Autoimmune Diseases; Female; Gastrins; Gastritis; Graves Disease; Humans; Immunoglobulins, Thyroid-Stimulating; Male; Middle Aged; Pepsinogens; Triiodothyronine

A follow-up of argyrophil cell hyperplasia in Helicobacter pylori-positive corpus gastritis in gastric ulcer patients during the natural course of ulcer disease.. Endoscopic biopsies (4 specimens) were obtained step-wise from the posterior wall of the corpus mucosa in 55 gastric ulcer (GU) patients. The natural course of GU was followed up in 38 patients during more than 10 years (maximum 19 years), and altogether 115 endoscopic examinations were made: 20 patients were re-examined once, 14 twice, and 4 three times. A total of 364 biopsies from 307 biopsy sites were stained by Grimelius' silver, hematoxylin-eosin, and Giemsa method for the analysis of the argyrophil endocrine cells, chronic gastritis, and H. pylori colonization, respectively, according to the Sydney System.. Of 307 biopsy sites, 153 (50%) showed some grade of ACH. Focal (linear/micronodular) hyperplasia was found in 118 (77%) of biopsy sites; it was detected in 78 (66%) cases of atrophic corpus mucosa, but was present in only 14 (12%) cases of gastritis without atrophy or in the normal mucosa. In the follow-up patients, ACH evolved in 17 and progressed in 6 cases, and a simultaneous development of atrophic corpus gastritis was found in 20 cases.. This study demonstrates that ACH evolves during the natural course of GU, alongside the development of chronic atrophic gastritis.

Topics: Adult; Aged; Antacids; Enteroendocrine Cells; Female; Follow-Up Studies; Gastrins; Gastritis; Helicobacter pylori; Humans; Hyperplasia; Male; Middle Aged; Stomach Ulcer

Autoantibodies against epitopes located at the canaliculi of human parietal cells occur in about 30% of Helicobacter pylori-infected patients. This has led to the hypothesis that gastric secretory function could be inhibited by anticanalicular autoantibodies in H. pylori gastritis.. Forty-four H. pylori-infected patients with and without duodenal ulcers were screened for anticanalicular autoantibodies by means of immunohistochemistry. Plasma gastrin levels and basal and maximal gastric acid output were determined.. Fasting gastrin levels were significantly increased in the group with anticanalicular autoantibodies. In the group of patients with non-ulcer dyspepsia the presence of anticanalicular autoantibodies was significantly correlated with an impaired basal acid secretion.. Antigastric autoimmunity in H. pylori gastritis seems to be relevant for gastric hyposecretion either directly by inhibiting the proton pump or indirectly through the development of gastric mucosa atrophy.

Topics: Adult; Autoantibodies; Autoimmunity; Duodenal Ulcer; Dyspepsia; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Male; Middle Aged; Stomach

Helicobacter pylori infection contributes to hypergastrinemia and hypersecretion of acid by blocking inhibitory reflex pathways to gastrin and parietal cells normally activated by antral distention. Our aim was to investigate whether a similar blockade of inhibitory responses could be provoked by inducing gastritis with aspirin, thus implicating a common inflammatory component, possibly a proinflammatory cytokine(s).. We studied the effects of antral distention on stimulated acid secretion and gastrin release in H. pylori-negative volunteers, before and after 3 days of aspirin therapy (2 g daily). Immediately before the examinations, the severity of gastric mucosal injury was evaluated macroscopically and histologically, and the production of interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma was determined by immunohistochemistry.. Most subjects had severe gastric injury after aspirin therapy, resulting in a substantially increased production of IL-1beta, IL-6, and IL-8 but not of TNF-alpha and IFN-gamma in the antral mucosa. In these subjects the acid-inhibitory response was abolished or markedly reduced. Conversely, aspirin therapy failed to affect the gastrin release in all subjects studied.. The disinhibition of acid secretion in response to antral distention is a joint feature of the gastritis induced by aspirin and H. pylori infection, possibly related to the increased production of IL-1beta, IL-6, and IL-8. The H. pylori-related hypergastrinemia apparently has a different background.

Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Cytokines; Female; Gastric Acid; Gastric Dilatation; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Male; Time Factors

How Helicobacter pylori infection affects gastric acid secretion is still unclear.. Gastric juice pH, ammonia concentration in gastric juice, serum gastrin level, and grade of gastritis in accordance with the Sydney System were determined for patients with gastric ulcer (GU) and duodenal ulcer (DU) before and after treatment with lansoprazole and amoxicillin, and results were compared with those of H. pylori-negative controls.. Scores for H. pylori density, atrophy, metaplasia, and activity of gastritis in the corpus were higher in patients with GU, especially those with proximally located GU, than in those with DU. Gastric juice pH was significantly higher in GU patients than in DU patients and controls. After H. pylori eradication, gastric juice pH and serum gastrin levels in both GU and DU patients were significantly decreased to control levels. In patients without eradication, no significant changes in these factors were observed.. These findings suggest that H. pylori infection and gastritis in the corpus suppress acid secretion and increase gastric juice pH, resulting in hypergastrinemia, and that eradication of H. pylori normalizes acid secretion and serum gastrin levels.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Ammonia; Amoxicillin; Anti-Ulcer Agents; Case-Control Studies; Drug Therapy, Combination; Duodenal Ulcer; Female; Gastric Acid; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Lansoprazole; Male; Middle Aged; Omeprazole; Penicillins; Proton Pump Inhibitors; Stomach Ulcer

The aim of this study was to clarify the mechanism of inappropriate hypergastrinemia in Helicobacter pylori (H. pylori)-infected subjects.. We measured fasting serum gastrin (SG) concentrations, and investigated immunohistochemically G and D cell numbers in 47 subjects with normal mucosa, 24 subjects with chronic gastritis, and 24 subjects with duodenal ulcer (DU). The degree of inflammation and atrophy were classified into four categories based on criteria established in the Sydney System: none, mild, moderate, and severe. Avidin-biotin complex methods were used to identify G and D cells, which were counted per unit square (0.25 mm2) in five random fields from each of two well-oriented antral and fundic biopsies. SG concentrations were measured by radioimmunoassay.. The G cell number was not significantly different between 24 subjects with H. pylori-associated gastritis and those with DU. However, the number of antral D cells was significantly lower and the G/D cell ratio was significantly higher in subjects with DU than in those with H. pylori-associated gastritis (p < 0.01), although the degree of inflammation and atrophy in the antrum and H. pylori status were similar between the two groups. The mean fasting SG concentration was higher in subjects with DU than in those with H. pylori-associated gastritis, but the difference was not statistically significant.. Our results demonstrate that a marked decrease in antral D cell number with a high G/D cell ratio may contribute to hypergastrinemia and the pathogenesis of DU.

Topics: Adult; Antibodies, Bacterial; Atrophy; Cell Count; Chronic Disease; Duodenal Ulcer; Female; Gastric Mucosa; Gastrin-Secreting Cells; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Inflammation; Male; Somatostatin-Secreting Cells

Topics: Adult; Female; Gastrins; Gastritis; Humans; Insulinoma; Pancreatic Neoplasms; Pancreatitis; Syndrome

To date, little is known about a possible relationship between H. pylori-related disturbances of gastric function and the bacterial virulence. The aim of this study was to assess whether certain gastric function indices as well as the pattern of symptoms in nonulcer dyspepsia (NUD) are related to CagA status.. A total of 56 consecutive patients with NUD (38 H. pylori-positive and 18 H. pylori-negative) were studied. Dyspeptic symptoms were categorized according to the predominant complaints and scored for severity and frequency. In all subjects, basal and pentagastrin-stimulated acid secretion, fasting and meal-induced gastrin release, fasting serum pepsinogen I (PG I) levels, and gastric emptying of solids were determined. CagA status was determined by assaying serum CagA IgG antibodies by western blotting.. Eighteen of 38 (47%) H. pylori-positive dyspeptics were CagA seropositive. Type and severity of dyspeptic symptoms did not significantly differ between CagA-positive and CagA-negative dyspeptics nor between H. pylori-positive and negative patients. Among the gastric function indices studied, only meal-stimulated gastrin was significantly influenced by CagA status (peak gastrin 129.9 [44.1] vs 99.1 [48.6] pg/ml in CagA-positive and negative NUD, respectively), but this was not accompanied by any significant modification of basal or stimulated acid secretion or gastric emptying of solids. The activities of both antral and corpus gastritis in NUD harboring CagA-positive strains were significantly higher than those of CagA-negative NUD. Accordingly, serum PG I levels were significantly higher in CagA-positive than CagA-negative or H. pylori-negative dyspeptics.. These findings support a role for CagA status in influencing the activity and perhaps the distribution of gastritis in NUD, as well as the degree of gastrin response to a meal; however, this is not accompanied by disturbances of acid secretion or gastric emptying or by differences in the type and severity of symptoms.

Topics: Adult; Aged; Antibodies, Bacterial; Antigens, Bacterial; Bacterial Proteins; Blotting, Western; Dyspepsia; Eating; Fasting; Female; Gastric Acid; Gastric Emptying; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Pentagastrin; Pepsinogens; Pyloric Antrum; Stomach; Virulence

Helicobacter pylori gastritis is common, but effects on gastric secretion are not well understood. We measured basal and pentagastrin-stimulated gastric acidity, pepsin activity, and fluid output, as well as serum gastrin concentrations and H. pylori antibody levels, before and after treatment of H. pylori gastritis in 28 men and women. Subjects were studied before and 1 and 3 mo after a course of bismuth, metronidazole, and tetracycline. Elimination of H. pylori gastritis, accomplished in 14 subjects, increased basal and pentagastrin-stimulated gastric acidity (by 15 meq/l) and basal acid output significantly (by 2.1 meq/h 1 mo after therapy). Elimination of H. pylori had an opposite effect on pepsin secretion, significantly decreasing pepsin output by 30%. Elimination of H. pylori significantly reduced nonparietal fluid output by 35%, without affecting fluid output from parietal cells. Serum gastrin and H. pylori antibody levels declined significantly after elimination of H. pylori. None of these changes was observed in 14 subjects whose H. pylori gastritis was resistant to antimicrobial therapy. In summary, eradication of H. pylori infection increases gastric acidity by reducing nonparietal gastric secretion from peptic and other cells.

Topics: Adult; Aged; Aged, 80 and over; Anti-Bacterial Agents; Antibodies, Bacterial; Female; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pentagastrin; Pepsin A

There is strong evidence accumulating that chronic infection with Helicobacter pylori (H. pylori) interferes with inhibitory pathways of the regulation of acid secretion. The increase in maximum acid output (MAO), and the increase in the sensitivity of the parietal cell to gastrin commonly observed in patients suffering from duodenal ulcer disease (DU), however, remains largely unexplained. Insufficient evidence is available concerning how these parameters are influenced by H. pylori infection in patients not suffering from peptic ulcer disease (PUD) and how they are related to H. pylori-induced gastritis. The aim of this study was to compare basal gastric acid secretion (BAO), MAO, and the sensitivity of the parietal cell to gastrin in H. pylori-positive and H. pylori-negative patients not suffering from PUD, and to study the relationship with their individual postprandial gastrin release and the degree of gastric antral and corpus gastritis.. H. pylori status was assessed by CLO test and histology (two biopsies each from the antrum and the corpus) in 14 H. pylori-positive and 16 H. pylori-negative nonulcer patients of comparable age, weight and gender. Gastritis score was assessed by a pathologist, who was unaware of the acid secretory data. Following determination of BAO, the relation of pentagastrin and gastric acid secretion was established with a cumulative pentagastrin dose response curve for the dose range 0.03-6.0 microg/kg(-1) h(-1) and MAO (Vmax) and pentagastrin sensitivity (ED50) were determined. Basal and postprandial gastrin release was measured by radioimmunoassay.. There was a significant higher gastritis score in the H. pylori-positive compared with the H. pylori-negative subjects. The dose response curves of the pentagastrin stimulated gastric acid secretion were not different between H. pylori-positive and H. pylori-negative groups. No correlation was seen between the gastritis score, basal acid output (BAO) peak acid output (PAO), maximum acid output (MAO), ED50 values and the plasma gastrin values. There was, however, a considerable larger variation of the PAO and MAO data of the H. pylori-infected subjects and >50% of the respective data was above or below the relatively low range of the respective values of the noninfected subjects.. H. pylori-induced gastritis does not regularly enhance maximum acid output in nonulcer patients, nor does it modify the sensitivity of the parietal cell to gastrin. H. pylori infection is thus unlikely to be directly responsible for an increase of these parameters in DU disease. Our data support, however, the concept that chronic H. pylori infection can either enhance or attenuate maximum acid secretory capacity in certain subgroups of patients.

Topics: Adult; Biopsy; Dose-Response Relationship, Drug; Female; Gastric Acid; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Linear Models; Male; Middle Aged; Pentagastrin; Peptic Ulcer; Postprandial Period; Statistics, Nonparametric; Stimulation, Chemical

Topics: Anemia, Pernicious; Autoimmunity; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Hyperplasia

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Cytokines; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Tumor Necrosis Factor-alpha

Recurrent abdominal pain (RAP) is a significant problem in the pediatric population, and there has been much recent interest in the role that Helicobacter pylori (Hp) might play in this disorder. In this case control study, the authors aimed to determine whether Hp is an agent responsible for RAP, and to assess fasting gastrin concentrations in children with and without RAP in the Hp-positive and -negative groups. The study was conducted in 42 patients with RAP and 50 healthy children attending routine day-case surgery as a control group, aged 3 to 15 years, over a 12-month period. Of the 42 children with RAP, 30 were seropositive (71.4%) for Hp IgG, and of 50 children in the control group, 32 were seropositive (64%) for Hp IgG (P > 0.05). We found that Hp infection was as high in healthy children as in children with RAP. The mean fasting gastrin levels in 62 Hp-seropositive children (60.4 ng/l) were not different from those in 30 Hp-seronegative children (57.3 ng/l) and those in 42 children with RAP (58.2 ng/l) were also not significantly different from those in 50 healthy children (62.9 ng/l). Thus, no association between childhood Hp infection, hypergastrinemia, and RAP was found in our Turkish population.

Topics: Abdominal Pain; Antibodies, Bacterial; Case-Control Studies; Child; Enzyme-Linked Immunosorbent Assay; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Recurrence; Turkey

Topics: Autoimmune Diseases; Endocrine Gland Neoplasms; Gastric Mucosa; Gastrins; Gastritis; Humans; Hyperplasia; Iatrogenic Disease; Pyloric Antrum

The mechanisms causing progression of fundic gastritis and changes in argyrophil cell morphology in patients undergoing long-term treatment with proton pump inhibitors are unknown. The hypothesis of this study was that Helicobacter pylori is a risk factor for both gastritis and argyrophil cell hyperplasia.. Forty-two patients with peptic disorders resistant to H2-blockers were treated with 30-90 mg lansoprazole daily for up to 5 years. Serum gastrin levels, antral gastrin cells, fundic argyrophil cells, parameters of gastritis, and H. pylori infection were evaluated regularly.. In nonantrectomized patients, serum gastrin levels increased from a median of 76 pg/mL to 163 pg/mL within 3 months. Antral gastrin cell density increased from 175 to 267 cells/mm2 (P < 0.001), and fundic argyrophil cell density increased from 83 to 149 cells/mm2 (P < 0.001). Chronic inflammation, activity, and atrophy of the oxyntic mucosa worsened exclusively in patients with H. pylori infection. Linear and/or micronodular argyrophil cell hyperplasia was diagnosed in 2.6% of patients before lansoprazole and in 29.2% after 5 years treatment. These changes were significantly related to serum gastrin levels, H. pylori infection, chronic inflammation, and atrophy of the oxyntic mucosa.. H. pylori represents an important factor for the progression of fundic gastritis and the development of argyrophil cell hyperplasia during long-term treatment with lansoprazole.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hyperplasia; Lansoprazole; Male; Middle Aged; Omeprazole; Proton Pump Inhibitors; Pyloric Antrum; Risk Factors

Topics: Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis; Helicobacter pylori; Humans; Proton Pump Inhibitors

Topics: Cell Count; Chronic Disease; Duodenal Ulcer; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Parietal Cells, Gastric

Primary biliary cirrhosis (PBC) is a chronic liver disease characterized by exocrine gland impairment. Up to now there have been no reports dealing with gastric mucosa involvement in this autoimmune condition, which is frequently associated with Sjögren's syndrome. The aim of this study was to investigate the morphologic, biochemical and immunological features of the gastric mucosa in PBC.. A cross-sectional study with matching was performed. Thirty-three PBC patients (30 F, 3 M, mean age 58 years; 17 with stage II-III, and 16 with stage IV disease) and 33 sex- and age-matched dyspeptic controls were included. Six biopsy specimens from the fundus (2), body (2) and antrum (2) were taken from all patients and controls. A serological assessment was performed for each subject, i.e. pepsinogen A (PGA), pepsinogen C (PGC), gastrin (G), and antibodies against Helicobacter pylori (anti-Hp IgG).. Endoscopic gastritis was found in 22 PBC patients (66.6%). There was no difference between PBC patients and controls regarding the percentage of subjects with mild, moderate, severe or atrophic gastritis (AG). There was no difference in gastric mucosal involvement between PBC subjects with or without secondary Sjögren's syndrome. A discrepancy was observed in the data obtained with respect to Helicobacter pylori (H. pylori) infection. H. pylori colonization was significantly more frequent in controls than in PBC patients (79% vs 49%, p < 0.002), but anti-Hp IgG were detected in the same percentage in the two groups (90% vs 83% respectively). There was no difference between the two groups in the PGA, PGC, PGA/PGC ratio, or gastrin. Eight PBC patients had esophageal varices.. PBC patients are not characterized by chronic atrophic gastritis. Even though they present chronic gastritis with the same prevalence as dyspeptic controls, and show signs of previous H. pylori infection as frequently as dyspeptic patients, they are actually much less frequently infected. The reasons for this observation are unclear.

Topics: Adult; Aged; Antibodies, Bacterial; Case-Control Studies; Chronic Disease; Cross-Sectional Studies; Dyspepsia; Female; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Liver Cirrhosis, Biliary; Male; Middle Aged; Pepsinogens; Sjogren's Syndrome

The aims of this study in 50 patients with H. pylori infection and duodenal ulcer were to examine the effect of eradication therapy on the serum levels of gastrin, pepsinogen I, and pepsinogen II and to investigate whether monitoring of the serum changes in these peptides after treatment could predict patient outcome. H. pylori status was assessed at entry and one and six months after therapy by culturing and microscopic analysis of the gastric mucosa and by [14C]urea breath test. Significant decreases were observed in the serum levels of gastrin (-11.4 +/- 3%), pepsinogen I (-28.9 +/- 4%), and pepsinogen II (-40.4 +/- 3%) in the 45 patients whose infection was eradicated, but not in the patients without eradication. Serum values of these peptides were unchanged in an additional group of 10 patients that only received omeprazol, none of whom had H. pylori eradicated. The best cutoff point of the percentage of each peptide to predict patient outcome was 10% for gastrin and pepsinogen I, and 15% for pepsinogen II. A pepsinogen II decrease > 15% resulted in the best marker of H. pylori clearance, accurately identifying patient outcome 86.6% of the time, whereas the diagnostic accuracy of gastrin and pepsinogen I was 61.7% and 76.6%, respectively. Significant correlations were found between the bacterial load assessed by histology with the serum concentrations of pepsinogen I and II and with the urease activity as measured by the amount of 14CO2 excreted. In conclusion, eradication of H. pylori infection is followed by a significant drop in serum levels of gastrin, pepsinogen I, and pepsinogen II. Changes in the latter are the most uniform and may be used as an indirect tool to predict treatment outcome.

Topics: Adult; Aged; Breath Tests; Duodenal Ulcer; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogens

We report a case of a gastric carcinoid tumor in an anemic woman with chronic atrophic gastritis and hypergastrinemia. An antrectomy with excision of a carcinoid tumor was performed; afterwards, gastrinemia was normal. Gastric carcinoids were considered uncommon gastric cancers; however, in recent years they have been studied with increasing interest because, as in chronic atrophic gastritis, it has been suggested that they might be produced by prolonged hypergastrinemia associated with therapeutic use of gastric acid supressors. We discuss the gastrin hypothesis, the different clinical types of gastric carcinoids and its therapeutical management.

Topics: Adult; Carcinoid Tumor; Female; Gastrins; Gastritis; Humans; Stomach Neoplasms

The influence of gastrin on the colonic mucosa is still uncertain. Some authors have suggested a stimulating effect on the growth of normal and malignant colonic epithelium, while others have shown no association between gastrin and neoplastic development.. To evaluate the effect of gastrin on colorectal cell proliferation, patients with chronic endogenous hypergastrinaemia underwent proctoscopy. Biopsy specimens were taken in order to study rectal cell kinetics.. Ten patients with chronic autoimmune gastritis (CAG), six patients with Zollinger-Ellison syndrome (ZES), and 16 hospital controls took part in this study. Patients with CAG and ZES had basal serum gastrin concentrations significantly higher than controls (p < 0.001).. Immunohistochemistry was performed on 3 microns sections of rectal biopsy specimens incubated with 5'-bromodeoxyuridine.. The percentage of proliferating cells in the entire crypts (overall labelling index) was similar in all the groups. However, the labelling frequency in the upper two fifths of the glands (phi h value) was significantly higher in patients with CAG or ZES compared with controls (p < 0.01 in both patient groups versus controls).. Endogenous hypergastrinaemia is associated with rectal cell proliferation defects, similar to those observed in conditions at high risk for colon cancer. The effect of the increased serum concentrations of gastrin on the colorectal mucosa after treatment with drugs inhibiting gastric acid secretion should be investigated.

Topics: Adult; Aged; Autoimmune Diseases; Cell Division; Chronic Disease; Colonic Neoplasms; Female; Gastrins; Gastritis; Humans; Immunohistochemistry; Male; Middle Aged; Rectum; Risk Factors; Zollinger-Ellison Syndrome

Gastric acid secretion in Japanese subjects decreases with aging. One of the possible causative mechanisms of this attenuated acid secretion is speculated to be a Helicobacter pylori induced chronic gastritis. The infection rate of this microorganism has decreased recently in Japan.. To investigate whether gastric acid secretion has altered over the past 20 years, and if so, what the influence of H pylori infection might be in the Japanese population.. Gastric acid secretion, serum gastrin and pepsinogen I and II concentrations, and H pylori infection were determined in 110 Japanese subjects in both the 1970s and 1990s.. Basal acid output as well as maximal acid output have greatly increased over the past 20 years, not only in individuals with H pylori infection but also in those without infection. Furthermore, subjects with H pylori infection tended to show decreased gastric acid secretion in comparison with those without infection, particularly in geriatric subjects. There was a positive correlation between gastric acid secretion and serum pepsinogen I concentrations.. In Japan, both basal and stimulated gastric acid secretion have increased over the past 20 years; some unknown factors other than the decrease in H pylori infection may play an important role in this phenomenon.

Topics: Adult; Aged; Aging; Female; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Japan; Male; Middle Aged; Pepsinogens; Regression Analysis; Secretory Rate; Statistics, Nonparametric

It has recently been shown that humoral antigastric autoreactivities occur in a substantial number of Helicobacter pylori infected patients.. To analyse the relevance of such antigastric autoantibodies for histological and serological parameters of the infection as well as for the clinical course.. Gastric biopsy samples and sera from 126 patients with upper abdominal complaints were investigated for evidence of H pylori infection using histology and serology. Autoantibodies against epitopes in human gastric mucosa were detected by immunohistochemical techniques. Histological and clinical findings of all patients were then correlated with the detection of antigastric autoantibodies.. H pylori infection was significantly associated with antigastric autoantibodies reactive with the luminal membrane of the foveolar epithelium and with canalicular structures within parietal cells. The presence of the latter autoantibodies was significantly correlated with the severity of body gastritis, gastric mucosa atrophy, elevated fasting gastrin concentrations, and a decreased ratio of serum pepsinogen I:II. Furthermore the presence of anticanalicular autoantibodies was associated with a greater than twofold reduced prevalence for duodenal ulcer.. The data indicate that antigastric autoantibodies play a role in the pathogenesis and outcome of H pylori gastritis, in particular in the development of gastric mucosal atrophy.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Atrophy; Autoantibodies; Chi-Square Distribution; Enzyme-Linked Immunosorbent Assay; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogens; Statistics, Nonparametric

Helicobacter pylori gastritis may spread proximally in the stomach during profound acid inhibition.. To examine histological gastric body changes and epithelial cell proliferation before and after treatment with lansoprazole.. Patients diagnosed as having reflux oesophagitis grade 1 or 2 were enrolled and treated for 12 weeks with lansoprazole (30 mg every morning). After 12 weeks, 103 of the 118 patients appeared endoscopically healed and were asymptomatic; they then received maintenance treatment with 15 or 30 mg lansoprazole daily. Biopsy specimens obtained from similar sites before and after treatment, were available from 90 patients after a median of 64 weeks (range 15-73 weeks). Epithelial cell proliferation was determined by the number of Ki-67 antigen positive cells per gland.. Of these 90 patients, 44 (49%) were found to be infected with H pylori. Their median inflammation score had increased from grade 1 before to grade 2 after treatment (p < 0.0001). Initially, the number of Ki-67 antigen positive cells per gland was significantly higher in the H pylori infected than in the uninfected group and increased further after treatment (p < 0.0001). In uninfected patients, no significant change in inflammation or proliferation occurred during treatment.. A marked increase in body gastritis was observed in H pylori infected individuals during long term treatment with the proton pump inhibitor lansoprazole. Epithelial cell proliferation and atrophy also increased in infected but not in uninfected patients.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Anti-Ulcer Agents; Cell Division; Epithelial Cells; Esophagitis, Peptic; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Lansoprazole; Middle Aged; Omeprazole; Proton Pump Inhibitors; Statistics, Nonparametric; Time Factors

Helicobacter pylori infection exerts variable effects on gastric acid secretion. It may increase acid secretion, decrease acid secretion or produce no overall change. The effect of the infection on acid secretion depends upon the relative extent to which the Helicobacter pylori gastritis affects the antral and body mucosa of the stomach. When there is antral predominant, body-sparing gastritis, there is increased gastrin release and this is accompanied by increased acid secretion. When there is a significant body gastritis, acid secretion is reduced and subjects may be completely achlorhydric. The majority of subjects have both antral gastritis and body gastritis and this results in no overall change in gastric acid secretion. There is now increasing evidence that the alteration which Helicobacter pylori infection exerts upon gastric acid secretion is a pivotal factor in determining the clinical outcome of the infection. Subjects in whom the infection produces acid hypersecretion develop duodenal ulcer disease due to the increased duodenal acid load. In subjects in whom the infection induces marked hypochlorhydria, there is an increased risk of gastric cancer. The hypochlorhydria probably plays an important role in the carcinogenic process as high intragastric pH markedly raises intragastric nitrite levels, profoundly lowers gastric juice ascorbic acid and allows colonization by nitrosating bacteria. The reason for the different functional responses to Helicobacter pylori infection is unclear but may be related to the host's pre-morbid acid secretory status.

Topics: Duodenal Ulcer; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Stomach; Stomach Neoplasms

The mechanism(s) by which sucralfate heals duodenal ulcers remains unclear. The aim of this study was to determine the effect of sucralfate on Helicobacter pylori infection and on the accompanying hypersecretion of gastric acid the infection induces in patients with duodenal ulcer.. Basal and gastrin-releasing peptide (GRP) stimulated gastrin release and acid secretion. H. pylori density, gastric urease activity, and severity of gastritis were studied in patients with duodenal ulcer who were positive for H. pylori before, during, and after 4 weeks' treatment with sucralfate (2 g twice daily).. The density of H. pylori decreased by 70% during sucralfate treatment and returned to the pretreatment level after discontinuation of therapy. This suppression of H. pylori infection was accompanied by an 80% decrease in gastric urease activity. GRP-stimulated plasma gastrin concentrations, GRP-stimulated acid output, and basal acid output all decreased by approximately 50% during sucralfate therapy and returned to pretreatment levels after treatment was discontinued.. These findings indicate that sucralfate markedly suppresses H. pylori infection and the accompanying hypersecretion of acid the infection induces in patients with duodenal ulcer. These effects are likely to be important mechanisms by which the drug promotes duodenal ulcer healing.

Topics: Adult; Aged; Anti-Ulcer Agents; Breath Tests; Duodenal Ulcer; Gastric Acid; Gastric Mucosa; Gastrin-Releasing Peptide; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Peptides; Stomach; Sucralfate; Urease

Persons infected with Helicobacter pylori show an enhanced meal-stimulated gastrin release compared with uninfected controls. The aim of this study was to determine in animal models whether this gastrin release could be related to chronic gastric inflammation, elevated luminal ammonia level, or a combination of these factors.. Two rat models of mild gastric inflammation were studied. Rats given a long-term diet of 20 g/dL ammonium acetate (AmAc) in rat chow or 0.1% iodoacetamide in drinking water for 2-3 weeks underwent a short-term challenge with a normal or AmAc-supplemented meal. Serum gastrin and antral gastrin messenger RNA levels were measured.. Compared with normal postprandial gastrin release, animals given the long-term AmAc feeding showed a normal response to rat chow but a greatly exaggerated response to rat chow plus 20 g/dL AmAc. Long-term feeding with iodoacetamide also resulted in enhanced gastrin release and antral gastrin messenger RNA in response to a meal supplemented with AmAc, but not to a normal meal or one supplemented with sodium acetate.. Inflamed gastric mucosa is more sensitive to the effects of luminal ammonia and responds with an increase in both synthesis and release of gastrin. These animal models may provide insight into the pathogenesis of hypergastrinemia associated the H. pylori infection.

Topics: Acetates; Ammonia; Animals; Disease Models, Animal; Gastric Mucosa; Gastrins; Gastritis; Iodoacetamide; Irritants; Male; Peroxidase; Radioimmunoassay; Rats; Rats, Sprague-Dawley; RNA, Messenger

Helicobacter pylori (Hp) infection is known to cause several gastroduodenal diseases. In patients with non-ulcer dyspepsia, we assessed the link between Hp infection and gastric mucosal inflammation, as well as the influence of Hp and inflammation on the serum levels of anti-Hp antibodies (IgG), pepsinogen A (PGA), pepsinogen C (PGC), and gastrin.. Entering the study were 221 patients with non-ulcer dyspepsia, all of whom underwent upper gastrointestinal endoscopy.. Of the 221 patients investigated, 135 (61%) were Hp positive. The higher the bacterial load, the worse the associated gastritis, the gastric antrum and body being considered. All of the serological indices studied were found to be influenced by gastritis. Serum IgG satisfactorily discriminated between Hp-positive and Hp-negative subjects, with a sensitivity of 84% and a specificity of 86%. PGC, PGA, and gastrin were less accurate. Only PGC only found to be correlated with Hp load. The product of IgG and PGC improved the diagnostic accuracy of IgG alone.. Hp infection, frequently found in patients with non-ulcer dyspepsia, is associated with gastric mucosal inflammation; of the indices studied, serum IgG and PGC most accurately indicated Hp infection, and their product may be proposed as an aid in diagnosing Hp infection in dyspeptic patients.

Topics: Adult; Aged; Aged, 80 and over; Chronic Disease; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Pepsinogens; Serologic Tests

To study basal gastrin levels in duodenal ulcer patients and in those with normal endoscopy, according to Helicobacter pylori infection.. Eighty-four duodenal ulcer patients and 164 with normal endoscopy were studied. Biopsy specimens were taken from gastric antrum and body, and investigated for microbiology (Gram stain and culture) and histology (hematoxilin-eosin stain). Basal gastrin levels were measured (RIA).. In duodenal ulcer patients the percentage of chronic gastritis was higher (p < 0.001) than in patients with normal endoscopy without H. pylori infection, and similar to patients infected by H. pylori. In patients with normal endoscopy (n = 164), those infected with H. pylori (n = 115) had higher (p = 0.02) gastrin levels (mean +/- SD) than non-infected (64 +/- 34 vs 51 +/- 14 pg/ml) and similar to duodenal ulcer patients (62 +/- 20 pg/ml). In the multiple regression model analysis H. pylori infection was the only variable which correlated with gastrin levels (regression coefficient 9.48 [SE = 4.59]; multiple correlation coefficient 0.22 [p = 0.008]). Additional variables (age, sex, duodenal ulcer) were not correlated with gastrin levels. Patients with chronic gastritis had higher gastrin levels (p < 0.01) than those with normal histologic mucosa.. In patients with normal endoscopy, those infected with H. pylori had significantly higher basal gastrin levels than non-infected individuals, and similar to duodenal ulcer patients. Therefore, hypergastrinaemia seems to be associated with H. pylori infection, and is not a distinctive feature of duodenal ulcer disease.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Biopsy; Chronic Disease; Duodenal Ulcer; Endoscopy; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Regression Analysis; Stomach

Age and close living conditions are known to be risk factors for the acquisition of Helicobacter pylori (HP) infection. It is unknown whether institutionalization of asymptomatic, elderly subjects is an additional risk factor and whether gastric function and nutritional status are affected by the HP infection. The study sample comprised 102 subjects over 65 years of age: 52 living in a nursing home and 50 at home. No subject had symptoms or previous pathology related to the upper digestive tract. In all subjects, serum levels of specific anti-HP antibodies were determined. Gastric function was evaluated by levels of pepsinogen A (PGA), pepsinogen C (PGC) and gastrin. The nutritional status of the subject was evaluated by measuring: albumin, haemoglobin, iron, ferritin, transferrin, vitamin B12, and folic acid in blood, and body mass index and mid-arm muscle area. The prevalence of anti-HP antibodies was 86.5% in institutionalized subjects (men: 100%; women:76.6%, p <0.05) and 82.0% in subjects living at home (men:86.3%; women:76.3%). No differences between the two groups were observed in levels of serum anti-HP antibodies and PGC was identified. In neither group were differences observed between serum positive (HP + ve) and negative (HP - ve) subjects with respect to the biohumoral and anthropometric indices of nutritional status. We conclude: (1) the seroprevalence of the HP infection was high (82-86%) in asymptomatic elderly patients living either at home or in an institution; (2) the presence of specific IgG anti-HP antibodies in asymptomatic elderly individuals, at home or in a nursing home, was not associated with changes in PGA levels in institutionalized subjects; (3) nutritional indices were not influenced by the presence of anti-HP antibodies.

Topics: Aged; Aged, 80 and over; Female; Gastrins; Gastritis; Geriatric Assessment; Helicobacter Infections; Helicobacter pylori; Home Nursing; Homes for the Aged; Humans; Italy; Male; Nursing Homes; Nutritional Status; Pepsinogens; Reference Values

The etiopathogenic relationship of Helicobacter pylori (HP) infection to chronic active antrumgastritis and peptic ulcer disease has been confirmed by a number of studies. The key role in the development of peptic lesions belongs to hypergastrinemia. This is supposed to be related to ammonium synthesis in the antral area influenced (promoted by HP and resulting in interruption) weakening of the negative feedback mechanism maintaining intraluminal acidity.. In our present study we focus our attention to the effectiveness of triple antimicrobial therapy in HP positive patients with chronic active antrumgastritis residing in the lowering of the level of serum gastrin.. There was a group of 15 patients in our current study with HP positivity as well as chronic active antrumgastritis documented by endoscopy, histology, microbiology and serology respectively. Endoscopical and histological findings were classified according to "The Sydney System". The whole group was evaluated on an ambulatory basis, those with active ulcer, endocrinopathy and biliary tract disorders were excluded. The basal level of serum gastrin was evaluated by RIA-test-gastrin before and after successful antimicrobial therapy.. In our group of 15 patients with HP infection in coexistence with chronic active antrumgastritis we have found a significant decrease in the basal level of serum gastrin (p = 0,01) after successful therapy.. The decrease in the basal level of serum gastrin after eradication of HP confirms the importance of HP infection in the pathogenesis of peptic lesions in stomach and duodenum. We consider the antimicrobial therapy in chronic active antrumgastritis in HP positive patients to be a fully indicated therapeutic approach. (Tab. 1, Fig. 1, Ref. 10.).

Topics: Adult; Amoxicillin; Drug Therapy, Combination; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged

The fact that H. pylori gastritis results in an increased secretion of basal and meal-stimulated gastrin, which is also a physiologic amplifier of insulin release directed us to investigate whether H. pylori gastritis may lead to an enhancement of nutrient-stimulated insulin secretion. For this purpose, we have investigated the insulin responses to both oral glucose and a mixed meal in 15 patients with H. pylori gastritis before and one month after the eradication therapy and also in 15 H. pylori-negative control subjects. The areas under the curve (AUC) for serum insulin following both oral glucose and a mixed meal in the patients with H. pylori gastritis before the eradication were significantly (P < 0.05) higher than those in the H. pylori-negative controls. After the eradication of H. pylori, the AUC for serum insulin following oral glucose and mixed meal decreased by 9.4% and 13.1%, respectively (P < 0.001 in both), and serum basal and meal-stimulated gastrin levels decreased significantly (P < 0.001). These results suggest that H. pylori gastritis enhances glucose and meal-stimulated insulin release probably by increasing gastrin secretion.

Topics: Adult; Blood Glucose; Eating; Female; Gastrins; Gastritis; Glucose Tolerance Test; Helicobacter Infections; Helicobacter pylori; Humans; Insulin; Male; Middle Aged

Topics: Duodenal Ulcer; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Parietal Cells, Gastric; Somatostatin

Topics: Carcinoid Tumor; Diagnostic Errors; Diarrhea; Female; Gastrins; Gastritis; Humans; Liver Neoplasms; Middle Aged; Pain; Stress, Psychological

The eradication of Helicobacter pylori (Hp) is known to reduce the recurrence rate of duodenal ulcer (DU) to similar extent as gastrectomy but it is not clear what is the prevalence of Hp in DU patients after surgical interventions such as gastrectomy or vagotomy. The purpose of this study was to evaluate the influence of gastrectomy or truncal vagotomy with pyloroplasty on the prevalence of Hp in 51 DU patients just before and 6-8 months after these procedures. Using C14-urea breath test (UTB), rapid CLO-test and histology of the biopsy samples of gastric mucosa obtained during gastroscopy, the Hp was detected in all DU subjects submitted to operation. Following distal gastric resection (antrectomy) with Billroth II anastomosis (N = 32) due to an ulcer resistance to conservative therapy, peptic ulceration was not observed during 6-8 months in any of the examined subjects and the Hp was only rarely observed (only in 3 out of 32 operated patients). Histologically, in antral biopsies taken prior to surgery, all DU patients presented chronic active gastritis. After the surgery, the absence of Hp was confirmed also by histology. Histological evaluation of gastrectomy stump biopsies revealed typical chronic gastritis with concomitant foveolar hyperplasia and focal gland dilation. Following selective vagotomy and pyloroplasty (N = 19), the scarring of duodenal bulb (without active ulcer) was seen in 4 out of 19 operated patients but the Hp was detected in all (100%) cases. Gastric biopsies prior and after vagotomy revealed chronic active gastritis associated with Hp infection. Basal plasma gastrin was reduced after gastrectomy by about 30% and basal and maximal pentagastrin-induced acid secretion was decreased by about 60% and 70%, respectively. Vagotomy did not reduce activity of the mucosal inflammation and the incidence of Hp. Basal plasma gastrin level was increased by about 60%, while basal and pentagastrin induced acid secretion was decreased by 25% and 40%, respectively. Because of the high ulcer recurrence rate after vagotomy as opposed to low recurrence after gastrectomy, it is reasonable to conclude that (1) the disappearance of Hp and reduction in plasma gastrin and gastric acid secretion were probably the major factors responsible for the high efficacy of gastrectomy in prevention of ulcer recurrence, (2) in non-complicated DU, gastric surgery should be avoided and replaced by conservative anti-Hp therapy involving both antisecretory or bismuth agen

Topics: Adult; Breath Tests; Duodenal Ulcer; Gastrectomy; Gastric Stump; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Prevalence; Urea; Vagotomy

Omeprazole treatment produces lower intragastric pH values 4 weeks after cure of Helicobacter pylori infection than before. We therefore investigated the effect of healing H. pylori-associated gastritis on intragastric pH in the presence and in the absence of omeprazole therapy.. Before and on day 8 of omeprazole, 20 mg once daily, 24-h intragastric pH-recordings were performed in 14 subjects with H. pylori infection and repeated 4 and 52 weeks after cure of infection. Gastritis severity in corpus and antrum was graded by using a modified Sydney system.. In the absence of omeprazole administration, median 24-h pH values before cure did not differ from those 4 and 52 weeks after cure. On day 8 of omeprazole administration, 24-h pH values were much higher before cure (median, 5.15; 95% confidence interval (CI), 4.3-6.0) than 4 weeks (3.6; 2.1-4.4; P < 0.001) and 52 weeks after cure (3.0; 2.1-4.4; P < 0.001). The activity of corpus and antral gastritis was not associated with the magnitude of H+ change induced by omeprazole.. The increased pH produced by omeprazole during H. pylori infection is likely to be due to neutralizing substances produced by H. pylori and not to H. pylori-induced gastritis.

Topics: Adult; Anti-Ulcer Agents; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Omeprazole; Radioimmunoassay

The present work analyzes the serie levels of pepsinogen I (PG I) and gastrin in relation to the histopathological findings with the optical microscope (OM) and electron microscope (EM) of different gastric mucosa biopsies obtained through fibrogastroscopy. 45 patients were studied (19 men and 26 women) with an average age of 63 with different clinical diagnoses documented later by fibrogastroscopy (peptic ulcer, neoplasia etc.), whose previous consent, two biopsies were taken at an antrum level and two biopsies at a fundic-body area level, analyzed later by OM and EM. The anatomopathological criteria followed in order to classify the condition of the mucosa was Whitehead's classification. The PG I and gastrin determination was carried out with RIA against a control group of 25 healthy individuals. Our study allows us to conclude that the normal or high serie concentration of PG I reflects a functional integrity of the fundic-body area, and low levels imply the presence of atrophic chronic gastritis at a fundic-body level. Thus a low level of PG I is a reliable marker of the atrophic condition of the mucosa and it can be considered as a precancerous factor.

Topics: Adult; Aged; Biomarkers; Biopsy; Chronic Disease; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Pepsinogens; Stomach Neoplasms

We have recently shown that antigastric autoantibodies occur in a considerable number of Helicobacter pylori (H. pylori) infected patients. Particularly, autoantibodies to canaliculi within parietal cells of human gastric body mucosa are strongly associated with H. pylori gastritis. In this study we analyzed the implications of this type of autoantibody for histological and for clinical parameters of the disease. 126 patients with upper abdominal complaints were included in our study. Several histological and clinical parameters were evaluated. Presence of anticanalicular autoantibodies is significantly correlated with a higher degree of gastritis in the body mucosa, with atrophic changes in the gastric mucosa, with elevated fasting gastrin levels and a decreased pepsinogen I/pepsinogen II ratio. These data indicate, that the host's autoimmune response to canaliculi of parietal cells is of relevance for the pathogenesis and outcome of H. pylori gastritis.

Topics: Atrophy; Autoantibodies; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Pepsinogens

The current study was designed to evaluate the effect of aging and Helicobacter pylori infection on the gastric mucosa in asymptomatic Japanese adults.. Eighty-five asymptomatic healthy adults were recruited from a health-screening center in Sapporo. All subjects underwent endoscopy and gastric biopsy, and serum was obtained for IgG antibodies to H. pylori, serum gastrin, and pepsinogen levels.. The prevalence of atrophic change of the gastric mucosa assessed by pathological findings increased with age (49% in the 30- to 39-year-old group compared to 89% in those 60 years and older, p < .001). The frequency of intestinal metaplasia also increased with age (38% in the 30- to 39-year-old group compared to 82% in those 60 years and older, p < .001). In contrast, the frequency of atrophic gastritis and intestinal metaplasia was extremely low in the H. pylori seronegative group regardless of age. Mean serum gastrin level in H. pylori-positive adults was significantly greater than in those who were H. pylori-negative (114.3 +/- 11.2 compared to 65.8 +/- 6.5 pg/ml, p < .03). The serum pepsinogen I-II ratio was significantly lower in those with H. pylori infection than in those without (3.1 compared to 6.6, p < .0001).. These results suggest that the chronological changes in the gastric mucosa in Japanese individuals are either entirely related to H. pylori infection or the process is greatly accelerated by H. pylori infection.

Topics: Adult; Aged; Antibodies, Bacterial; Atrophy; Duodenum; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Japan; Male; Metaplasia; Middle Aged; Pepsinogens

Among the various themes related to Helicobacter pylori (HP) which is still a subject of discussion, there is the possible influence of this bacterium on gastric secretory physiology. In the present study, an evaluation has been carried out of stimulated gastrinemia, stimulated acid secretion and total peptic activity in gastric juice in the course of a paradigmatic condition, as autonomous chronic gastritis, in order to reveal possible modifications induced by the HP infection. In cases of HP positive chronic superficial antral gastritis associated either with normal body-fundic mucosa or with superficial gastritis, there is a significant increase of stimulated gastrinemia in comparison to HP negative groups and controls. In the course of body-fundic atrophic and preatrophic chronic gastritis associated either with antral superficial chronic gastritis or with antral atrophic gastritis, there are no statistically significant differences between HP positive and HP negative subjects. As regards acid and pepsin secretion no significant differences emerge in any group between HP positive and HP negative subjects. In the HP positive subjects with antral superficial gastritis and higher gastrin values the study of acid and pepsin secretion has yielded no significant variations. From the results of this study it emerges how gastric secretory parameters vary exclusively according to the histologic state of gastric mucosa. Therefore, the lesion action of HP may mainly be attributed to a direct action, rather than to substantial gastric secretory changes.

Topics: Adult; Aged; Biopsy; Chronic Disease; Female; Gastric Fundus; Gastric Juice; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pyloric Antrum; Stomach

Topics: Animals; Disease Models, Animal; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Humans; Immunity, Mucosal; Lymphocytes; Mice; Mice, Inbred BALB C; Phenotype

The pathogenic role played by Helicobacter pylori in gastric mucosal defense was investigated in Japanese monkeys infected with H. pylori. Serum gastrin levels and ammonia concentrations in gastric juice were compared in H. pylori-infected (n = 6) and control (n = 7) groups. The gastritis score, the intracellular content of periodic acid-Schiff (PAS)-positive substance and hexosamine, and the bromodeoxyuridine (BrdU) labeling index in the gastric mucosa were compared in the two groups in the antrum and the corpus. The ammonia concentration in the gastric juice was significantly higher in the infected group (P < 0.01). The gastritis scores were significantly higher in the antrum and corpus in the infected group (P < 0.01, and P < 0.05, respectively). The content of PAS-positive substance and hexosamine was significantly decreased in the antrum of the infected group compared with that in the controls (P < 0.01, and P < 0.05, respectively), but there was no significant difference between the two groups in the corpus. The BrdU labeling indices were significantly higher in the antrum and corpus of the infected group (P < 0.01, and P < 0.01, respectively). Colonization by H. pylori injures the gastric mucosa by depressing the gastric mucosal defense factors, and, consequently, the cell kinetics are accelerated.

Topics: Ammonia; Animals; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Hexosamines; Immunity, Innate; Macaca; Periodic Acid-Schiff Reaction; Pyloric Antrum

Many studies have confirmed the close association of Helicobacter pylori with duodenal ulcer (DU) in adults. However, in the subtype of DU known as 'childhood' or 'early onset DU' genetic factors seem to play a prominent role in the pathogenesis. The aim of this study was to investigate the prevalence of H. pylori in teen-age subjects with DU, gastritis, and normal mucosa and to examine the relationship of H. pylori to serum gastrin levels and gastric acid secretion.. Sixty-one teen-age subjects (24 with DU, 14 with gastritis, and 23 normal subjects) were investigated for the presence of H. pylori, antral histology, gastrin levels, basal acid output (BAO), and maximal acid output (MAO).. All 24 patients with DU and 8 of 14 with gastritis were infected with H. pylori; none of the normal subjects were infected. Mean gastritis scores and fasting serum gastrin levels were significantly higher in patients with DU or H. pylori-positive gastritis than in subjects with H. pylori-negative gastritis or normal mucosa (p < 0.05). The difference in serum gastrin levels was also significant when patients with DU were compared with those with H. pylori-positive gastritis (p < 0.05). BAO and MAO were significantly higher in patients with DU than in subjects with H. pylori-positive gastritis or normal mucosa (p < 0.05), but there was no difference between subjects with H. pylori-positive gastritis and those with normal mucosa.. H. pylori infection is associated closely with teen-age DU and gastritis and with hypergastrinemia but does not affect BAO and MAO in most infected teen-age subjects.

Topics: Adolescent; Adult; Duodenal Ulcer; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Prevalence; Retrospective Studies

The patients with chronic superficial gastritis were perfused in the stomach with 20 g of Dendrobium nobile to observe the variations in gastric acidity output, serum gastrin and plasma somatostatin concentration. The result showed a significant increase in both acidity output and serum gastrin concentration (P < 0.01). No significant change occurred in plasma somatostatin concentration (P > 0.05).

Topics: Adult; Drugs, Chinese Herbal; Gastric Acid; Gastrins; Gastritis; Humans; Middle Aged; Somatostatin

Experimental chronic gastritis (ECG) models were established in rats by inserting a spring into pyloric canal as well as feeding sodium deoxycholate. An experiment was undertaken to observe the therapeutic effects of three formulas of traditional Chinese medicine "Shipitong" (SPT), "Ganpingyangwei" (GPYW) and "Weile" (WL). The experimental results show that all of the three decoctions can make serum gastrin, gastrin cell density and amount of antral mucosal PGE2 of the ECG rats return to normal levels.

Topics: Animals; Cell Count; Chronic Disease; Dinoprostone; Drug Combinations; Drugs, Chinese Herbal; Gastric Mucosa; Gastrins; Gastritis; Male; Rats; Rats, Wistar

Acute Helicobacter pylori associated gastritis causes achlorhydria, a powerful stimulus to gastrin secretion. If H pylori infection is acquired primarily in early childhood, then the degree of hypergastrinaemia in seropositive children should be age dependent. Anti-Helicobacter antibodies and fasting gastrin concentrations were measured in 439 children aged 4 to 13 years attending hospital for routine day case surgery not connected with any gastrointestinal disorder. Thirty per cent were seropositive for H pylori. There was an inverse relationship between the fasting gastrin concentration and age; the mean fasting gastrin in children aged 4-5 years, 155 ng/l, was significantly higher than that seen in children aged 12-13 years, 90 ng/l. The more noticeable hypergastrinaemia seen in young children with H pylori associated gastritis may reflect achlorhydria associated with acute H pylori infection and suggests that this is primarily acquired in early childhood.

Topics: Adolescent; Age Factors; Child; Child, Preschool; Enzyme-Linked Immunosorbent Assay; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Socioeconomic Factors

Topics: Data Interpretation, Statistical; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Pepsinogens; Regression Analysis

The association between Helicobacter pylori and recurrent abdominal pain (RAP) is controversial. In this cross-sectional study, the authors aim to determine whether hypergastrinaemia causes RAP in children with H pylori gastritis. In 439 children age 4 to 13 years (mean 7.3 years) attending for nongastrointestinal day-case surgery, anti-Helicobacter immunoglobulin G (IgG) was identified in serum by an enzyme-linked immunosorbent assay (ELISA) method validated in children and fasting plasma gastrin was measured. A history of RAP was sought. One hundred twenty-seven children (29%) tested seropositive for H pylori. Fifty-one seronegative children (16.3%) and 22 seropositive children (17.3%) gave a history of RAP. The mean fasting gastrin in seronegative children was 52 ng/L compared with 117 ng/L in seropositive children (P < .001). The mean fasting gastrin in seropositive children with RAP (124 ng/L) was not significantly different from that of seropositive children without RAP (115 ng/L). The high prevalence of H pylori seropositivity in this study is at variance with other reported paediatric data from the developed world. No association between childhood H pylori gastritis, hypergastrinaemia, and RAP was found. In children with H pylori gastritis, the increase in circulating gastrin (mean 140% increase) is greater than that seen in adults (50% increase).

Topics: Abdominal Pain; Case-Control Studies; Child; Cross-Sectional Studies; Enzyme-Linked Immunosorbent Assay; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Prevalence; Recurrence; Seroepidemiologic Studies

The present report describes two patients with fasting hypergastrinemia, gastric acid hypersecretion, and Helicobacter pylori gastritis. Provocative testing for Zollinger-Ellison syndrome was negative and imaging studies did not demonstrate an intra-abdominal mass. Following eradication of the Helicobacter pylori infection, the fasting hypergastrinemia resolved in both patients and in one patient the gastric acid hypersecretion also resolved. The implications of this case on the differential diagnosis of Zollinger-Ellison syndrome are discussed.

Topics: Adolescent; Adult; Diagnosis, Differential; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Zollinger-Ellison Syndrome

A 48-year-old woman with type II diabetes developed fatigue, arthralgia and myalgia. A few weeks later she was found to have hepatomegaly. The erythrocyte sedimentation rate was raised (53/93 mm), as were liver enzyme activities (GOT 186 U/l; GPT 240 U/l; gamma-GT 199 U/l), the gamma-globulin levels (40.7%;IgG 4470 mg/dl, IgA 698 mg/dl, IgM 245 mg/dl), antinuclear antibodies and antibodies against double-strand DNA, smooth muscles and actin. Laparoscopy revealed small-nodular liver cirrhosis. The autoimmune hepatitis was treated with prednisolone (initially 60 mg daily, then reduced to 10 mg daily) and azathioprine (initially 100 mg daily, reduced to 50 mg daily). The symptoms markedly improved. But one year later, during follow-up examination, gastric polyps were found, excised and histologically found to be carcinoid. The gastrin level was raised to 765 pg/ml. Another year later the liver cirrhosis had advanced further and the type A gastritis was still present, but there was no sign of carcinoid recurrence.

Topics: Autoimmune Diseases; Azathioprine; Carcinoid Tumor; Cholangiopancreatography, Endoscopic Retrograde; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Endoscopy, Digestive System; Female; Follow-Up Studies; Gastrins; Gastritis; Hepatitis; Humans; Liver Cirrhosis; Middle Aged; Prednisolone; Stomach Neoplasms

This study was undertaken in healthy volunteers to determine the relation between serum levels of pepsinogen A, pepsinogen C, pepsinogen A:C ratio, and gastrin on the one hand and histology of the gastric mucosa on the other. The grade of gastritis was scored separately for antral and fundic mucosa by three different classifications: Whitehead, activity, and the Sydney score. Among 48 healthy volunteers studied, 17 were found to have gastritis according to the criteria of Whitehead. Fourteen of these 17 subjects with gastritis had H. pylori in gastric biopsies. In all 48 subjects serum pepsinogen A (r = 0.298-0.506; P < 0.01-P < 0.05), pepsinogen A:C ratio (r between -0.377 and -0.495; P < 0.001-P < 0.05) and gastrin (r = 0.38-0.695; P = 0.007-P < 0.01) were significantly correlated to the severity of both antral and body gastritis as assessed by all three classifications. In contrast, there was no significant correlation between serum pepsinogen C and any of the gastritis scores. When the 17 subjects with gastritis were analyzed separately, there were no correlations between the parameters studied and gastritis of the antrum. Regarding the corpus mucosa, serum PgA correlated significantly with the activity score (r = 0.520; P = 0.03), weakly with the Sydney score (r = 0.465; P = 0.06), but not with the Whitehead score. Serum PgC correlated with the Whitehead (r = 0.555; P = 0.02) and Sydney score (r = 0.523; P = 0.03), but only weakly with the activity score (r = 0.441; P = 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Biomarkers; Biopsy; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Pepsinogens; Pyloric Antrum; Radioimmunoassay

The aim of the present study was to clarify the effects of Helicobacter pylori infection and its eradication on gastric emptying.. Out of a total of 52 patients with non-ulcerative dyspepsia, 34 H.pylori-positive patients were enrolled. Antimicrobial drugs for the eradication of H. pylori were administered to 19 out of the 34 H. pylori-positive patients. Gastric emptying was evaluated according to the acetaminophen method. Inflammatory changes and intracellular periodic acid-Schiff-positive substances in the antral mucosa were examined in biopsy specimens.. Although gastric emptying was significantly prolonged in the patients with non-ulcerative dyspepsia compared with the control group (P < 0.01), there was no difference in gastric emptying between H. pylori-positive and -negative patients, with all patients showing significantly less gastric emptying than the control group. The H. pylori eradication rate was 58% (11 out of 19) and gastric emptying improved significantly in seven patients whose infection was eradicated and whose dyspeptic symptoms disappeared. The ammonia concentration in gastric juice, inflammatory changes in the gastric mucosa and the index of periodic acid-Schiff-positive substances improved significantly when H. pylori was successfully eradicated compared with patients in whom eradication was unsuccessful. As gut hormones may affect gastroduodenal motility associated with H. pylori infection, we also studied the levels of serum gastrin and cholecystokinin. In the patients whose infection was eradicated, serum gastrin decreased significantly, but the cholecystokinin level did not change significantly, although there was a non-significant trend for cholecystokinin to increase.. These results suggest that delayed gastric emptying is partly associated with H. pylori infection and that the infection may contribute to the development of non-ulcerative dyspepsia.

Topics: Adult; Aged; Amoxicillin; Cholecystokinin; Dyspepsia; Female; Gastric Emptying; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Penicillins

The aims were to study gastrin concentrations and gastric mucosal somatostatin and gastrin concentrations in relation to the extent of gastritis in Helicobacter infection.. We measured basal serum gastrin concentrations in antral mucosal biopsy specimens and somatostatin concentrations in corpus biopsy specimens in 88 consecutive dyspeptic subjects undergoing endoscopy. These subjects were divided into three categories on the basis of histology, serology, and culture: H. pylori-positive pangastritis, H. pylori positive antral gastritis with normal body histology, and H. pylori-negative controls. Statistical evaluation was done with the Wilcoxon rank sum test.. Basal serum gastrin concentrations were significantly increased only in subjects with pangastritis and not in those with antral gastritis only, as compared with controls (mean +/- SEM: 72 +/- 7, 46 +/- 10, and 42 +/- 7 ng/l, respectively). Subjects with pangastritis or antral gastritis had significantly lower antral somatostatin concentrations than controls (mean +/- SEM: 0.80 +/- 0.07, 1.03 +/- 0.15, and 2.40 +/- 0.31 micrograms/g(protein), respectively). We also found significantly lower antral gastritis only as compared with controls (mean +/- SEM: 62 +/- 13, 78 +/- 16, and 165 +/- 25 micrograms/g(protein), respectively). In subjects with pangastritis a significantly lower concentration of somatostatin was found in the corpus biopsy specimens than in those with antral gastritis only and controls.. These results suggest that hypergastrinemia in H. pylori gastritis is not caused by antral gastritis and antral somatostatin deficiency alone but that corpus inflammation plays a key role in the origin of hypergastrinemia. Furthermore, in patients with pangastritis a corpus mucosal somatostatin deficiency was found.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pyloric Antrum; Somatostatin

Radioimmunoassays are sensitive and specific methods for measurement of the concentrations of regulatory peptides. However, aspects of physiological, pathophysiological and pharmacological research require knowledge about the biological activity which does not necessarily vary concomitantly with immunological activity. The present work describes a simplified bioassay for gastrin based on the gastric histamine releasing properties of this peptide, using an isolated vascularly perfused rat stomach preparation with a crystalline perfusate and a specific radioimmunoassay for histamine. The establishment of a dose-response curve is described, as well as the utilization of the bioassay on sera from patients with hypergastrinaemia. The method is sensitive for gastrin in the low (4 pmol L-1) picomolar range.

Topics: Anemia, Pernicious; Animals; Biological Assay; Gastric Mucosa; Gastrins; Gastritis; Histamine Release; Humans; Male; Perfusion; Rats; Rats, Wistar; Reproducibility of Results; Sensitivity and Specificity; Stomach; Zollinger-Ellison Syndrome

Helicobacter pylori infection of the antral mucosa is responsible for an increase in basal and stimulated serum gastrin. In the present study we have investigated whether gastritis induced by H. pylori is responsible for abnormalities in the processing of gastrin in dyspeptic patients.. Basal serum gastrin was measured by radioimmunoassay before, 5 weeks, and 1 year after anti-H. pylori therapy in 73 H. pylori positive functional dyspeptic patients. Three region-specific antisera were used, specific for the biologically active carboxy-terminal part, the biologically inactive amino-terminal part of gastrin 1-17, and for the non-sulphated tyrosyl residue in gastrin 1-17.. Basal serum gastrin levels were markedly (P < 0.01) decreased 5 weeks and 1 year after successful eradication of H. pylori (n = 39) but not in the patients in whom treatment failed (n = 34). A decline of gastrin was observed for each of the three radioimmunoassays.. The decrease of serum gastrin levels in all three radioimmunoassays after a successful eradication of H. pylori does not point to major changes in the processing of gastrin. These results suggest that G-cells in the antral mucosa are not functionally affected by the inflammation.

Topics: Adult; Aged; Chromatography; Dextrans; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Radioimmunoassay; Sensitivity and Specificity; Time Factors

21 patients with mild type of chronic superficial gastritis were selected in this study. The effect of electroacupuncture in Zhongwan (RM12), Neiguan (P6) and Sanyinjiao (Sp6) on gastric acid secretion, serum gastrin, plasma somatostatin, plasma motilin concentration and erythrocyte acetylcholinesterase (AchE) activity were observed. The results were as follows: There were significant decreases in gastric acid output, serum gastrin concentration and AchE activity (P < 0.05), but no significant changes in plasma somatostatin and motilin concentration (P > 0.05) after simultaneous electroacupuncture in Zhongwan, Neiguan and Sanyinjiao.

Topics: Acetylcholinesterase; Adult; Chronic Disease; Electroacupuncture; Erythrocytes; Female; Gastric Acid; Gastrins; Gastritis; Humans; Male; Middle Aged

It is well known that acupuncture is effective for treatment of gastric disease in human. We have observed the effect of acupuncturing "Zhongwan" "Neiguan" "Zusanli" on fluorohistochemical changes of G cells of antral mucosa in 42 patients with gastric disease. The results show that after acupuncture treatment the amount of fluorescent G cells and the fluorescent intensity of gastrin in the G cells were obviously decreased in patients with duodenal ulcer, as compared with that before acupuncture treatment. However, the amount of G cells was increased by acupuncture treatment in patients with chronic atrophic gastritis. These data indicate the acupuncture may regulate G cell from abnormal to normal condition in gastric mucosa of gastric disease.

Topics: Acupuncture Therapy; Chronic Disease; Duodenal Ulcer; Enterochromaffin Cells; Gastric Mucosa; Gastrins; Gastritis; Humans; Pyloric Antrum

This study examined the effects of eradication of Helicobacter pylori (H pylori) infection on gastric mucosal morphology and acid secretion. Sixteen H pylori positive patients with enlarged gastric body folds were divided into two groups: (a) patients with moderate enlargement (fold width: 6 to 10 mm, n = 8) and (b) patients with severe enlargement (> 10 mm, n = 8). After successful treatment, gastric body fold width was reduced in both groups (p < 0.01) with an associated decrease in inflammatory infiltrates in the body mucosa (p < 0.01 and p < 0.05). Basal acid output and tetragastrin stimulated maximal acid output (mean (SEM)) in all 16 patients significantly increased from 1.1 (0.5) to 2.9 (0.9) mmol/h (p < 0.05) and from 5.4 (1.3) to 18.7 (2.3) mmol/h (p < 0.01), respectively, with a significant decrease in fasting serum gastrin concentrations, from 127.1 (16.1) to 59.6 (3.8) pg/ml (p < 0.01). The increase in acid secretion after eradication of H pylori was more noticeable in the severe group, who had shown lower acid secretion and higher serum gastrin concentrations (p < 0.05) before eradication, than the increase seen in the moderate group. The decreases in ammonia nitrogen content seen after eradication were significant in basal (from 0.91 (0.17) to 0.37 (0.08) mmol/h, p < 0.05) and stimulated gastric secretions (from 1.57 (0.19) to 0.37 (0.13) mmol/h, p < 0.01), although these changes were too small to explain the increases in basal acid output and maximal acid output. These results suggest that inflammation of the gastric body mucosa caused by H pylori infection is associated with enlarged gastric body folds and inhibition of acid secretion in H pylori positive patients with enlarged gastric body folds.

Topics: Adult; Aged; Ammonia; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Stomach

The prevalence of peptic ulcer in cirrhotic patients is similar to that reported for the general population. Although gastric acid outputs ar normal or lower in cirrhotic subjects compared with non-cirrhotics, the frequency of non-response to histamine H2-receptor antagonists is higher. Peptic ulcer disease in the cirrhotic seems to pursue a more virulent course compared with that in the non-cirrhotic subject. Peptic ulcer prevalences in patients dying of uraemia or in uraemic patients on maintenance dialysis treatment are comparable with those in the general population. However, the frequency of peptic ulcer, especially complicated ulcer, is increased following renal transplantation. Ulcer complications in this context are associated with a high mortality rate. Pre-transplant risk factors for subsequent development of peptic ulcer remain to be identified and the value of histamine H2-receptor antagonists in prophylaxis is as yet unproven.

Topics: Duodenitis; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Peptic Ulcer; Peptic Ulcer Hemorrhage; Uremia

Helicobacter pylori infection is associated with abnormalities in serum gastrin concentration, antral gastrin and somatostatin content, and D-cell density in adults. We have studied the effects of H pylori infection in children. We studied 13 children positive for H pylori and 7 negative children. The median antral somatostatin content was significantly lower in the positive than in the negative group (0.69 [range 0.35-0.91] vs 1.31 [0.73-1.67] ng/mg, p = 0.007). Both antral and serum gastrin concentrations were significantly higher in the positive group (30.1 [15.3-83.6] vs 14.8 [13.8-28.8] ng/mg, p = 0.008; and 89.9 [59.4-313.2] vs 29.5 [13.9-71.1] pg/mL, p = 0.006). Treatment to eradicate H pylori was successful in 11 of the 13 positive patients. With eradication antral somatostatin increased to within the normal range (by a median of 0.41 [0.21-0.86] ng/mg to 1.10 [0.81-1.55] ng/mg, p = 0.016). Serum and antral gastrin decreased (by 37.1 [5.5-265.2] pg/mL to 52.8 [21.4-267.5] ng/mg, p = 0.001; and by 8.0 [2.0-47.2] ng/mg to 22.1 [10.9-37.5] ng/mg, p = 0.001). Eradication of H pylori also significantly increased antral D-cell density (8 [5-22] to 15 [9-22] cells per mm, p = 0.031) and decreased G-cell density (138 [89-161] to 88 [33-121] cells per mm, p = 0.016). The hypergastrinaemia in children positive for H pylori may be due to a deficiency of antral somatostatin, which inhibits gastrin synthesis and release.

Topics: Adolescent; Amoxicillin; Cell Count; Child; Drug Therapy, Combination; Female; Furazolidone; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Pyloric Antrum; Somatostatin

The patients with chronic superficial gastritis were selected in the study. The variation in gastric acidity output, serum gastrin and plasma somatostatin concentration were observed during the Saussurea lappa decoction (SLD) perfusion into the stomach. There was no significant changes in acidity output, serum gastrin and plasma somatostatin concentration after the perfusion of SLD (P > 0.05). Changes in gastric emptying and plasma motilin concentration were observed after oral administration of the SLD in 5 healthy volunteers. The time of gastric emptying was markedly shortened after oral administration of SLD (P < 0.01). A significant increase occurred in plasma motilin concentration at 30 min. after oral administration of SLD (P < 0.01). It revealed that SLD could accelerate the gastric emptying and increase the endogenous motilin release.

Topics: Adult; Drugs, Chinese Herbal; Female; Gastric Acid; Gastric Emptying; Gastrins; Gastritis; Humans; Male; Middle Aged; Motilin; Somatostatin

To study the relationship between Helicobacter pylori infection, gastric inflammatory scores, and fasting gastrin and pepsinogen A and C concentrations, and to evaluate the effect of treatment on these parameters.. Gastrin and pepsinogen A and C concentrations were measured in 36 patients with gastritis, 10 gastric ulcer patients, 12 duodenal ulcer patients, and in 15 subjects with normal gastric mucosa, by standard radioimmunoassay techniques. Fifteen patients with H. pylori infection underwent triple therapy (bismuth subsalicylate, amoxicillin, metronidazole) and were reassessed 1 month later.. Fasting gastrin and pepsinogen A and C concentrations were significantly higher in H. pylori-positive gastritis and peptic ulcer patients than in subjects with normal mucosa and in patients with H. pylori-negative gastritis. There was a significant correlation between inflammatory scores and serum gastrin (r = 0.45, p < 0.0001), and pepsinogen A (r = 0.33, p < 0.006) and pepsinogen C (r = 0.55, p < 0.0001) concentrations. Neither sex nor age affected basal gastrin and pepsinogen concentrations. Eradication of H. pylori infection was successful in 12 patients and resulted in a significant fall in serum gastrin and in pepsinogen A and C concentrations, and in a concomitant improvement of the inflammatory scores. Serum peptide levels and gastritis scores were unchanged in those patients in whom H. pylori infection persisted.. These findings suggest that hypergastrinemia and hyperpepsinogenemia are secondary to H. pylori infection and are related to mucosal inflammation.

Topics: Amoxicillin; Bismuth; Drug Therapy, Combination; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged; Organometallic Compounds; Pepsinogens; Peptic Ulcer; Salicylates

The density of antral gastrin (G)- and somatostatin (D)-immunoreactive cells and the contents of antral gastrin and somatostatin were investigated in endoscopic antral biopsy specimens from patients with duodenal ulcer before and after eradication of Helicobacter pylori. After H. pylori eradication both antral somatostatin concentration (p = 0.0002) and antral D-cell density (p = 0.01) increased significantly. Conversely, although the number of G-cells was unchanged, antral (p = 0.0002) and serum (p = 0.001) gastrin contents decreased significantly. The number of oxyntic D-cells did not change significantly. These results strongly suggest that the hypergastrinaemia observed in H. pylori-positive patients may be due to a deficiency in antral somatostatin, which normally inhibits the synthesis and release of gastrin.

Topics: Adult; Biopsy; Cell Count; Chronic Disease; Duodenal Ulcer; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pilot Projects; Pyloric Antrum; Somatostatin; Time Factors

The number, size, and volume density of endocrine cells was determined in biopsies obtained endoscopically in patients after proximal selective vagotomy (PSV; N = 31), antrectomy (N = 9), untreated duodenal ulcer (DU) disease (N = 11), and in controls (N = 15). Serum gastrin was significantly elevated after PSV (mean 60 pg/ml) compared to DU patients (29 pg/ml), controls (26 pg/ml), and after antrectomy (11 pg/ml). Volume density of fundic argyrophil (largely enterochromaffin-like) cells after PSV (0.74%) and in DU disease (0.63%) were significantly (P < 0.001) higher when compared with controls (0.37%) but lower after antrectomy (0.24%; P < 0.02). The density of argyrophil cells was not influenced by the interval following PSV or the magnitude of hypergastrinemia. Antral gastrin cells were increased after vagotomy, whereas the antral and fundic somatostatin cell numbers were reduced after PSV. It is concluded that: (1) a major role of the vagal nerve as a trophic factor for enterochromaffin-like cells could not be demonstrated after PSV, and (2) moderate hypergastrinemia after PSV did not induce proliferation of ECL cells.

Topics: Adult; Aged; Biopsy; Duodenal Ulcer; Enterochromaffin Cells; Female; Gastrectomy; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Pyloric Antrum; Somatostatin; Vagotomy, Proximal Gastric

A 63-year-old woman was diagnosed as autoimmune gastritis by the presence of serum antibody against alpha-subunit of gastric H+,K(+)-ATPase. The patient did not have pernicious anemia, but showed achlorhydria, marked hypergastrinemia, enterochromaffin-like cell hyperplasia and an extremely high histidine decarboxylase activity in the gastric fundic mucosa. Intragastric acidification by infusion of hydrochloric acid via a nasogastric tube induced a transient reduction of serum gastrin level and fundic mucosal histidine decarboxylase activity. A marked increase in fundic mucosal histidine decarboxylase activity as well as hypergastrinemia appears to be the pathophysiologic response to achlorhydria caused by autoimmunity against gastric H+,K(+)-ATPase.

Topics: Achlorhydria; Autoimmune Diseases; Enterochromaffin Cells; Female; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis; Graves Disease; H(+)-K(+)-Exchanging ATPase; Histidine Decarboxylase; Humans; Hyperplasia; Middle Aged; Parietal Cells, Gastric; Polyps; Stomach Neoplasms

To investigate whether antral colonization by Helicobacter pylori (Hp) modifies gastrin-cell population, the number of G-cells was evaluated in antral biopsy specimens from 22 apparently healthy subjects and from 48 duodenal ulcer patients using a morphometric method. The level of serum immunoreactive gastrin in a sample of fasting serum obtained at the time of biopsy was also measured. In healthy subjects the G-cell count (evaluated according to G/I index) and the serum gastrin levels were not significantly different than those found in duodenal ulcer patients. When the antral colonization by Hp was assessed, we found that, both controls and duodenal ulcer Hp-positive patients had a mean G-cell count and fasting serum gastrin levels not significantly higher than in patients without Hp.

Topics: Adult; Biopsy; Cell Count; Chronic Disease; Duodenal Ulcer; Female; Gastric Mucosa; Gastrins; Gastritis; Helicobacter pylori; Humans; Male; Pyloric Antrum

Topics: Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans

The effects of chronic drug-induced hypergastrinemia on the exocrine and endocrine stomach are still incompletely understood. Chronic hypergastrinemia in rats and humans is associated with gastric argyrophil cell hyperplasia.. Seventy-four patients with chronic ranitidine-resistant ulcerations were treated chronically with omeprazole (median observation period 48 [6-84] months).. Median fasting serum gastrin levels increased from a pretreatment value of 74-145 pg/mL after 3 months. No further increase was observed thereafter. The finding of atrophic gastritis increased from 1.8% to 20.8% after 5 years. A doubling of the mean argyrophil cell volume density (0.36% vs. 0.74% after 5 years; P < 0.01%) was paralleled by a decrease in the normal endocrine cell growth pattern from 64.3% to 33.3% and an increase in micronodular hyperplasia (8.9% vs. 16.7%). These changes correlated with the severity of corpus gastritis and seemed to be more disease- than drug-related. No statistically significant changes were observed in the antral G- and D-cell volume densities under therapy.. Long-term omeprazole therapy in humans results in moderate hypergastrinemia and a significant argyrophil cell hyperplasia, which are correlated to the grade of corpus gastritis. Because hypergastrinemia and gastritis are closely related, it is difficult to quantitatively assess their respective role in this process.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Cell Division; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole; Peptic Ulcer; Stomach; Time Factors

The presence of autoimmune gastritis was investigated in 54 women with postpartum thyroiditis. Parietal cell antibodies (PCA) specific against H+, K(+)-adenosine triphosphatase (EC 3.6.1.36) were found in 18 women during pregnancy; in 10 of them, a 2-9-fold increase in the PCA level was observed in the postpartum period. At a 5-year follow-up, the initially PCA-positive women still had elevated antibody levels. Hypergastrinemia and low pepsinogen levels were noted in 4 women. In 2 of these women low serum vitamin B12 levels had developed. In 6 of 9 PCA-positive women examined by gastroscopy, biopsy specimens from the gastric body mucosa contained mononuclear cells, mainly T lymphocytes (CD3+) and macrophages (Leu-M3+) combined with an aberrant epithelial expression of HLA-DR. In four patients with chronic gastritis, all parietal cells, as defined by a specific monoclonal antibody, were found to have immunoglobulin G (IgG) deposits by a double-immunostaining method. Three of them had microscopic evidence of atrophy, whereas in 1 patient the body mucosa was intact. In 1 further patient with intact glands at histological examination, the basolateral membrane of some oxyntic glands was coated with IgG. The selective in situ deposition of antibodies associated with histologically intact parietal cells may support the concept that specific autoantibodies participate in the early pathogenesis of parietal cell destruction.

Topics: Adenosine Triphosphatases; Adult; Antibodies; Autoimmune Diseases; Biopsy; Female; Fluorescent Antibody Technique; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis; H(+)-K(+)-Exchanging ATPase; Humans; Immunoglobulin A; Immunoglobulin G; Iron; Pepsinogens; Pregnancy; Puerperal Disorders; Thyroiditis, Autoimmune; Vitamin B 12

Hypergastrinemia is a very important clinical condition for the reason that a growing body of evidence obtained from animal and human experiments has revealed gastric carcinoids induced by hypergastrinemia. We investigated 35 patients with Basedow's disease (BD) to elucidate the mechanism of hypergastrinemia associated with BD as well as the relationship between type A gastritis and BD. Fasting serum gastrin levels in BD (296.1 +/- 251.4 pg/ml; mean +/- S.D.) were significantly (p less than 0.001) higher than those in age-matched 27 healthy subjects (106.1 +/- 69.2), and in the BD group, significant positive correlation was detected between fasting serum gastrin levels and thyroid hormones (i.e. T3 and free T4). In the hyperchlorhydria group in BD with hypergastrinemia, the levels of fasting serum gastrin were normalized after euthyroidism was attained due to antithyroidal drugs. On the other hand, in the achlorhydria group in BD significant hypergastrinemia was persisted in spite of normalization of thyroid function. Twenty % of the BD patients had histologically proved type A gastritis with achlorhydria, and all patients with type A gastritis were older than 60 years old. Endoscopic examination revealed that one patient with type A gastritis had an early gastric cancer. However, no gastric carcinoids were demonstrated in this study. In conclusion, the results described as above suggested, 1) hypergastrinemia observed in patients with BD may be induced by gastrin hypersecretion due to hyperthyroidism as well as type A gastritis, 2) BD patients with type A gastritis were recommended to undertake regular endoscopic examination for detecting gastric cancers as well as gastric carcinoids.

Topics: Adult; Aged; Female; Gastrins; Gastritis; Graves Disease; Humans; Male; Middle Aged

Studies were performed in patients with and without renal failure to investigate the role of bacterial ammonia production in the pathogenesis of the mucosal abnormalities caused by Helicobacter pylori. The high rate of H pylori ammonia production in uraemic patients should accentuate any ammonia induced effects. The median (range) gastric juice ammonium concentration in the H pylori positive patients with renal failure was 19 mmol/l (II-43) compared with 5 mmol/l (1-11) in the H pylori positive patients without renal failure (p < 0.005). In the H pylori negative patients the values were 3 mmol/l (0.5-11) and 0.7 mmol/l (0.1-1.4) respectively in the patients with and without renal failure (p < 0.01). Despite the much higher ammonia production in the H pylori positive uraemic patients, the nature and severity of their gastritis was the same as that in the H pylori positive non-uraemic patients. The median (range) fasting serum gastrin concentration was raised in the uraemic patients compared with the non-uraemic patients but was similar in the uraemic patients with (95 pmol/l (52-333)) or without (114 pmol/l (47-533)) H pylori infection. The median (range) serum pepsinogen I concentration was also high in the uraemic compared with the non-uraemic patients and was significantly higher in uraemic patients with H pylori (352 ng/ml, range 280-653) than in those without H pylori infection (165 ng/ml, range 86-337) (p < 0.01). These findings indicate that the gastritis and hypergastrinaemia associated with H pylori infection are not the result of mucosal damage induced by the organism's ammonia production.

Topics: Adult; Aged; Ammonia; Gastric Juice; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Middle Aged; Pepsinogens; Renal Insufficiency; Stomach Diseases

Eradication of Helicobacter pylori is associated with a fall in serum gastrin but the way in which the infection raises the serum gastrin concentration is not clear. It may be related to the ammonia produced by the bacterium's urease stimulating gastrin release by the antral G cells. Alternatively, the antral gastritis induced by the infection may modify the regulation of gastrin release. We have examined serum gastrin in 10 patients before and 24 hours after starting triple anti-H pylori treatment consisting of tripotassium dicitrato bismuthate 120 mg four times daily, metronidazole 400 mg three times daily, and amoxycillin 500 mg three times daily. The urease activity, assessed by the 20 minute value of the 14C-urea breath test, fell from a median of 176 (range 116-504) kg% dose/mmol CO2 x 100 pretreatment to 5 (2-15) at 24 hours (p less than 0.005). The median antral gastritis score was 6 (4-6) pretreatment and fell to 3 (2-5) at 24 hours (p less than 0.02), and this was due to resolution of the polymorphonuclear component. Despite this complete suppression of bacterial urease activity and partial resolution of antral gastritis the median basal gastrin concentration remained unchanged, being 57 ng/l (45-77) pretreatment and 59 ng/l (45-80) at 24 hours and the median integrated gastrin response to a standardised meal was also unaltered, being 4265 ng/l/min (range 1975-8350) and 4272 ng/l/min (range 2075-6495) respectively. These findings do not support a causal association between H pylori urease activity and hypergastrinaemia and show rapid improvement of antral gastritis after starting anti-H pylori treatment.

Topics: Adult; Aged; Drug Therapy, Combination; Eating; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Urease

The relationship between different features of gastric mucosal inflammation, intragastric pH and serum gastrin concentration and the distribution and quantity of Helicobacter pylori was studied in a series of 107 dyspepsia patients. H. pylori was identified in 62 cases (59%), and its presence was associated with increased amounts of mononuclear inflammatory cells and neutrophilic and eosinophilic leucocytes in both the antrum and the corpus. The number of H. pylori in the antral mucosa was significantly associated with the quantity of mononuclear inflammatory cells. It was also associated with glandular atrophy in antral mucosa, so that slight and moderate glandular atrophy were significantly more common in cases with abundant H. pylori. Intragastric pH and serum gastrin concentration were inversely related to the number of H. pylori in both the antral and corpus mucosa. H. pylori positive patients were also divided into groups according to proportions of H. pylori in the antral and corpus mucosa. In 5 of these patients (8%) the bacteria were present only in the corpus, and this group had a significantly more pronounced degree of glandular atrophy in the corpus mucosa, higher intragastric pH and a higher serum gastrin concentration than the other H. pylori positive patients. The other patients with a higher corpus H. pylori than antral H. pylori score (n = 25; 34%) also had a significantly higher intragastric pH and serum gastrin concentration than those with a corpus H. pylori score lower than or equal to the antral score, while the latter had more severe inflammation in the antral mucosa and a lower intragastric pH and serum gastrin concentration. The results suggest that inflammation in the antrum forms a favourable environment for H. pylori, while atrophy of the corpus glands, being connected with increased pH, leads to a diminished amount of H. pylori. They thus support the view that proliferation of H. pylori is dependent on acid produced by the corpus mucosa.

Topics: Adult; Aged; Colony Count, Microbial; Dyspepsia; Female; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis; Helicobacter pylori; Humans; Leukocytes, Mononuclear; Male; Middle Aged; Neutrophils

Nine patients with Helicobacter pylori-related antral gastritis and history of duodenal ulceration were studied before and at 1 and 7 months after eradication of the infection by a 4-week course of tripotassium dicitrato bismuthate, metronidazole, and amoxycillin. The median basal gastrin concentration before eradication was 30 ng/l (range, 20-60) and fell to 20 ng/l (5-20) at 1 month (p less than 0.02) and 15 ng/l (5-20) at 7 months (p less than 0.01) after eradication. The integrated gastrin response to a peptide meal was 3650 ng/l.min (range, 1875-6025) before treatment compared with 1800 ng/l.min (range, 1200-3075) at 1 month (p less than 0.01) and 1312 ng/l.min (875-2625) at 7 months (p less than 0.03). Daytime intragastric pH (0900-2100 h) was similar before treatment (median, 1.4; range, 1.1-2.1) and at 1 month (1.4; 1.1-2.3) and 7 months (1.4; 1-2.2) after eradication. In five of the patients nighttime acid output (2300-0900 h) was also studied and was similar before (median, 86 mmol/10 h; range, 52-114) and at 1 month (76 mmol/10 h; 50-143) and 7 months (94 mmol/10 h; 63-106) after eradication. In conclusion, eradication of H. pylori is accompanied by a sustained fall in serum gastrin concentrations but is not accompanied by an early or late reduction of daytime intragastric acidity or nighttime acid output.

Topics: Adult; Aged; Amoxicillin; Anti-Ulcer Agents; Bismuth; Circadian Rhythm; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Metronidazole; Middle Aged; Organometallic Compounds; Stomach; Time Factors

The content of basal gastrin and ultrastructure of gastrinproducing cells was studied in 81 patients showing chronic gastritis with secretory insufficiency. The highest level of gastrin was revealed in the blood of patients with diffuse atrophic gastritis, moderately increased--focal atrophic gastritis. The blood gastrin was reduced in patients with antral gastritis. A study of the ultrastructure of gastrinproducing cells revealed their high functional activity in diffuse atrophic gastritis and a moderate in focal atrophic gastritis. Changes of the gastrin level and ultrastructure of gastrinproducing cells should be considered in the choice of treatment methods.

Topics: Adult; Chronic Disease; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Parietal Cells, Gastric

We studied histologically antral biopsies from 89 consecutive patients with chronic renal failure for Helicobacter pylori (previously Campylobacter pylori). A dose-response gastric secretion test was also performed. The frequency of Helicobacter-positive subjects was low (15/89, 17%), corresponding to figures reported in the literature for young symptomless volunteers. Helicobacter-positive patients had significantly more frequently upper gastrointestinal symptoms than Helicobacter-negative individuals (P less than 0.05). Antral gastritis was more common in the Helicobacter-positive than in the Helicobacter-negative renal patients (P less than 0.01), but the incidence of body gastritis did not differ between them. The Helicobacter-positive patients had lower serum urea levels (P less than 0.01) and higher acid outputs (P less than 0.001) than Helicobacter-negative subjects. All patients had raised fasting serum gastrin levels, which possibly obscured the difference between Helicobacter-positive (283 pg/ml) and -negative (331 pg/ml) patients. We conclude that in chronic renal failure gastric colonization of Helicobacter pylori is not more frequent than usual. It correlates positively with antral gastritis, gastric acid output and upper gastrointestinal symptoms, but negatively with serum urea levels.

Topics: Biopsy; Female; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Incidence; Kidney Failure, Chronic; Male; Middle Aged; Pyloric Antrum

Since Helicobacter pylori infects the gastric mucosa in most patients with chronic duodenal ulcer, infection with this organism has been implicated in the pathogenesis of this common disease. We postulated that if H. pylori is pathogenic in the usual type of duodenal ulcer, it should be less common when duodenal ulcer has another, specific etiology, such as Zollinger-Ellison syndrome. Gastric mucosa was compared from 18 patients with proven Zollinger-Ellison syndrome (17 of whom had had duodenal ulcer disease) and 18 controls with chronic duodenal ulcer without such a diagnosis. All subjects, who were matched for age and sex, had undergone elective gastric resections. Gastric tissues were stained by hematoxylin-eosin and Giemsa and were reviewed by an experienced pathologist who was unaware of the diagnosis. The frequency of H. pylori in patients with Zollinger-Ellison syndrome (8/18) was lower than in controls with duodenal ulcer (16/18; P less than 0.02). Moreover, chronic antral gastritis scores were higher in patients with duodenal ulcer (P less than 0.01). In Zollinger-Ellison syndrome, peak acid output was lower in patients positive (median 22 meq/30 min) compared to those negative for H. pylori (median 32 meq/30 min; P less than 0.02) but serum gastrin was correspondingly lower in patients positive for H. pylori (P less than 0.05). H. pylori infection appears to be more frequent when duodenal ulceration is not associated with another etiology, such as acid hypersecretion in Zollinger-Ellison syndrome. H. pylori infection in Zollinger-Ellison syndrome may also be associated with decreased gastric acid secretion.

Topics: Adolescent; Adult; Aged; Child; Chronic Disease; Duodenal Ulcer; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Zollinger-Ellison Syndrome

Topics: Age Factors; Aged; Campylobacter; Chronic Disease; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Middle Aged; Pepsin A; Peptic Ulcer; Recurrence; Risk Factors

The study investigated whether cimetidine could heal chronic erosive gastritis induced experimentally in rats by the administration of taurocholate for 6 months. Taurocholate gastritis is associated with mucosal erosions, the infiltration of inflammatory cells, reduction of the parietal cell mass, reduction of mucosal thickness, and interstitial fibrosis, a histopathological picture similar to that of human erosive gastritis. Microscopic quantitative morphological studies were used to determine the effect of cimetidine administered freely to rats for two weeks in the form of food containing 0.4 or 0.8% of the agent after the withdrawal of taurocholate. Basal acid secretion was analysed in rats with pyloric ligation 12 hours after withdrawal of the cimetidine-containing food. Basal gastrin levels were determined after a 12-hour fast by radioimmunoassay. The total length of the mucosal erosions was significantly decreased in the cimetidine-treated rats of Group A (cimetidine: 400 mg/kg/day: median 294.6 mm) and Group B (800 mg/kg/day; 225.7 mm) when compared to Group C (control gastritis group; 626.4 mm). Both the grade of inflammatory cell infiltration and fibrosis were also significantly reduced in Groups A and B compared with Group C. The number of parietal cells per unit area (A: 101.0, B: 108.8) and the mucosal thickness of the fundic mucosa (A: 0.610, B: 0.710) and of the antral mucosa (A: 0.220, B: 0.240) were greater in Groups A and B than in Group C (85.1 and 0.52 of the fundic mucosa, 0.170 of the antral mucosa, respectively). Basal acid secretion was significantly inhibited in Groups A and B (31.8 and 26.3 mu Eq/hr/100 g body weight, respectively) when compared to Group C (69.6 mu Eq/hr/100 g body weight). Basal serum gastrin levels were significantly higher in Groups A and B (198.1 and 210.5 pg/ml, respectively) than in Group C (98.7 pg/ml). It was concluded from these results that cimetidine had a curative effect on chronic erosive gastritis induced experimentally by taurocholate. The inhibition of acid and gastrin secretion may play an important role in the mechanism of its action.

Topics: Animals; Cimetidine; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Male; Rats; Rats, Inbred Strains; Taurocholic Acid

According to the day-prescription of acupoint mentioned by Xu Feng in Encyclopaedia of Acupuncture and Moxibustion, the authors used opening acupoints to treat 31 chronic superficial gastritis patients (young male) and closing points to treat 15 patients for comparison. Besides, the authors observed the changes of hydrochloric acid of gastric juice, volume of juice and serum gastrin of the patients before and after the acupuncture. Results of clinical treatment: In the opening acupoint group, 13 were cured, 12 effected, 4 improved and 2 ineffective. The total effective rate was 93.55%. There was no significant difference between the results of the two groups. Results of experiment: to the hyperacidity patients of the two groups, the content of hydrochloric acid tended to fall after acupuncture while to the hypoacidity patients the content tended to rise after acupuncture. The changes of the gastric juice volume were different in the two groups. In the opening group, we could also see that the low volume rose and high volume fell after acupuncture. However, the closing group showed that the low volume fell after acupuncture. There was not any significant difference. The changes of serum gastrin indicated that, after acupuncture, all the serum gastrin in the two groups went up. But the peak value in the opening group appeared at 30 minutes after acupuncture while in the closing group it appeared at one hour. In both groups, there were significant differences between those results before and after acupuncture.

Topics: Acupuncture Therapy; Adolescent; Adult; Circadian Rhythm; Gastric Acid; Gastrins; Gastritis; Humans; Male

The stomachs of cirrhotic patients are frequently subject to a number of alterations, detectable by endoscopy, the presence of which indicates a disturbance in the mucosa. Several investigators believe that portal hypertension plays an etiopathogenetic role. Three groups of subjects were studied prospectively: 83 cirrhotic patients with portal hypertension, 53 cirrhotic patients without portal hypertension, and 135 control subjects. Snake skin, scarlatina rash, and petechia were the most frequent endoscopic findings in the cirrhotic patients with portal hypertension (P less than 0.001); these findings were also most frequently present in association with each other in this group. There was no correlation between the endoscopic findings, the clinical gravity of liver cirrhosis (Child-Pugh grade), and the gravity of esophageal varices (Beppu score). There were no characteristic inflammatory findings in the gastric mucosa. Hypergastrinemia was often observed in cirrhotic patients with and without angiodysplasias.

Topics: Aged; Biopsy; Chronic Disease; Cluster Analysis; Female; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Gastroscopy; Humans; Hypertension, Portal; Liver Cirrhosis; Male; Middle Aged; Prospective Studies

161 cases of chronic gastritis (including 59 superficial gastritis, 86 atrophic gastritis, 16 superficial gastritis combined with atrophic gastritis) typed in deficiency syndrome (including 64 Spleen-deficiency syndrome, 97 Spleen-Kidney-deficiency syndrome) were studied clinically with modern medicinal multiple-index. The gastroscope image, pathologic changes of gastric mucosa, stomach barium meal examination, gastric acid, serum gastrin, urine pepsinogen, urine 17-ketosteroid, vegetative nerve function, peripheral blood picture, etc. were selected as observation indices. The preliminary findings showed that in Spleen-deficiency patients, the superficial gastritis constituted the majority, the asthenic stomach constituted the minority, the gastric secretion and the serum gastrin were on the high side, the urine pepsinogen, the adrenocortical function and the hemoglobin were on the low side, but the white blood cell was rather normal; otherwise, in Spleen-Kidney deficiency patients, the atrophic gastritis and the asthenic stomach constituted the majority, the gastric secretion decreased, the serum gastrin level was higher, while the urine pepsinogen, the adrenocortical function, white blood cell and the hemoglobin were on the low side. It was also found that in certain same inflammation changes, the gastric secretion of the Spleen-Kidney-deficiency syndrome was markedly than that of Spleen-deficiency syndrome. With the treatment method of invigorating the Spleen and reinforcing the Spleen-Kidney, each index was relatively improved. The degree of seriousness to inflammation changes of gastric mucosa and the disturbance or imbalance of gastric secretion function were reflected from the Spleen-deficiency and the Spleen-Kidney-deficiency syndromes of chronic gastritis. It is suggested that hemopoiesis and hypothalamo-adenohypophysial-adrenal cortical axis be influenced.

Topics: Adult; Aged; Chronic Disease; Female; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Male; Medicine, Chinese Traditional; Middle Aged

Serum pepsinogen I, serum gastrin concentration, and inflammatory scores were measured in a population of 71 children undergoing upper gastrointestinal endoscopy for investigation of upper abdominal pain. Forty four were initially colonised with Helicobacter pylori. The indices were measured before treatment (in 71 children), one month (in 41 children), and six months (in 21 children) after stopping treatment. Before treatment there was a significant correlation between serum pepsinogen concentration, total inflammatory score, and H pylori state, but no correlation between serum gastrin concentrations and H pylori state. Similarly, the total inflammatory score and serum pepsinogen concentrations were significantly correlated. There was no such correlation in children negative for H pylori. After treatment the inflammatory score improved in those patients in whom H pylori had been eradicated. There was also a significant fall in serum pepsinogen I and serum gastrin concentration in those patients in whom H pylori had been eradicated. These results were similar to those found six months after treatment had been stopped. These findings suggest that the serum pepsinogen I concentration could be considered a useful marker for gastritis and can be used as an index of severity of gastritis in H pylori positive subjects. The measurement of serum gastrin concentrations does not give useful information.

Topics: Adolescent; Biomarkers; Child; Child, Preschool; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Infant; Male; Pepsinogens; Prospective Studies; Severity of Illness Index

The aim of our study was to investigate the relationship between gastrin producing cell density with antral mucosa, luminal and serum gastrin concentration in antral atrophic gastritis. Our study group consisted of 17 patients: six with mild atrophic gastritis, seven with moderate atrophic gastritis and four with severe atrophic gastritis. None of the patients had type-A atrophic gastritis but the body mucosa was affected by superficial gastritis at various extent in some. A group of 15 healthy subjects served as control. All subjects underwent gastroscopic examination with multiple bioptic sampling. Radioimmunoassay was used for gastrin determination and photomicroscopy for gastrin producing cell density assessment. Electron microscopy was used to assess the gastrin producing granule density index. Patients with moderate and severe atrophic gastritis showed a lower gastric acidity and acid output as compared to control. Serum gastrin did not show significant differences among the groups. In moderate and severe atrophic gastritis, gastrin producing cell granule density index, gastrin producing cell density and antral mucosa gastrin concentration were significantly lower when compared with control and decreased with advancing of the severity of atrophic gastritis. In atrophic gastritis, however, the latter two measurements were not correlated. In moderate and severe atrophic gastritis luminal gastrin concentration significantly increased, compared with control, after the severity of atrophic gastritis. Gastrin producing cell granule density index and luminal gastrin concentration showed a significant correlation with gastric pH. These data suggest that in antral atrophic gastritis with reduced gastric acidity, the decrement of gastrin producing cells is followed by gastrin producing cell hyperfunction with increased luminal release of gastrin.

Topics: Adult; Cell Count; Female; Gastric Acid; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Male; Middle Aged; Pyloric Antrum

The amount of gastrin-like immunostaining in gastrin (G) cells of the antral mucosa was quantified using a computer-assisted method of measuring immunoreaction product. Biopsies from 25 patients without Heliobacter-like organisms and 60 patients with varying degrees of infection were immunostained for gastrin. Twenty-five G cells from each patient were measured both subjectively and by image analysis. Gastrin-like immunoreactivity was found to be significantly increased in the presence of Heliobacter-like organisms.

Topics: Biopsy; Campylobacter Infections; Gastric Mucosa; Gastrins; Gastritis; Humans; Immunohistochemistry

Gastric mucosal histology and function were evaluated in 57 Italian subjects with dermatitis herpetiformis (DH), by means of multiple endoscopic biopsies, gastrin and pepsinogen I (Pg I) serum levels, and parietal cell antibodies (PCA). One hundred and forty-nine patients with nonulcer dyspepsia served as reference population for the prevalence of atrophic gastritis of the body. Seventeen DH patients (30%) and 23 controls (15.4%) showed atrophic gastritis of the body mucosa (p less than 0.05). Nine of the DH patients with atrophic gastritis of the body also had atrophic changes in the antrum. Six patients, all with severe atrophic gastritis, had high gastrin levels and PCA; five of these six also had low Pg I levels. We found an increased prevalence of abnormal indirect function tests among patients with atrophic gastritis is due to the younger age of the patients in our series. Thus, atrophic gastritis can be detected early on a histologic basis, but functional impairment occurs later, as the mucosal damage increases in severity.

Topics: Adolescent; Adult; Age Factors; Aged; Autoantibodies; Dermatitis Herpetiformis; Female; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Italy; Male; Middle Aged; Parietal Cells, Gastric; Pepsinogens; Prevalence

The relationship of fasting serum gastrin (FSG) levels to the histologic state of antral and body mucosa and to the stimulated acid output (PAO) was examined in 860 subjects. The FSG levels correlated with PAO and atrophy of the body mucosa: the FSG increased linearly with an increase in the grade of body atrophy and increased exponentially when the PAO decreased from 'normal' (greater than 10 meq/h) to zero. In subjects with achlorhydria or marked hypochlorhydria (PAO less than 1.1 meq/h) accompanying moderate or severe atrophy in the gastric body mucosa, FSG decreased linearly with increasing grade of atrophy in the antral mucosa. No such relationship between antral atrophy and FSG was found in subjects who had a PAO above 1.1 meq/h or who had non-atrophic gastric body mucosa. We conclude that the state of the antral mucosa influences the FSG level, but only when the function of antral G cells is maximal--that is, in achlorhydric or nearly achlorhydric conditions in which the inhibitory effect of intragastric acidity on the G cells' secretion of gastrin into the circulation is minimal.

Topics: Atrophy; Fasting; Finland; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Humans; Pyloric Antrum; Radioimmunoassay; Stomach Diseases

Topics: Antacids; Campylobacter; Campylobacter Infections; Duodenal Ulcer; Gastrins; Gastritis; Humans; Metronidazole; Organometallic Compounds; Pyloric Antrum

32 children (mean age 12 years, range 6-18) with non-specific abdominal pain and Campylobacter pylori positive gastritis received a six week course of daily oral amoxycillin (50 mg/kg) and tinidazole (20 mg/kg). Before treatment and one month after stopping treatment, endoscopic biopsy samples were taken from the antral mucosa and serum C pylori IgG antibody, pepsinogen I, and gastrin levels were measured in fasting blood samples. One month after treatment 30 children (94%) were cleared of C pylori and gastritis had resolved in 27 (84%) and was improved in the remaining 5. Serum IgG, pepsinogen I, and gastrin levels were significantly decreased after treatment. Of 12 children assessed at six months, 9 remained free of C pylori. Increases or decreases in IgG level indicated clearance or recurrence, respectively, of C pylori.

Topics: Administration, Oral; Adolescent; Amoxicillin; Antibodies, Bacterial; Campylobacter; Campylobacter Infections; Child; Drug Evaluation; Drug Therapy, Combination; Female; Follow-Up Studies; Gastrins; Gastritis; Humans; Immunoglobulin G; Male; Nitroimidazoles; Pepsinogens; Pyloric Antrum; Recurrence; Tinidazole

Campylobacter pylori (C.p.) infection is often found in patients with antral gastritis and peptic ulcer disease. Pathophysiological links are still unclear, and we therefore tested the hypothesis whether C.p. affects the gastrointestinal peptides and thus influences gastric acid secretion and protective factors. 94 patients were examined by upper GI endoscopy and blood analyzed for gastrin, somatostatin, pancreatic polypeptide and neurotensin. Biopsies of antral mucosa were investigated for C.p. in urease testing, culture and microscopy. C.p. was found in 42 patients (45%). In microscopy all of these patients had chronic gastritis (100%). A significant increase in gastrin uninfluenced by C.p. was found in patients with antral gastritis (normal: 6.4 +/- 0.7, [n = 27]; gastritis without C.p.: 18.4 +/- 5.9 [p less than 0.02], [n = 7]; gastritis with C.p.: 10.7 +/- 2.2, [n = 22]). Somatostatin, pancreatic polypeptide and neurotensin showed no difference.

Topics: Campylobacter; Campylobacter Infections; Gastrins; Gastritis; Humans; Neurotensin; Pancreatic Polypeptide; Pyloric Antrum; Somatostatin

Topics: Adult; Campylobacter Infections; Duodenal Ulcer; Evaluation Studies as Topic; Gastric Acidity Determination; Gastrins; Gastritis; Humans; Middle Aged

To investigate whether hypergastrinemia and low serum levels of pepsinogen I are associated with gastric hypoacidity in cirrhosis with capillary ectasia of gastric mucosa and whether this alteration is secondary to the presence of atrophic gastritis, two groups of patients were studied: 1) 12 cirrhotic patients with diffuse gastric red spots at the endoscopic examination, and 2) 12 cirrhotic patients with endoscopically normal mucosa. Vascular ectasia of the gastric mucosa was histologically confirmed in all patients with gastric red spots. The study of base-line and stimulated acid gastric secretion showed that 9 of 12 (75%) cirrhotics with gastric vascular ectasia had achlorhydria and that 8 of these 9 patients had high base-line gastrin serum levels (greater than 130 pg/ml) and low base-line pepsinogen I serum levels (less than 20 ng/ml). Base-line gastrin and pepsinogen I serum levels were significantly greater and lower, respectively, in patients with gastric vascular ectasias than in cirrhotics without these lesions. None of the patients of either group had complete atrophy in the corpus of the stomach, and only 4 of the 9 cirrhotics with gastric vascular ectasia and achlorhydria had moderate atrophy. These results show that achlorhydria is frequently associated with hypergastrinemia and low pepsinogen I serum levels in patients with cirrhosis and gastric vascular ectasias and suggest that this disturbance is not secondary to a morphologic abnormality of the gastric mucosa.

Topics: Atrophy; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Liver Cirrhosis; Pepsinogens

In this paper, 89 Spleen deficiency (SD) patients' gastric mucosa specimens obtained during fibrogastroscopy mucosal biopsy were observed with immunocytochemical-stereologic-quantitative analysis method. The number of G cells counted and the content of basic gastrin in serum measured. This study found that the difference of the number of G cells and the content of gastrin in serum possessed statistical significance between two types of SD. The results suggested the hyperplasia and hypersecretion of G cells in gastric antrum might be an important pathological mechanism for different types of SD.

Topics: Adolescent; Adult; Aged; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Immunohistochemistry; Male; Medicine, Chinese Traditional; Middle Aged; Peptic Ulcer; Pyloric Antrum; Splenic Diseases

We report a case of gastric enterochromaffin-like carcinoid tumour associated with fundic chronic atrophic gastritis and hypergastrinaemia of antral origin. The clinical and pathological features of this association are reviewed. The probable causal relationship between these argyrophil carcinoids and hypergastrinaemia is also discussed.

Topics: Adult; Carcinoid Tumor; Female; Gastrins; Gastritis; Humans; Stomach Neoplasms

1. Ranitidine hydrochloride was administered orally to Beagles at doses equivalent to 50 mg once daily, or 5 mg twice daily, of ranitidine base/kg for more than 7 years. 2. Apart from looseness of faeces, seen mainly after doses of 50 mg/kg and only rarely after the first year of such treatment, there were no adverse clinical effects. There were no deaths related to treatment. 3. Periodic gastroscopy revealed nothing abnormal. 4. Peak plasma levels of ranitidine occurred within 2 h of dosing; levels were proportional to the doses administered. 5. There were no major differences in fasting plasma gastrin levels between treated and untreated dogs; the expected increase occurred in response to the provision of food and, predictably, this was greater following a dose of ranitidine. 6. A normal histamine-induced gastric secretory response was demonstrated. 7. Necropsy revealed no lesions of toxicological significance. Macroscopically the stomachs appeared normal but microscopic examination showed some gastritis in both treated and control dogs. No changes in enterochromaffin-like (ECL) cells were detected. Electron microscopy showed unimpaired secretory activity of parietal cells. 8. Thus, after more than 7 years administration to beagle dogs of doses in excess of the normal daily therapeutic dose, the stomachs showed no changes attributable to treatment and their secretory capacity was unimpaired.

Topics: Administration, Oral; Animals; Diarrhea; Dogs; Dose-Response Relationship, Drug; Female; Gastric Mucosa; Gastrins; Gastritis; Male; Microscopy, Electron; Ranitidine; Stomach; Time Factors

Topics: Autoimmune Diseases; Campylobacter Infections; Chronic Disease; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Parietal Cells, Gastric

Thirty patients with bile reflux gastritis, proven by gastroscopy and Milk 99mTc-EHIDA Test, were studied and their clinical features were compared with those of patients with non-bile reflux gastritis. The symptoms were similar in both groups of patients, whereas histologically in bile reflux gastritis there were more hyperemia of mucosa, more obvious edema in lamina propria and more polymorphonuclear infiltration. Furthermore, in bile reflux gastritis the histological changes were more severe in the antrum and decreased in severity toward the cardia. Acid secretion was significantly lower in patients with bile reflux gastritis than in patients with non-bile reflux gastritis while the serum gastrin level was significantly higher in the former than in the latter group. The authors suggest that there may be a vicious cycle among duodenogastric reflux, low level of gastric acidity and high level of serum gastrin. When duodenogastric reflux occurs, not only the bile salts damage the gastric mucosa and subsequently cause the back diffusion of hydrogen ion but also the alkaline duodenal juice neutralizes the gastric acid, resulting in decrease of gastric acidity. The bile salts and low acidity can stimulate the release of serum gastrin which antagonizes the effects of cholecystokinin and secretin on pyloric tone and aggravates the duodenogastric reflux.

Topics: Adult; Aged; Bile Reflux; Biliary Tract Diseases; Female; Gastric Acidity Determination; Gastrins; Gastritis; Humans; Male; Middle Aged

Thirty-five patients with fundic atrophic gastritis and achlorhydria were classified in two groups according to the presence or absence of fundic argyrophil, mostly enterochromaffinlike cell hyperplasia. Among the biologic and histologic parameters studied, the hyperplasic group differed only by a circulating hypergastrinemia and an antral G-cell hyperplasia. The histamine content, the histidine decarboxylase activity, and the mast cell number of fundic biopsies were determined in 10 controls, 16 of the preceding patients (11 with and 5 without fundic argyrophil-cell hyperplasia), and 5 patients with fundic atrophic gastritis and neither achlorhydria nor hyperplasia. Histamine content and histidine decarboxylase activity were increased only in the hyperplasic group despite an unchanged mast cell number. For all fundic biopsies the argyrophil-cell density was positively related to the histamine content. Finally, the argyrophil-cell hyperplasia occurring in fundic atrophic gastritis with achlorhydria is associated not with the gastritis intensity, as assessed by histologic and secretory criteria, but with a circulating hypergastrinemia and an increase of both fundic histamine content and histidine decarboxylase activity.

Topics: Adult; Aged; Aged, 80 and over; Biopsy; Carboxy-Lyases; Chromaffin System; Enterochromaffin Cells; Female; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Histamine; Histidine Decarboxylase; Humans; Male; Mast Cells; Microscopy, Electron; Middle Aged

Two groups of volunteers (199 in total, 149 of whom were a random sample of an urban population) were examined twice, with a 6-year interval, for the occurrence of parietal cell antibody (PCA) and thyroid microsomal antibodies (TMA). The antibody findings were compared with the antral and fundal gastric mucosal state, and with the fasting serum gastrin-17 level. During the study period, two new PCA and four new TMA cases appeared. There were no significant changes in the state of gastric antral/fundal mucosa in relation to PCA and/or TMA persistence or appearance, as compared with the gastric mucosa changes in the whole random population sample. However, a good correlation was observed between PCA and basal serum gastrin elevation.

Topics: Adult; Aged; Autoantibodies; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Parietal Cells, Gastric

Analysis of specific features of stomach pathology in 174 patients with various clinical manifestations of chronic glomerulonephritis has demonstrated peculiar nephrogenous gastropathy in these patients. Clinical assessment of the secretion-excretion relationship was carried out in patients with intact renal function and chronic renal insufficiency of various degree of manifestation.

Topics: Chronic Disease; Gastric Mucosa; Gastrins; Gastritis; Glomerulonephritis; Humans; Nephrotic Syndrome

Using radioimmunoassays specific for essential processing sites of human progastrin in combination with chromatography before and after cleavage with trypsin and carboxypeptidase B, we have examined antral biopsy specimens and serum from 10 hypergastrinemic patients with fundic atrophic gastritis and 7 normal control subjects. Four types of processing were studied: N-terminal proteolysis (at the N-terminus of component I, gastrin 34, and gastrin 17); C-terminal proteolysis (at the C-terminus of the amide donor, glycine93 in preprogastrin); alpha-carboxyamidation (of phenylalanine92); and O-sulfation (of tyrosine87). The results show that progastrin during permanent G-cell hypersecretion is less completely processed with respect to C-terminal proteolysis, alpha-amidation, and tyrosine-sulfation. In contrast, the degree of N-terminal proteolysis is normal. Thus, the processing of progastrin adjacent to the active site of gastrin is more restrictively controlled than N-terminal processing during G-cell hypersecretion associated with pernicious anemia.

Topics: Carboxypeptidase B; Carboxypeptidases; Chromatography, Gel; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Protein Precursors; Pyloric Antrum; Radioimmunoassay; Trypsin

The human gastric fundal mucosa contains a variety of endocrine cells, the most numerous of which are the so-called enterochromaffin-like (ECL) cells. We have studied the variations with age and sex of the ECL cell populations, utilizing an assessment based on multiple endoscopic biopsies from four groups of subjects. Plasma gastrin levels were also determined in these subjects. In males, endocrine cell densities declined with age but the ECL cell numbers in females opposed this trend. ECL cell counts showed no appreciable differences between young and old females. In older females, there was a high rate of gastritis and increased levels of circulating gastrin. Concentrations in older females (29.6 +/- 8.7 pmol/l) were higher than in both younger (less than 45 years) males (5.3 +/- 1.1 pmol/l) and older (greater than 55 years) males (6.3 +/- 0.6 pmol/l) (P less than 0.05). The plasma gastrin level was also higher in older females than in young females (13.1 +/- 4.5 pmol/l), although this difference failed to reach statistical significance. In conclusion, clinically silent gastritis, raised gastrin levels, and maintenance or rise of ECL cells numbers, in opposition to a general decrease in endocrine cells with age, appear to be features of women of more than 55 years of age. The variations in ECL cell populations reported here should be taken into account when evaluating possible pathological alterations of the stomach.

Topics: Adult; Age Factors; Aged; Cell Count; Chromaffin System; Enterochromaffin Cells; Female; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Retrospective Studies; Sex Factors

Of 86 cases of aged patients with chronic gastritis treated with Trimebutine or Flutazolam, we evaluated the changes of serum pepsinogen-I and gastrin levels in their clinical courses from the points of the correlation with severity of chronic gastritis, aging phenomenon and the changes of symptom and endoscopic findings. In order to elucidate the multidimensional interrelation among these items, we used Hayashi's quantification theory II as a conventional analysis method. In aged patients, generally, although the serum gastrin levels were rather high compared with younger generation, the serum pepsinogen-I levels were consistently low throughout their clinical courses. There were some correlation between the levels of serum gastrin and the severity of chronic gastritis. When the drugs were effective on improving the condition of the disease, the level of gastrin revealed gradual decrease. These changes of gastrin were more typical in patients treated with Trimebutine.

Topics: Aged; Anti-Anxiety Agents; Benzodiazepines; Benzodiazepinones; Chronic Disease; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Pepsinogens; Trimebutine

We have identified ten children who developed gastritis after prolonged anticonvulsant therapy that included either valproic acid or divalproex sodium. Presenting symptoms were primarily feeding difficulties, including anorexia and refusal to eat. Vomiting was present in two thirds of the patients, with diarrhea, weight loss, and abdominal pain occurring less frequently. Occult blood in stool samples was a late development. All patients responded to therapy with H2-receptor antagonists, oral antacids, or both, with prolonged treatment often necessary to prevent relapse. Although gastrointestinal tract side effects are common with the initiation of valproate sodium therapy, feeding difficulties after long-term treatment are less common. Gastritis should be suspected in children receiving valproate therapy when feeding difficulties arise, particularly if the symptoms are persistent or recurrent.

Topics: Adolescent; Antacids; Anticonvulsants; Child; Child, Preschool; Drug Therapy, Combination; Epilepsy; Female; Gastrins; Gastritis; Histamine H2 Antagonists; Humans; Male; Phenytoin; Valproic Acid

In 40 young patients with chronic renal failure (CRF) on maintenance hemodialysis and 22 control subjects, (1) basal and test meal-stimulated gastrin concentrations, (2) basal and pentagastrin-stimulated gastric acid outputs, and (3) endoscopic examinations were studied. Age-matched CRF patients with control subjects had higher circulating gastrin levels both in the fasting and the test meal-stimulated state and they also had hypochlorhydria. After a test meal, the peak increment of serum gastrin in the CRF patients was more prolonged and greater than in controls. Endoscopic findings showed that the most predominant lesion in the CRF patients was hemorrhagic gastritis. Nine (64.2%) out of 14 patients were hyposecretors and none were hypersecretors. Patients with hyposecretion had higher gastrin levels as well as the same incidence of abnormal endoscopic findings as patients with normosecretion. It is concluded that hypergastrinemia in young CRF patients might be due to a combined effect of impaired renal clearance capacity and overproduction of gastrin associated with hypochlorhydria and also that the cause of gastritis in the young CRF patients might partly be due to a relative impairment of the mucosal defensive mechanism to acid. Our data suggest that the parietal cell response to gastrin in CRF patient may be impaired.

Topics: Adult; Eating; Female; Gastric Juice; Gastrins; Gastritis; Gastroscopy; Humans; Kidney Failure, Chronic; Male; Pentagastrin

Pepsinogen (PG) I and PG II levels were determined in sera from 147 patients with pernicious anemia. Race, sex, age, gastrin level, and antibody status did not influence pepsinogen levels. PG I values less than 30 micrograms/L were found in 92% of cases and PG I to PG II ratios less than 3.0 in 82% of cases. At least one of these two results was abnormal in 97% of all patients with pernicious anemia. In comparison, results of other blood tests used in the investigation of pernicious anemia were less often abnormal. Serum gastrin level exceeded 200 ng/L in 90% of patients with pernicious anemia and was second to pepsinogen abnormality in diagnostic sensitivity. Results for anti-intrinsic factor antibody were positive in 73% of cases and anti-parietal cell antibody in only 52%. Although its specificity is limited, the presence of low PG I level and/or low PG I-PG II ratio is currently the most sensitive serum indicator for pernicious anemia, and absence of both can be taken as a strong argument against the diagnosis. This highly sensitive test can be combined further with the highly specific serum anti-intrinsic factor antibody test for the presumptive diagnosis of pernicious anemia when definitive tests (the Schilling test or gastric analysis for intrinsic factor) cannot be done or results are inconclusive.

Topics: Adolescent; Adult; Age Factors; Aged; Anemia, Pernicious; Autoantibodies; Biomarkers; Child; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Pepsinogens

Topics: Adolescent; Child; Child, Preschool; Duodenal Ulcer; Eating; Gastric Mucosa; Gastrins; Gastritis; Humans

In 15 undialyzed (UD) patients and 26 hemodialyzed (HD) patients, (1) basal and test meal-stimulated gastrin concentrations, (2) basal and pentagastrin-stimulated gastric acid outputs, and (3) endoscopic examinations were studied. Also studied were the morphological and functional differences of the gastrointestinal tract between UD and HD patients. HD patients had lower gastric acid outputs and higher circulating gastrin levels in the fasting state. After a test meal, the peak increment of serum gastrin in UD and HD patients occurred 30 and 60 min later, respectively, and the response was prolonged in each group. Endoscopic findings showed that the incidence of abnormalities in each group was very similar, that is, the most predominant lesions in each group were hemorrhagic and atrophic gastritis. The data suggested that the response to gastrin of parietal cell and the defensive mechanism of gastrointestinal mucosa in HD patients may be impaired.

Topics: Adult; Eating; Female; Gastric Juice; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Gastroscopy; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

Campylobacter pylori may cause gastritis and has been proposed as an etiologic factor in the development of peptic ulcer. However, it may be an acid-sensitive microbe and before it can be implicated in the pathogenesis of peptic ulcer, it should be consistently found in ulcer patients with normal acid secretion. Thirty-six patients with C. pylori by Warthin-Starry stain underwent gastric analysis; 25 were normochlorhydric and 11 hypochlorhydric. Ulcers were present in 19 normochlorhydric patients (10, gastric; 9, duodenal) and 2 hypochlorhydric patients (gastric). Median basal acid output was higher for those with duodenal ulcer (38 mmol/h) than gastric ulcer (28 mmol/h) or miscellaneous endoscopic features (33 mmol/h). The hypergastrinemia seen in 12 patients with negative secretin provocation tests was believed to be due to various nongastrinoma conditions. Campylobacter pylori was found in 6 normogastrinemic patients with elevated acid output and in 1 gastrinoma patient with marked acid hypersecretion. Histologic chronic gastritis was present in all subjects and 29 had active chronic gastritis. Twenty-three patients were taking H2-receptor antagonists at the time of diagnosis which did not seem to interfere with culture results. Using standard acid secretory tests, we conclude that C. pylori can survive in a wide range of acid conditions.

Topics: Adult; Campylobacter; Campylobacter Infections; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Gastritis; Humans; Male; Stomach Ulcer

Conflicting results are reported in the literature on the structure and function of gastric mucosa in patients with chronic renal failure (CRF). In the present endoscopic study of 68 CRF patients on conservative treatment (regular dialyses or transplantations had not yet been undertaken), we sought to clarify whether CRF leads to hypertrophic or hypotrophic phenomena in gastric mucosa, as interpreted by the presence and grade of gastritis and by the thickness of the gastric mucosa. We found that the mean progression of gastritis in both antrum and body was significantly slower than expected in CFR patients, and that the thickness of both antral and body mucosa was significantly lower in CFR patients than in non-CRF controls. Furthermore, although the thickness of the oxyntic body mucosa in CRF showed a positive correlation to serum gastrin (SeGa) levels and even though 12 of the patients showed high SeGa levels corresponding to those seen in the Zollinger-Ellison synbdrome (300-1500 ng/l), the thickness of the oxyntic body mucosa in CRF patients did not exceed that seen in control subjects with normal SeGa. We conclude that CRF exerts inhibitory effects on the gastric mucosa resulting in retardation in the progression of chronic gastritis and hypotrophy of the gastric mucous membrane.

Topics: Adult; Age Factors; Aged; Creatinine; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Kidney Failure, Chronic; Male; Middle Aged; Pyloric Antrum

Two patients with chronic abdominal pain and fasting hypergastrinemia had increases in serum gastrin of 440 and 300 pg/ml after injection of 2 U/kg Secretin-KABI. Both subsequently proved to have pentagastrin-fast achlorhydria. Intragastric instillation of 0.1 N HCl suppressed serum gastrin concentration by greater than 60%. In both, the pancreas was normal by sonography or computed tomography (CT) scan and at laparotomy in one. Both are currently asymptomatic 12 and 18 months later. We conclude that achlorhydria may be associated after injection of Secretin-KABI with a false-positive rise in fasting serum gastrin concentration of greater than 200 pg/ml and that gastric analysis for hypochlorhydria should be performed before secretin provocation testing.

Topics: Achlorhydria; Adult; Chronic Disease; False Positive Reactions; Female; Gastric Acidity Determination; Gastrins; Gastritis; Humans; Middle Aged; Pentagastrin; Secretin

Topics: Adult; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Male; Pyloric Antrum

The authors tried to clarify relations between autoimmune gastritis and isolated atrophic corpus gastritis by bioptic corporal and antral examinations from 150 probands as well as examinations of gastrin in serum and parietal cell antibody tests. Only 30% of all patients examined with isolated atrophic gastritis of the corpus part revealed criteria of an autoimmune gastritis. Therefore investigations of antibodies against parietal cells are necessary to mark off both clinical pictures. This differentiation seems to be necessary regarding the high risk of gastric cancer following an autoimmune gastritis.

Topics: Autoantibodies; Autoimmune Diseases; Biopsy; Fluorescent Antibody Technique; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Gastroscopy; Humans; Parietal Cells, Gastric

Topics: Adolescent; Biopsy; Child; Child, Preschool; Cimetidine; Female; Fiber Optic Technology; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Male

Topics: Adolescent; Child; Child, Preschool; Duodenal Ulcer; Duodenum; Eating; Gastric Mucosa; Gastrins; Gastritis; Humans; Intestinal Mucosa

Topics: Adult; Aged; Calcitonin; Female; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

The prevalence of gastric carcinoid in fundic atrophic gastritis is probably greater than previously recognized. To help elucidate the clinicopathology of this syndrome, we report a series of 11 patients with solitary or multicentric carcinoid tumors. In these patients, basal gastrin levels and density of fundic mucosal endocrine cells were greater than that for patients with uncomplicated fundic atrophic gastritis (p = 0.02 and p = 0.002, respectively). The polypoid tumors, of which the largest measured 30 mm, frequently showed characteristic endoscopic features. They were all situated in the fundic mucosa, which showed micronodular endocrine cell hyperplasia. Small, endoscopically evident tumorlets, or "early carcinoids," limited to the lamina propria were observed in some patients. These lesions may represent intermediate stages between micronodules and invasive carcinoids, all of which infiltrated at least into the muscularis mucosae of the gastric wall. Although some consistent characteristics features were noted, there were structural variations. The cells were argyrophil but nonargentaffin and did not stain with conventional mucus stains. They did not stain significantly for carcinoembryonic antigen (CEA). The secretory product of these tumors remains to be identified. Ultrastructurally, some tumors were mainly composed of enterochromaffinlike (ECL) cells, but in other tumors most of the cells could not be classified.

Topics: Carcinoid Tumor; Endoscopy; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Microscopy, Electron; Prospective Studies; Stomach Neoplasms; Syndrome

Topics: Animals; Gastric Mucosa; Gastrins; Gastritis; Glutamine; Male; Proglumide; Rats; Rats, Inbred Strains; Taurocholic Acid

Morphofunctional studies of parietal and gastrin-producing cells in 30 children with chronic gastroduodenitis with (10 patients) or without (20) recurrent erosions in the pyloroduodenal region showed functional inhibition of G cells and hyperplasia of P cells in the antral part of the stomach in children with recurring erosions. In these children, the increased surface area and density of parietal cells, the increased perimeters of secretory canaliculi's membranes, and the consequent elevated gastric juice acidity were probably due to P-cell hyperplasia in the gastric antrum and G-cell hyperplasia in the duodenal bulb. In children, gastroduodenitis with recurrent erosions should be considered a pathogenetic variant of duodenal ulcerous disease.

Topics: Adolescent; Biopsy; Child; Chronic Disease; Duodenitis; Duodenum; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Microscopy, Electron; Parietal Cells, Gastric; Recurrence

The normal microscopic and gross morphologic features of the stomach are described. Emphasis is given to mucosal anatomy and the recognition of minor alterations seen in disease that may be identified on an endoscopic biopsy. Advice is given in the interpretation of biopsy artefact that may present diagnostic problems. The various types of gastric metaplasia are discussed both in relation to altered morphology and to changes in mucin histochemistry.

Topics: Biopsy; Epithelial Cells; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis; Histamine; Humans; Lymphatic System; Metaplasia; Muscle, Smooth; Pyloric Antrum; Serotonin; Somatostatin; Stomach

It is argued that all chronic gastroduodenal peptic ulcers result from localised increase in mucosal susceptibility to acid attack at the interface between a segment of gastroduodenitis and gastric fundus or duodenal mucosa. The site is predetermined by the background mucosal pattern. Changes can occur in the differentiated gastroduodenal mucosa that closely resemble cell population transformations described in embryology and regeneration biology. A second pathological process, gastroduodenitis, may develop that does not of itself predispose to ulceration, but the combination of factors can produce a zone of increased acid susceptibility. These complex changes could be generated by immunologically activated gastroduodenitis. Destructive or stimulatory immune reactions, analogous to those seen in the thyroid gland, could affect the gastrin-secreting G cells and other paracrine cells. The resulting tropic and inflammatory reactions would provide the background for peptic ulceration.

Topics: Autoantibodies; Chronic Disease; Duodenitis; Duodenum; Gastric Fundus; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Intestinal Mucosa; Parietal Cells, Gastric; Peptic Ulcer; Zollinger-Ellison Syndrome

Serotonin-containing EC cells in human fetal, infantile and adult stomachs both normal and affected by gastritis, were studied by immunohistochemical, electron microscopic and autoradiographic methods. EC cells were sparse in fetal and infantile stomachs, while they occurred in the lower half of the gastric mucosa in adult stomachs showing no atrophic changes and their distribution density was higher than that of D cells. With the progress of chronic gastritis, the number of EC cells gradually decreased, but intestinal type of EC cells appeared in intestinalized gastric mucosa, often showing hyperplasia. Most of EC cells showed argyrophil reaction, but only about 10-20% of them were positive with argentaffin. Epithelial cells with 3H-TdR labeled nuclei were frequently detected in the gastric mucosa where EC cells were sparse or almost absent. Electron microscopically, EC cells had typical electron dense granules in both the normal gastric mucosa and in the intestinal metaplastic glands, but the number of secretory granules was greater in the latter than in the former. These findings suggested that EC cells are preferentially present in the gastric mucosa with a small number of labeled nuclei and have morphological heterogeneity.

Topics: Adult; Aged; Autoradiography; Duodenal Ulcer; Female; Gastric Mucosa; Gastrins; Gastritis; Histocytochemistry; Humans; Infant; Microscopy, Electron; Pregnancy; Serotonin; Somatostatin; Stomach Ulcer

Topics: Adult; Duodenal Ulcer; Endorphins; Gastric Mucosa; Gastrins; Gastritis; Humans; Intestinal Mucosa; Male; Middle Aged; Somatostatin

Clinical and experimental evidence indicates that carcinoid tumours of the stomach fundic mucosa represent another example of hormone-dependent neoplasm, gastrin being the hormone involved in tumour induction. In this context hyperplasia of fundic endocrine cells associated with chronic atrophic gastritis (CAG) and hypergastrinaemia is regarded as the most frequent preneoplastic lesion. However, the cell type involved in this hyperplasia has not been clarified. To elucidate this problem fundic endocrine cells were characterized ultrastructurally in 9 patients from which endoscopic gastric biopsies were obtained. ECL cells were the most frequent cell type in 8 cases, in 4 of which they were more numerous than all other cell types taken together. D1 cells were the most frequent type in one case while they were inconspicuous in the other cases. P cells were found with a frequency in each case intermediate between that of ECL cells and that of D1 cells. These results indicate that fundic endocrine cell hyperplasia occurring in hypergastrinaemic CAG is in most cases cytologically similar to that found in other hypergastrinemic conditions, in which the gastrin-dependent ECL cells were already found to prevail. They also explain why fundic carcinoids arising in CAG are mostly composed of ECL cells. The relation between ECL, D1 and P cells, if any, remains obscure.

Topics: Adolescent; Aged; Biopsy; Carcinoid Tumor; Chronic Disease; Female; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Hyperplasia; Male; Microscopy, Electron; Middle Aged; Precancerous Conditions

In 40 patients with insulin-dependent diabetes mellitus, the number of gastrin cells in the mucous membrane of the antrum of the stomach was measured by immunohistochemistry according to the method of L. Sternberger. The number of the cells depended on the gravity of antral gastritis, namely their number decreased as the lesion was aggravated. The basal level of serum gastrin was determined by radioimmunoassay in 144 patients with insulin-dependent diabetes mellitus. The high basal level of gastrin was recorded in patients with achlorhydria. However, no correlation was established between the gravity of antral gastritis and the basal level of serum gastrin. If the basal gastrin level is too high, the possibility of asymptomatic paresis of the stomach should be taken into account together with the other factors.

Topics: Achlorhydria; Adult; Biopsy; Cell Count; Diabetes Mellitus, Type 1; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Immunoenzyme Techniques; Male; Middle Aged

To demonstrate the immunoreactive alpha-subunit of human chorionic gonadotropin (hCG) or glycoprotein hormones in non-neoplastic gastric mucosa, and to clarify the nature and significance of alpha-subunit-immunoreactive cells, immunohistochemical studies were performed on gastric mucosa using polyclonal antibodies for hCG alpha and beta, hLH beta, hFSH beta, hTSH beta, and gastrin, and a monoclonal antibody for hCG alpha. Surgically resected stomachs were classified as follows: nearly normal (Group A); antral gastritis (Group B); fundic gastritis with pseudopyloric glands (Group C); and intestinal metaplasia (Group D). Cells immunoreactive for the alpha-subunit were present in the pyloric glands and to a lesser extent in the fundic glands (Groups A and B). Almost all alpha-subunit-immunoreactive cells were nonreactive for the beta-subunits of the four glycoprotein hormones. alpha-subunit-immunoreactive cells corresponded to gastrin-containing cells in the pyloric glands, but were unrelated to gastrin in the fundic glands. In fundic gastritis, alpha-subunit-immunoreactive cells appeared to increase (Group C), and many hyperplastic foci were observed in atrophic glands with hyperplasia of the argyrophilic cells (Groups C and D). Isolated hCG alpha or the alpha-subunit of glycoprotein hormones may be present in the endocrine cells of gastric mucosa, and alpha-subunit-immunoreactive cells in the fundic glands seem to proliferate in fundic gastritis.

Topics: Adult; Aged; Chorionic Gonadotropin; Female; Gastric Mucosa; Gastrins; Gastritis; Glycoproteins; Histocytochemistry; Humans; Immunoenzyme Techniques; Male; Middle Aged; Radioimmunoassay

Hypertrophic gastritis, histologically characterized by a depletion of parietal and chief cells and by varying degrees of lymphocyte infiltration along the thickened muscularis mucosa, could be induced by neonatal thymectomy (Tx) without any additional treatment in about 50% of mice (C3H/HeMs X 129/J)F1 (C3.129). The thickness of the mucosa in gastritic mice increased with age, forming giant folds. In Tx mice with an early stage of abnormal mucosal folds at 6 months of age, numbers of parietal cells per mucosal tissue unit area (parietal cell densities) and ratios of parietal cells to mucous cells became lower than in control mice, and serum gastrin levels became contrastingly higher with the increasing severity of gastritis. Circulating antibodies against parietal cells (APA) were detected by indirect immunofluorescence (IFL) in the mice. A good correlation was observed between APA and gastritis: APA with high titers (more than 1,000-fold dilutions) appeared when severe lesions were found. In mice with giant mucosal folds at 18 months of age, serum protein levels were within normal limits, but fecal clearance rates of 125I-labelled polyvinylpyrrolidone (125I-PVP) were significantly increased. These results suggest that the hypertrophic gastritis induced by neonatal Tx is characterized by hypergastrinemia due to parietal cell depletion caused by the presence of circulating APA and the protein loss from the hypertrophic mucosa. Both histological and physiopathological similarities were found between the gastritis in the mice and Menetrier's disease in man.

Topics: Animals; Animals, Newborn; Autoantibodies; Blood Proteins; Disease Models, Animal; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Hypertrophic; Hypertrophy; Immunoglobulin G; Male; Mice; Thymectomy

It has been suggested that gastrin may be a causative factor in the proliferation of gastric fundic mucosal endocrine cells, as seen in the Zollinger-Ellison syndrome and in atrophic gastritis with hypergastrinemia of antral origin. In the present study, morphometrically determined densities of endocrine cells in fundic mucosal biopsy specimens were related to basal levels of serum gastrin in 10 normal controls and 60 patients with achlorhydric fundic atrophic gastritis, of which 45 had pernicious anemia (5 with fundic mucosal carcinoid) and 15 had atrophic gastritis without pernicious anemia. The densities of fundic mucosal endocrine cells were positively related to the levels of serum gastrin (atrophic gastritis, rs = 0.65; atrophic gastritis and normal controls, rs = 0.72). The highest levels of serum gastrin were found in patients with carcinoid tumors (mean, 1659.3 pmol/l), followed by those in patients with focal hyperplasias (cluster formation) of endocrine cells (mean, 503.2 pmol/l) and those in patients without focal hyperplasias (mean, 304.4 pmol/l) (p = 0.03 and p = 0.04, respectively).

Topics: Adult; Aged; Cell Division; Endocrine Glands; Female; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Male; Middle Aged

Topics: Duodenal Ulcer; Gastrins; Gastritis; Humans; Radioimmunoassay; Vagotomy

Gastric biopsies, and measurements of fasting serum gastrin levels and titers of antihuman parietal cell antibodies have been performed in 65 unselected patients with vitiligo. Histologic evidence of autoimmune atrophic gastritis has been obtained in 10 cases (15%), who were all positive for the antibodies and who had elevated gastrin levels. The study of gastric secretion after pentagastrin stimulation, performed in 7 of these patients, showed a markedly reduced acid output. The present study provides definite evidence of the association of autoimmune atrophic gastritis with a proportion of vitiligo cases and suggests the need for surveillance of these patients in terms of gastric neoplasia.

Topics: Adolescent; Adult; Autoantibodies; Autoimmune Diseases; Female; Gastric Acid; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Male; Middle Aged; Vitiligo

Folic acid absorption was studied in 12 elderly subjects with atrophic gastritis and 10 elderly normal controls using tritium-labeled pteroylmonoglutamic acid. Two folic acid absorption tests were carried out on each subject with 120 ml of either water or 0.1 N HCl. Folic acid absorption was significantly lower in subjects with atrophic gastritis than in normal controls (31% vs. 51%, respectively; p less than 0.01). In subjects with atrophic gastritis, folic acid absorption rose significantly to 54% (p less than 0.001) when administered with acid, but did not change in normal controls (50%). Serum folate levels were normal in all subjects. Proximal small intestinal pH was higher in atrophic gastritis subjects than in normal controls (7.1 vs. 6.7, respectively; p less than 0.05), as were bacterial counts of small intestinal fluid (p less than 0.01). Bacteria cultured from the aspirates of subjects with atrophic gastritis were able to synthesize folate in vitro when incubated in a folate-free medium. Atrophic gastritis results in folic acid malabsorption but not in folate deficiency, possibly due to increased bacterial synthesis of folate in the small intestine.

Topics: Aged; Bacteria; Female; Folic Acid; Gastric Acidity Determination; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Hydrogen-Ion Concentration; Intestinal Absorption; Intestinal Mucosa; Intestines; Male; Middle Aged; Pepsinogens

The ratio of pepsinogen I to pepsinogen II in the circulation decreases progressively with increasing severity of atrophic gastritis of the fundic gland mucosa. Fasting blood was obtained from 359 free-living and institutionalized elderly people (age range, 60 to 99 years). A pepsinogen I/pepsinogen II ratio less than 2.9, indicating atrophic gastritis, was found in 113 (31.5%) subjects. The prevalence of atrophic gastritis increased significantly with advancing age (P less than .05). Within the atrophic gastritis group, 84 had a pepsinogen I level greater than or equal to 20 micrograms/L, indicating mild to moderate atrophic gastritis, and 29 had a pepsinogen I level less than 20 micrograms/L, indicating severe atrophic gastritis or gastric atrophy. A significant increase in the prevalences of elevated serum gastrin levels (P less than .005), low serum vitamin B12 levels (P less than .005), circulating intrinsic factor antibody (P less than .005), and anemia (P less than .025) was observed with stepwise increases in severity of atrophic gastritis. Subjects with atrophic gastritis exhibited a lower mean serum vitamin B12 level (P less than .05) and a higher mean folate level (P less than .05), but no difference was detected in mean hemoglobin levels or serum levels of iron, ferritin, retinol or alpha-tocopherol. It is concluded that serum pepsinogen I and pepsinogen II levels can be used to determine the prevalence and severity of atrophic gastritis, that atrophic gastritis is common in an elderly population, and that atrophic gastritis is associated with vitamin B12 deficiency and anemia. Further, higher folate levels in atrophic gastritis may be related to an accumulation of 5-methyl tetrahydrofolate in serum due to vitamin B12 deficiency and/or greater folate synthesis by the intestinal flora resulting from bacterial overgrowth secondary to hypo- or achlorhydria.

Topics: Aged; Aged, 80 and over; Aging; Boston; Female; Gastrins; Gastritis; Gastritis, Atrophic; Hemoglobins; Humans; Intrinsic Factor; Male; Middle Aged; Nutritional Status; Pepsinogens; Vitamin B 12 Deficiency

Topics: Adolescent; Adult; Autoimmune Diseases; Female; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Hyperthyroidism; Immunoglobulin G; Immunoglobulins, Thyroid-Stimulating; Male; Middle Aged; Parietal Cells, Gastric

Topics: Adolescent; Adrenocorticotropic Hormone; Child; Chronic Disease; Duodenitis; Gastric Juice; Gastrins; Gastritis; Growth Hormone; Histamine; Humans

The sulfation of gastrin in serum, antrum and duodenum was studied in 22 normo- and 20 hypergastrinemic patients. The ratio between gastrin-17 and gastrin-34 was measured in antrum and duodenum. The degree of sulfation was reduced in the antrum of hypergastrinemic patients (35.3 +/- 1.3%, mean +/- SEM) compared with 48.0 +/- 2.1% in normo-gastrinemic patients (p less than 0.001). The degree of sulfation in serum and duodenum was similar to that of the antral gastrins in all patients. The percentage of gastrin-34 in antrum was increased (7.3 +/- 0.7%) in hypergastrinemic compared with 4.9 +/- 0.3% in normogastrinemic patients (p less than 0.01). In the duodenum the percentage of gastrin-34 was similar in normo- and hypergastrinemia. When classified according to clinical diagnosis, sulfation of antral gastrin was normal in duodenal ulcer (47.6 +/- 4.5%) but decreased in gastric ulcer (36.7 +/- 1.6%, p less than 0.01) and pernicious anemia (31.3 +/- 1.9%, p less than 0.001) compared with 48.2 +/- 2.2% in control patients. In pernicious anemia a larger proportion of antral gastrins occurred as gastrin-34 (8.2 +/- 0.9%) compared with 4.8 +/- 0.4% in control patients (p less than 0.01). Our study suggests that both sulfation and proteolytic processing of the gastrin precursor is diminished in hypergastrinemia of antral origin.

Topics: Anemia, Pernicious; Duodenal Ulcer; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Protein Precursors; Pyloric Antrum; Radioimmunoassay; Stomach Ulcer; Sulfuric Acids

We determined total gastrin and pepsinogen I in frozen serum samples from 175 overnight-fasted women 54 years old, and from 81 overnight-fasted women 60 years old, who took part in a population study in 1968-69. We also assayed samples from some of these women, who participated in clinical follow-up studies in 1974-75 and 1980-81: all of the women in the initial group whose serum gastrin concentration exceeded the 85th centile value and, as a reference group, a randomized subsample of women whose initial serum gastrin concentration was less than the 80th centile. Samples with total gastrin concentration greater than 400 ng/L were also assayed for gastrin-17 and gastrin-34. We found that: a pronounced increase of serum gastrin persisted throughout the study period for most of these postmenopausal women, indicating that conversion of type A gastritis (antrum-sparing) to pan-gastritis is uncommon; unexplained high concentrations of pepsinogen I in relation to the reference interval for young and middle-aged adults, as well as in relation to serum gastrin, were common; and the gastrin-17/gastrin-34 ratio is not correlated with the outcome of pronounced hypergastrinemia.

Topics: Achlorhydria; Fasting; Female; Follow-Up Studies; Food; Gastrins; Gastritis; Humans; Longitudinal Studies; Middle Aged; Pepsinogens; Sweden

There has not come to any definite conclusion on morphological changes in post-vagotomy gastric mucosa. And, it was reported that duodenogastric reflux in consequence of pyloroplasty or gastroenterostomy could aggravate these gastric mucosal changes. To elucidate this problem, 34 Wistar male rats were subjected to either truncal vagotomy, duodenogastric reflux procedure (transection of the lower part of the duodenum and gastrojejunostomy), or truncal vagotomy with duodenogastric reflux procedure. After 12 weeks, rats were killed for histologic studies of gastric mucosa. Rats subjected to vagotomy with duodenogastric reflux procedure showed marked atrophy of gastric glands, reduction in number of parietal cells and gastrin cells, formation of small ulcer, and generation of heterotopic glands. Rats subjected to duodenogastric reflux also showed chronic ulceration in the prepyloric region on the lesser curvature and hyperplasia of gastric glands. However, no remarkable changes were observed in the stomach of rats with vagotomy. These results indicate that chronic influence of postvagotomy duodenogastric reflux can lead to severe gastritis as well as altered structure of gastric mucosa.

Topics: Animals; Duodenogastric Reflux; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Male; Parietal Cells, Gastric; Postoperative Period; Rats; Rats, Inbred Strains; Vagotomy

A consecutive series of 357 endoscopic gastric biopsies was investigated after staining of histological sections with the Grimelius silver method. Argyrophil cells were classified according to the type of mucosa (fundic, antropyloric or intestinalized) in which they were located. Cases of argyrophil cell hyperplasia detectable on a qualitative basis were selected and their associations with various gastroduodenal disorders of the patients as well as with functional and pathological findings of the gastric mucosa were investigated. Hyperplasia of fundic argyrophil cells was more frequent in patients with atrophic gastritis of the fundic mucosa and a relatively well preserved antral mucosa as well as in patients with hyperplastic polyps. In contrast, it was infrequent in patients with duodenal ulcer and gastric stump. Hyperplasia of antropyloric argyrophil (non-G) cells was most frequent in patients with gastric peptic ulcer or with hyperplastic polyps as well as in those with atrophic gastritis of the fundic mucosa irrespective of the concomitant condition of antral mucosa. Hyperplasia of metaplastic argyrophil cells was more frequent in intestinal metaplasia of the antral mucosa than in that of fundic mucosa. Moreover, it was more frequent in patients with gastric cancer.

Topics: Adolescent; Adult; Aged; Biopsy; Female; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Diseases; Gastroscopy; Humans; Hyperplasia; Intestinal Mucosa; Male; Metaplasia; Middle Aged; Peptic Ulcer; Polyps; Silver; Staining and Labeling; Stomach Neoplasms

Topics: Animals; Gastric Mucosa; Gastrins; Gastritis; Mice; Mice, Inbred BALB C; Pyloric Antrum; Somatostatin; Thymectomy

In this study we have investigated the mucin profile and the endocrine cell population in gastric endoscopic biopsies from 22 patients affected by chronic gastritis and intestinal metaplasia and in five surgical specimens of stomachs removed because of intestinal-type carcinoma (4) or peptic ulcer (1). High iron diamine-Alcian blue (HID-Ab) staining and peptide immunocytochemistry (peroxidase anti-peroxidase technique) were used. Forty-one foci of intestinal metaplasia were detected, 15 produced sulphomucins and 26 sialomucins. Of the endocrine cells investigated, gastrin and somatostatin cells were the most frequently observed, while cholecystokinin, glucose-dependent insulinotropic peptide-, secretin- and enteroglucagon-containing cells were also found in the metaplastic areas, but less frequently. No significant correlation was found between the type of mucin and the types of endocrine cells present, the latter usually resembling those normally found in the small intestine. On the basis of these results we conclude that intestinal metaplasia involves mucin- and peptide-producing cells of the stomach in a variable manner, with no correlation between the two.

Topics: Adult; Cholecystokinin; Gastric Inhibitory Polypeptide; Gastric Mucosa; Gastrins; Gastritis; Glucagon-Like Peptides; Humans; Immunoenzyme Techniques; Intestines; Metaplasia; Middle Aged; Mucins; Secretin; Somatostatin

In the present study we used the highly sensitive avidin-biotin complex technique (ABC) for detection of gastrin cell (G cell) autoantibodies. Serum samples were studied from 56 patients with histologically proven antral gastritis, 20 adult subjects with histologically proven normal antral and fundal mucosa and from 25 healthy children. The presence of G cell autoantibodies was assessed by both immunofluorescence (IFL) and the ABC-peroxidase method, using sections from paraformaldehyde-lysine-periodate fixed and paraffin embedded human antral mucosa as antigen. Other organ specific and non-organ specific autoantibodies were demonstrated with IFL. Using the ABC method, G cell autoantibodies were found at a dilution of 1:100 in nine of 56 sera with antral gastritis. One of the control sera was positive. The ABC method was considered superior to IFL in demonstrating G cell antibodies, since positively stained G cells could be easily distinguished from the histiocytic cells in lamina propria which sometimes give false positive staining. Furthermore, higher antibody titres results in the ABC method. Thus it is suggested that by analogy to fundal gastritis, some cases of antral gastritis may have autoimmune aetiology.

Topics: Adult; Aged; Autoantibodies; Avidin; Biotin; Child; Female; Fluorescent Antibody Technique; Gastric Mucosa; Gastrins; Gastritis; Humans; Immunoenzyme Techniques; Male; Middle Aged; Pyloric Antrum

The occurrence of tissue autoantibodies in relationship to fundal and antral gastritis was examined in an Estonian rural population sample, consisting of 227 persons 15 to 69 years of age. The state of the gastric mucosa was verified with multiple biopsy specimens obtained at direct-vision gastroscopy. Isolated fundal gastritis was characterized as the presence of parietal cell (PCA) and/or thyroid antibodies. PCA was seen only in persons with normal antral mucosa. On the other hand, gastrin cell antibodies (GCA) showed no correlation to the extent of antral gastritis, being seen in normal antrum or in superficial or slight atrophic gastritis but not in moderate or severe gastritis. The findings of our present study thus strengthen the view that the occurrence of PCA is mainly limited to isolated fundal gastritis and excludes the occurrence of antral gastritis. On the other hand, an association of GCA and antral gastritis could not be established.

Topics: Adolescent; Adult; Aged; Autoantibodies; Estonia; Female; Fluorescent Antibody Technique; Gastric Mucosa; Gastrins; Gastritis; Humans; Immunoenzyme Techniques; Male; Middle Aged; Parietal Cells, Gastric; Rural Population; Thyroid Gland

Topics: Adult; Atrophy; Female; Gastrins; Gastritis; Humans; Myxedema; Stomach

A method for measurement of gastrin in human antral mucosa or in extragastric tissue has been developed and validated. Tissue gastrin was extracted by boiling followed by homogenization at neutral pH. Extractable gastrin immunoreactivity was measured by radioimmunoassay using an antiserum with equal affinity towards G-17 I, G-17 II, G-34 I and G-34 II molecular forms. Almost all extractable gastrin immunoreactivity was recovered after a single extraction and no significant interference by other peptides and/or substances present in tissue was found. The mean gastrin concentration in antral mucosa of healthy subjects was similar to that observed in duodenal ulcer patients, while patients with type A chronic atrophic gastritis or with antral gastrin cell hyperplasia had mean values significantly higher. Gastrin concentration in all specimens from gastrinoma or its metastases was above the upper limit of the range of control tissue. Measurement of tissue gastrin seems to be a valuable tool in the diagnosis of antral gastrin cell hyperplasia and Zollinger-Ellison syndrome.

Topics: Adolescent; Adult; Aged; Cholecystitis; Chronic Disease; Duodenal Ulcer; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Hyperplasia; Male; Middle Aged; Pancreatic Neoplasms; Pyloric Antrum; Zollinger-Ellison Syndrome

The effects of proximal selective vagotomy (PSV) on parietal cell morphology and the degree of gastric inflammation were investigated and correlated with changes in gastric acid secretion and serum gastrin concentrations in 17 duodenal ulcer patients. Endoscopy, acid secretion tests, and blood sampling were performed preoperatively and 2 months, 1 year, and 3 years postoperatively. The mucosal biopsy specimens obtained at endoscopy were analyzed both light- and electron-microscopically. Five healthy persons also underwent gastroscopy and biopsy for comparison. Preoperatively, the duodenal ulcer patients differed significantly from this control group, 33% of whose parietal cells appeared 'secretory'; the corresponding figure for the duodenal ulcer patients was 47%. Two months after the operation the number of secretory parietal cells had fallen to 30%, after which the percentage increased slightly again to 35% 3 years after PSV. A similar phenomenon was observed in the acid secretion capacities, which were maximally depressed 2 months postoperatively and recovered slightly but significantly during the 3-year follow-up period. There was a significant increase in the degree of gastric inflammation after the operation.

Topics: Adult; Aged; Duodenal Ulcer; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Parietal Cells, Gastric; Vagotomy; Vagotomy, Proximal Gastric

The authors analyzed 380 autopsies for chronic glomerulo- and pyelonephritis and studied the clinical and functional features of gastric pathology in 240 patients with the same disease entities. The hypotheses are suggested about a 3-stage successive formation of uremic gastropathy. The importance of hypergastrinemia as one of the pathogenetic factors, as a vicarious organ as regards nitrogenous products at early stages of chronic renal insufficiency is discussed.

Topics: Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Hydrogen-Ion Concentration; Urea; Uremia

The gastric mucosa of 19 mongrel dogs was submitted to a bilio-pancreatic, isolated biliary or isolated pancreatic reflux. With an isolated biliary reflux, there is a more rapid and more severe hyperaemia and foveolar hyperplasia of the mucosa of the fundus than with an isolated pancreatic reflux. There was no significant change in the basal serum level of gastrin with any of these different types of alkaline reflux, but we observed a statistically significant increase in the level of histamine in the gastric mucosa. Hyperaemia and foveolar hyperplasia of the fundic mucosa both disappeared when the alkaline reflux was suppressed, and there was a statistically significant decrease in the basal serum level of gastrin and in the level of histamine in the gastric mucosa.

Topics: Animals; Bile Reflux; Biliary Tract Diseases; Dogs; Duodenogastric Reflux; Gastric Mucosa; Gastrins; Gastritis; Gastrostomy; Histamine; Hyperemia; Jejunum; Time Factors

Maximal acid outputs were determined during intravenous pentagastrin tests (6 micrograms/kg/h) in 119 male subjects: 17 controls, 74 patients with duodenal ulcer and 28 with atrophic gastritis. Basal and postprandial serum gastrin levels were also determined in order to estimate the integrated gastrin response to the meal. In patients with atrophic gastritis the maximal acid output was decreased (p less than 0.01) and the integrated gastric response was increased (p less than 0.01) but the basal gastrin levels in these patients did not differ from that of controls. An integrated gastrin response greater than 2.5 ng/ml/100 min was observed in 89 p. 100 of patients with atrophic gastritis. An integrated gastrin response smaller than 2.5 ng/ml/100 min was observed in 76 p. 100 of controls. The maximal acid output was smaller than 20 mmol/l in all patients with atrophic gastritis but was greater than this value in all controls. In duodenal ulcer patients, the measured parameters were not significantly different from control values. The measure of the integrated gastrin response which reflects the presence of an antral endocrine hyperactivity may be useful to detect patients with atrophic gastritis, but this test is less sensitive and less specific than the determination of the maximal acid output.

Topics: Duodenal Ulcer; Eating; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Male; Pentagastrin

Topics: Animals; Female; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Male; Mice; Mice, Inbred BALB C; Somatostatin

Topics: Animals; Atrophy; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Male; Neoplasms, Experimental; Pilot Projects; Rats; Rats, Inbred Strains; Stomach Neoplasms

In 118 patients with histological proven chronic gastritis, was performed a study of seric antibodies against parietal cells (ACCP), following the indirect inmuno-fluorescence method. The results were positives in 36 cases (30%). Four positives cases were found in 40 normal controls (10%), two of them were compensated diabetics, one have the thyrohyoid Hashimoto's disease, and the remainder, brother of a patient with chronic gastritis, was a positive ACCP. A major positiveness (44.4%) was obtained in 9 cases of gastric atrophy than in 65 cases with atrophic gastritis (32%) and in 44 cases of superficial gastritis (25%); although due to the few cases of gastric atrophy regarding other histological types, conclusions cannot be obtained about the incidence of ACCP and histological variety of chronic gastritis. If we do group the patients according to their acid secretory debit, 53 achlorhydric patients had a positiveness of ACCP of 45%, while over 63 with decreased secretory capability, only 18.4%, was positive. The distribution by age groups, shows a major incidence of ACCP about the 4th and 5th decade of life. Thirty seven patients with chronic atrophic gastritis and achlorhydria, and seven with chronic superficial gastritis and hypochlorhydria, besides the antibodies study were on a basal dosage of gastrinemia and antral endoscopic biopsy, finding out that, achlorhydric patients (15 on 19) with normal or slightly altered antrus, have gastrinemia (222 +/- 123 Pgo/oo) and the majority of patients with normal gastrinemia (32 +/- 16 pgo/oo) have more important antral lesions. The ratio between antral histology and ACCP in auto--immune gastritis (Type A), conciliates only partially with the observation by Strickland et al., as only 52.4% of achlorhydric patients and ACCP have a normal antrus or al least with mild lesions. Our results suggest the possibility of that on auto--immune gastritis could act other pathogenic factors of antral lesion.

Topics: Adult; Aged; Autoantibodies; Autoimmune Diseases; Chronic Disease; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Pyloric Antrum

Topics: Chronic Disease; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Stomach Neoplasms

Factors that may influence the magnitude of the gastrin response to a test meal have been examined in vitro by use of isolated sheets of antral mucosa obtained from 78 patients who underwent gastric resection. The amount of immunoreactive gastrin (IG) released during stimulation with the luminal pH at 7.4 increased linearly with the passage of time and stopped abruptly when the luminal pH was lowered to 2.5. The rate at which IG was released by the same stimulus at pH 7.4 was linearly related to the IG content in antral tissue (r = 0.66). The IG content in antral tissue increased during stimulation in vitro (10.05 +/- 2.09 to 19.77 +/- 3.38 pmol/mg tissue protein, P less than 0.03). These in vitro data suggest that the magnitude of the gastrin response to a test meal may be indicative of the IG content in antral tissue provided that: the tissue is in an unstimulated state when the stimulus is applied; the stimulus is applied for a standard span of time; the stimulus is applied to the antrum alone; and the inhibitory effects of acid are prevented by clamping the intraluminal pH at 7.4.

Topics: Acetylcholine; Antigens; Arginine; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Glycine; Humans; Hydrogen-Ion Concentration; In Vitro Techniques; Pyloric Antrum; Radioimmunoassay

The concentration of the NH2-terminal fragment of gastrin-17 in serum was determined by radioimmunochemistry. Two antisera were used, one specific for the COOH-terminus and the other for the NH2-terminus of gastrin-17. The NH2-terminal gastrin-17 immunoreactivity in unfractionated serum correlated well with the amount of fragment found after gel filtration of the same sera (p less than 0.001). In healthy subjects (no. = 100), the NH2- and COOH-terminal gastrin immunoreactivity was 8 +/- 1 and 20 +/- 1 pmol/l (mean +/- SEM), respectively. In patients with acute duodenal ulcer (no. = 30) and acute gastritis (no. = 10) the NH2-terminal immunoreactivity was fourfold increased compared with in healthy subjects (p less than 0.001), whereas the COOH-terminal was identical, the NH2- and COOH-terminal concentrations being 33 +/- 7 and 22 +/- 2 pmol/l in duodenal ulcer and 35 +/- 6 and 21 +/- 1 pmol/l in acute gastritis. Other groups of patients had NH2- and COOH-terminal gastrin concentrations in serum similar to those measured in healthy subjects. The results suggest that gastrin cells process gastrin-17 abnormally during the acute phase of duodenal ulcer and gastritis.

Topics: Acute Disease; Adolescent; Adult; Aged; Amino Acid Sequence; Chromatography, Gel; Duodenal Ulcer; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Peptide Fragments; Radioimmunoassay

The gastrin-producing G-cells of the antropyloric mucosa are affected by a variety of disorders. By immunoperoxidase methods, employing a specific anti-gastrin I and II antibody, we demonstrated G cells in antropyloric biopsies of 15 patients with chronic gastritis, 6 of them with gastric ulcer and 1 with duodenal ulcer disease. As controls we studied 5 biopsies of histologically normal antropyloric mucosa. We correlated the numbers of G cells per gland with the histological, clinical and endoscopic findings. Normal antropyloric mucosa contained a mean of 2.11 G cells per gland. Patients with chronic gastritis had decreased numbers of G cells (mean 0.75) The difference was statistically significant. The cases with chronic gastritis and intestinal metaplasia had lower numbers of G cells (mean 0.38). The case with duodenal ulcer had a number of G-cells similar of normal cases (1.57). This finding give a morphologic basis for the low gastrin serum levels usually present in these entities.

Topics: Adult; Gastric Mucosa; Gastrins; Gastritis; Humans; Middle Aged

Two brothers with pachydermoperiostosis, an autosomal dominant syndrome characterized by digital clubbing, periosteal new bone formation, coarse facial features with thick, furrowed, and oily skin, presented in their twenties with severe complicated duodenal ulcer disease requiring multiple operations. Their father and one paternal uncle also had pachydermoperiostosis and a past history of ulcer dyspepsia. The mother, one sister, two maternal aunts, and one other paternal uncle were healthy. Both brothers had giant hypertrophic gastritis (Ménétrier's disease). Their pentagastrin-stimulated acid output and fasting and meal-stimulated serum gastrin levels were normal, but their serum pepsinogen I and II levels were markedly elevated. The father had hypochlorhydria and a low serum pepsinogen I/II ratio, suggesting atrophic gastritis. This family study raises the possibility that pachydermoperiostosis, hypertrophic gastropathy, and peptic ulcer may be genetically related.

Topics: Adult; Aged; Dyspepsia; Facial Expression; Female; Gastric Acidity Determination; Gastrins; Gastritis; Gastritis, Hypertrophic; Genes, Dominant; Humans; Male; Middle Aged; Osteoarthropathy, Primary Hypertrophic; Pepsinogens; Peptic Ulcer; Skin Diseases; Syndrome

We tested the validity of the concept that chronic atrophic gastritis can be subdivided into type A and B in hospital patients and normal subjects with proven pentagastrin-refractory achlorhydria. Classification was based on the determination of the basal serum gastrin and parietal cell antibodies. Of 59 hospital patients with achlorhydria, 71% could be classified as belonging to either type A or B; for 29% the criteria for neither type were fulfilled. Of 14 asymptomatic persons with achlorhydria found in 564 normal persons, five could be classified as having type A gastritis, and one as type B gastritis. In eight (53%) persons, an elevated serum gastrin was found in the absence of parietal cell antibodies, representing an intermediate type of atrophic gastritis. Because one-third of the hospital patients and more than half the persons with achlorhydria in a normal population had to be classified as belonging to an intermediate type, the discrimination between type A and B atrophic gastritis in achlorhydria seems to be of limited practical value.

Topics: Achlorhydria; Antibodies; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans

The number of G- and D-cells per area and the ratio of G/D-cells were investigated in biopsy specimens of the pyloric antrum from normochlorhydric subjects without peptic ulcer, from patients with duodenal ulcer, gastrinoma, pernicious anaemia, and after selective proximal vagotomy. Compared with normochlorhydric subjects antral G-cell density was significantly raised in pernicious anaemia, unchanged in duodenal ulcer, and diminished in gastrinoma patients. After vagotomy G-cell density was found to be raised if compared with patients with duodenal ulcer. D-cell density was significantly increased in gastrinoma patients, unchanged in duodenal ulcer, and diminished in pernicious anaemia and after vagotomy. The G/D-cell ratio was increased in pernicious anaemia and after vagotomy, unchanged in duodenal ulcer, and decreased in gastrinoma patients. It is concluded that the antral pH governs the ratio of G- and D-cells. Therefore, the G/D cell ratio increases in states of reduced acid secretion and decreases in massive hyperchlorhydria. Hypergastrinaemia as such does not affect the G/D-cell ratio.

Topics: Adult; Anemia, Pernicious; Cell Count; Duodenal Ulcer; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Pyloric Antrum; Somatostatin; Vagotomy, Proximal Gastric; Zollinger-Ellison Syndrome

Topics: Adrenocorticotropic Hormone; Chronic Disease; Dietary Proteins; Duodenal Ulcer; Fasting; Female; Gastrins; Gastritis; Humans; Insulin; Male; Middle Aged; Time Factors

Topics: Cell Division; Female; Gastrins; Gastritis; Humans; Immunoenzyme Techniques; Male; Microscopy, Electron; Middle Aged; Peptic Ulcer; Pyloric Antrum

Topics: Adult; Aged; Antibodies; Female; Gastrins; Gastritis; Gastritis, Atrophic; Gastroscopy; Humans; Male; Microscopy, Electron; Middle Aged

Topics: Adult; Aged; Female; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Pyloric Antrum; Stomach Neoplasms

Topics: Cell Count; Chromaffin System; Enterochromaffin Cells; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Pyloric Antrum

Topics: Anemia, Pernicious; Female; Gastric Acid; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Male; Mass Screening; Pepsinogens

Topics: Adult; Aged; Antibodies; Female; Gastric Mucosa; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Male; Middle Aged

Measurements of basal and stimulated gastric acid secretion, serum gastrin, and serum pepsinogen I cannot replace direct radiologic and endoscopic examination of the gastroduodenal mucosa for diagnosis of peptic ulcer disease, or histological examination for classification of gastritis and duodenitis. These tests, however, can provide information about the functional status of the gastric mucosa and sometimes indicate the etiology of gastric acid hypersecretion. The most diagnostic combination of tests comprises markedly increased fasting serum gastrin, positive serum gastrin response to secretin challenge, and increased levels of basal acid secretion and serum pepsinogen I found in patients with gastrinoma. The same combination of results, except for negative response to secretin and marked stimulation of gastrin by food, is found in patients with antral gastrin cell hyperfunction. Increased serum gastrin concentrations often are found in patients with hyposecretion of gastric acid, including those with atrophic gastritis, and in patients with renal failure, or previous vagotomy. Patients with atrophic gastritis have a low serum pepsinogen I level, while an increased level is found with renal failure and a normal level is found after vagotomy. Thus, the concurrent measurement of serum pepsinogen I and creatinine provides a useful initial step in the evaluation of hypergastrinemia.

Topics: Creatinine; Duodenitis; Gastric Acid; Gastrins; Gastritis; Humans; Pepsinogens; Peptic Ulcer; Radioimmunoassay; Secretin

Topics: Adolescent; Adult; Aged; Aging; Autoantibodies; Complement System Proteins; Female; Gastric Emptying; Gastrins; Gastritis; Gastritis, Atrophic; HLA Antigens; Humans; Hypersensitivity, Delayed; Leukocyte Count; Lymphocytes; Male; Middle Aged; Phenotype; Skin Tests

Topics: Adolescent; Adult; Female; Gastrins; Gastritis; Humans; Hyperthyroidism; Isoproterenol; Male; Middle Aged; Propranolol; Receptors, Adrenergic; Receptors, Adrenergic, beta

Endoscopy of the upper gastrointestinal tract was performed on 84 patients with end-stage chronic renal failure undergoing hemodialysis. Gastric acid secretion and fasting plasma gastrin levels were also examined in these patients. Hemorrhagic gastritis was most frequently observed (23 cases) followed by erosive gastritis (18 cases). No patients had gastric ulcers. Duodenal ulcers were observed in only two patients. Gastrointestinal bleeding was observed in 15 cases (17.9%). Thirteen of these 15 cases had hemorrhagic gastritis, one of which had a duodenal ulcer as a complication. Fasting plasma gastrin levels (359.6 +/- 336.5 pg/ml) were significantly higher than those of normal subjects (35.2 +/- 37.1 pg/ml), but no acceleration in gastric acid secretion was observed either in the basal condition (BAO 0.8 +/- 0.7 mEq/h) or following tetragastrin stimulation (MAO 9.0 +/- 6.9 mEq/h). Our results were inconsistent with the previous reports that high frequencies of peptic ulcers and increased gastric acid secretion were observed in patients with chronic renal failure. Our data suggest that the defensive factors rather than the aggressive factors of the gastroduodenal mucosa may be involved in chronic renal failure.

Topics: Adolescent; Adult; Aged; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Gastroscopy; Humans; Kidney Failure, Chronic; Male; Middle Aged

Topics: Child; Chronic Disease; Duodenitis; Fasting; Feeding Behavior; Female; Gastrins; Gastritis; Humans; Insulin; Male; Peptic Ulcer; Time Factors

Topics: Adenocarcinoma; Gastrins; Gastritis; Humans; Peptic Ulcer; Radioimmunoassay; Stomach Neoplasms

Previous studies of gastric secretory function and serum gastrin levels in patients with chronic renal failure (CRF) have yielded conflicting results. In a study of 30 patients on regular hemodialysis, serum gastrin levels were higher than normal (p less than 0.05), and the gastric secretory response to pentagastrin was normal for the group as a whole. There were, however, 8 patients who were hypochlorhydric (4 achlorhydric) and 7 who were hyperchlorhydric. The patients with gastric hyposecretion were older, predominantly male and this group was associated with the highest gastrin levels as well as the highest incidence of gastrointestinal hemorrhage. Chronic gastritis is thus more common in CRF than generally believed and may be responsible for much of the morbidity from gastrointestinal complications during hemodialysis.

Topics: Adolescent; Adult; Female; Gastric Juice; Gastrins; Gastritis; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

Topics: Adult; Alcoholism; Female; Gastrins; Gastritis; Humans; Male; Middle Aged

The hypothesis that reflux of upper intestinal content, particularly of bile acids (BA), is responsible for a unique postgastrectomy syndrome, alkaline reflux gastritis, was tested on 28 occasions in 21 postoperative patients (14 symptomatic patients, 7 controls). Parameters evaluated: recumbent (rec.), upright, p.c. intragastric pH, {BA}, net BA reflux per hour, specific BA fractions, fasting and p.c. gastrin, maximal acid output (MAO), gastric emptying of solids by delta-scintigraphy), and the severity of nonstomal histologic gastritis, the "gastritis score," graded 0-15 by an independent senior pathologist. For the entire group, gastritis severity correlated positively with intragastric {BA} and net BA reflux per hour, both in recumbency and p.c. Five symptomatic patients demonstrated rec. and p.c. {BA} and net BA reflux per hour greater than two standard deviations from comparable mean values in control patients. They differed significantly from the remaining symptomatic patients as follows: increased intragastric {BA} and net BA reflux per hour, increased intragastric pH and decreased MAO. They also demonstrated a more severe grade of gastritis. Lithocholic acid was present in their reflux content significantly more often. Bilious vomiting was also more frequent. No other differences could be identified, either objectively or clinically, between the symptomatic groups. Four patients with excessive reflux underwent Roux-en-Y revision and restudy 6-22 months later. BA reflux was completely abolished, histologic gastritis improved, hematocrit rose, MAO increased, and gastric emptying slowed. Burning pain, bilious vomiting, and symptoms of esophageal reflux were eliminated. Vomiting and nausea were improved. Diarrhea was unchanged. The objective criteria outlined can identify symptomatic postgastrectomy patients with a greater than normal reflux and gastritis. Clinical criteria alone cannot. Revisional surgery in these patients eliminates reflux, improves gastritis, and produces symptomatic improvement. The hypothesis under consideration is strengthened but not proven.

Topics: Adult; Bile Acids and Salts; Female; Gastric Acid; Gastric Emptying; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Postgastrectomy Syndromes

Hypergastrinaemia was found in 11 out of 24 untreated hyperthyroid patients (Graves' disease or nodular goitre). Seven patients had a co-existent (autoimmune) atrophic gastritis. In the remaining 17 patients plasma T3 was positively related to plasma gastrin, and negatively to gastric acid output; there was no relation between gastrin levels and acid output. Acid instillation into the stomach revealed a normal negative feedback of acid upon gastrin release. Sixteen hyperthyroid patients were restudied when euthyroid. Plasma gastrin decreased from 171 (51-1188) ng/l before treatment to 69 (39-392 ng/l after treatment (P < 0.002), and maximal acid output increased from 1.55 (0.00-22.75) to 8.03 (0.00-26.60) mmol H+/h (P < 0.01) (median values; range in brackets). However, in 4 patients with complete achlorhydria before and after treatment plasma gastrin decreased to the same extent as in the patients with gastric acid secretion. We conclude that thyrotoxic hypergastrinaemia cannot be fully explained by the low gastric acid output in hyperthyroidism.

Topics: Adult; Aged; Female; Gastric Acid; Gastrins; Gastritis; Humans; Hyperthyroidism; Hypothyroidism; Male; Middle Aged; Thyroid Hormones

Topics: Adult; Aged; Cell Count; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Male; Middle Aged; Pyloric Antrum

Topics: Adult; Female; Gastrins; Gastritis; Gastritis, Hypertrophic; Humans; Stomach

Topics: Adult; Chronic Disease; Dyspepsia; Female; Gastrins; Gastritis; Gastritis, Atrophic; Humans; Male; Middle Aged; Renal Dialysis; Uremia

Gastric function and histology were investigated in 24 patients with untreated chronic renal failure. At endoscopy nine patients had oesophagitis, 12 patients were considered to have gastritis, and the duodenum appeared inflamed in 20 patients. Endoscopic biopsies were taken at standard sites in the stomach and duodenum; gastritis was found in all patients, and 17 patients had duodenitis. Stimulated acid secretion was impaired in seven out of 20 patients and acid hypersecretion was found in a further two patients. Pepsin output correlated well with acid output in these patients. Fasting serum gastrin levels were elevated in 12 of the 19 patients tested. Patients with atrophic gastritis had low acid outputs and hypergastrinaemia, and when extensive gastritis was present, the patients tended to have more severe renal failure and hyposecretion of acid. Three patients were studied again after regular haemodialysis or renal transplantation and were found to show marked endoscopic and histological improvement.

Topics: Adult; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Intestinal Mucosa; Kidney Failure, Chronic; Male; Middle Aged; Pepsin A; Renal Dialysis

Autoantibodies that react exclusively with the gastrin-secreting cell of human antrum have been detected by immunofluorescence in eight of 106 patients with histologic evidence of chronic atrophic gastritis, Type B, involving mainly the antrum. These antibodies were of the IgG class and of low titer. However, follow-up studies one to two years later showed persistently positive reactions, despite symptomatic treatment. These data support the concept of an autoimmune variant of chronic "antral" gastritis, Type B.

Topics: Adult; Aged; Atrophy; Autoantibodies; Autoimmune Diseases; Chronic Disease; Female; Fluorescent Antibody Technique; Follow-Up Studies; Gastrins; Gastritis; Humans; Immunoglobulin G; Male; Middle Aged; Pyloric Antrum

Topics: Brunner Glands; Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Intestinal Mucosa; Kidney Transplantation; Postoperative Complications; Transplantation, Homologous

Topics: Atrophy; Fluorescent Antibody Technique; Gastric Mucosa; Gastrins; Gastritis; Humans

The histological changes and gastric function alterations in 19 patients who had intrathoracic stomach replacement following esophagectomy were studied. Atrophic gastritis was noted in 13 of the 19 patients. The mechanical response of the stomach to distention by food was largely retained. The basal and maximal acid output was reduced markedly, and the serum gastrin was elevated. An association between the degree of gastritis, the percentage of gastric motility at rest, and acid secretion is demonstrated. These changes are consistent with patients with duodenal ulcer following vagotomy and dyloroplasty. Postprandial elevation in serum gastrin was noted in patients with or without vagotomy. The lack of significant difference in integrated gastrin response suggests that the vagus may not be important in the control of postprandial gastrin release.

Topics: Adult; Aged; Biopsy; Esophageal Neoplasms; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Motility; Humans; Male; Metoclopramide; Middle Aged; Pentagastrin; Secretory Rate; Stimulation, Chemical; Stomach; Vagotomy

Parietal cell autoantibody (PCA), basal gastrin, and calcium-stimulated gastrin were measured in twenty patients with achlorhydria, in eight patients with the Zollinger-Ellison syndrome, and in fifty control subjects. In twelve patients with achlorhydria with a spared antrum, PCA was positive and basal gastrin was elevated. In contrast, eight achlorhydric patients with antral gastritis had negative PCA and significantly lower basal gastrin levels. Patients with the Zollinger-Ellison syndrome did not demonstrate positive PCA despite elevated levels of basal gastrin, nor was PCA present in normal controls. This study suggests that certain achlorhydric states are caused by an autoimmune response, particularly if antral function is spared.

Topics: Achlorhydria; Anemia, Pernicious; Autoantibodies; Calcium; Gastrins; Gastritis; Humans; Stomach; Zollinger-Ellison Syndrome

To determine the effect of varying degrees of gastritis on the distribution of immuno-reactive gastrin cells 38 partial gastrectomy specimens have been studied. Routinely stained histological sections of mucosa were compared with serial and adjacent sections stained by specific immunohistochemistry using peroxidase and fluorescent techniques. While chronic superficial gastritis had no obvious effect, mild atrophic gastritis was associated with an uneven distribution of gastrin cells which became more marked with increasing severity of gastritis. In the region of intestinal metaplasia gastrin cells were almost totally absent. Small numbers of gastrin cells were found within areas of pseudopyloric metaplasia in the fundus, a region where those cells are not normally seen. Similarly, gastrin cells were detected within regenerative gastric polypi in both antrum and fundus.

Topics: Chronic Disease; Gastric Mucosa; Gastrins; Gastritis; Humans; Metaplasia; Pyloric Antrum

Gastric morphology, function, and immunology was studied in 68 patients with pernicious anemia (PA), 183 of their first-degree relatives, and 354 control subjects. The PA relatives and controls were comparable in age and sex distribution. In both groups, mean gastric acid output decreased and mean fasting serum gastrin levels and the prevalence of atrophic gastritis increased with age. The total prevalence of chronic gastritis was similar in the two groups, but severe atrophic gastritis of the body of the stomach (AGB), achlorhydria, parietal cell antibodies, and a raised fasting serum gastrin level were significantly more common in PA relatives than in controls. Of the PA relatives 23 had severe AGB which was indistinguishable from the gastric mucosal lesion found in PA probands and was, as a rule, accompanied by several other characteristics of type A gastritis. These included a normal antrum (78%), slight or absent inflammatory cell infiltration in the gastric mucosa (70%), achlorhydria (91%), high fasting serum gastrin level (83%), parietal cell antibodies (65%), and intrinsic factor antibodies (22%). The mean age and the proportion of subjects with slight and moderate AGB of all AGB subjects was significantly lower in PA relatives than in controls. This suggests an early onset and a rapid progression from mild to severe AGB in PA relatives. Thus, the PA relatives appear to consist of two populations, one with a high and one with little or no proneness to severe AGB. This bimodal distribution suggests the participation of a single major factor, probably genetic, in the pathogenesis of severe AGB in PA relatives.

Topics: Adolescent; Adult; Age Factors; Anemia, Pernicious; Atrophy; Autoantibodies; Consanguinity; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Intestines; Intrinsic Factor; Male; Metaplasia; Middle Aged; Pyloric Antrum; Vitamin B 12

Seventeen of 37 healthy volunteers participating in studies of acid secretion and 1 patient with Zollinger-Ellison syndrome became rapidly and profoundly hypochlorhydric. A mild illness with epigastric pain occurred in 9 subjects, usually several days before detection of hypochlorhydria. Gastric mucosal biopsy specimens taken from subjects during hypochlorhydria revealed severe fundal and antral gastritis; however, even when acid secretion was severely depressed, parietal cells were abundant and appeared normal histologically. During hypochlorhydria, gastric permeability to hydrogen, sodium, and lithium was normal in 4 subjects. Serum gastrin concentrations were usually normal, whereas serum pepsinogen concentrations were invariably elevated. Serum parietal cell antibodies were not present. Acid secretion returned to near baseline levels in 14 of 17 subjects after a mean of 126 days (range 53--235); severity of gastritis diminished concurrently in 7 of 10 subjects on whom biopsies were serially performed. An infectious etiology is suspected, although serologic studies and bacterial and conventional viral cultures of stool and gastric juice have not identified a candidate agent.

Topics: Achlorhydria; Adult; Aged; Dietary Proteins; Disease Outbreaks; Female; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Pepsinogens; Pyloric Antrum; Zollinger-Ellison Syndrome

The sensitivities, specificities, and predictive values of parietal cell antibody, serum gastrin, and serum pepsinogen I (PG I) for severe atrophic gastritis of the oxyntic gland mucosa have been determined in 171 first-degree relatives of 62 patients with pernicious anemia. Parietal cell antibody had the lowest sensitivity (65%), specificity (87%), and predictive value (44%). A low serum PG I and a high serum gastrin had identical specificities (97%), and similar predictive values (84 vs 83%), but the sensitivity of a low serum PG I was greater than that of a high serum gastrin (91 vs 83%). Parietal cell antibody was found in 19 of 148 relatives without severe atrophic gastritis and occurred as an isolated finding in 17. In contrast, 14 of the 15 relatives with severe atrophic gastritis who had parietal cell antibody also had a high serum gastrin and a low serum PG I. A high serum gastrin together with a low serum PG I had a specificity of 100%. The results recommend serum PG I and serum gastrin, but not parietal cell antibody, as tests for severe atrophic gastritis in relatives of patients with pernicious anemia.

Topics: Anemia, Pernicious; Atrophy; Autoantibodies; Evaluation Studies as Topic; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Pepsinogens

Topics: Duodenal Diseases; Enteritis; Esophagus; Ethanol; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Motility; Humans; Intestinal Absorption; Intestinal Mucosa; Lipoproteins

A progression in the development of gastritis is not observed following selective proximal vagotomy. Morphometrically, a moderate compensatory foveolar hyperplasia can be noticed in addition to a reduction of parietal cells. Paralleles can be found concerning the ultrastructural alterations of parietal cells following vagotomy or after anticholinergic treatment. They consist in an increase of lamellar osmiophilic bodies, reduction of tubulovesicles, a narrow canalicular lumen and sparse mitochondria. A few years after vagotomy, the parietal cells appear rather unstimulated. After vagotomy, numerous antral G-cells can be demonstrated, with ultrastructural features of increased secretory activity in correlation to raised plasma gastrin levels. This moderate G-cells hyperplasia may, however, already exist preoperatively with the duodenal ulcer. 5 years after vagotomy, there is no pronounced alteration concerning the number of granular or agranular vesicles inside the terminal axons. Experimentally, a degeneration of sympathetic nerves has been described a few days after vagotomy.

Topics: Adult; Aged; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis; Humans; Middle Aged; Mitochondria; Nerve Degeneration; Sympathetic Nervous System; Vagotomy

131 patients operated on for gastric ulcer according to Gillroth II were investigated with gastroscopy and biopsy. The histology of the gastric mucosa was correlated with the time elapsed since resection. In most cases gastritis shows no difference between anastomosis and stump. In up to 12% gastritis in the stump was more pronounced that at the anastomosis. In the stump any form of gastritis can be seen even more than 20 years afer resection. Atrophic changes are more often to be found in the resected stomach and develop more rapidly than in the normal stomach. They probably result from the coincidence of the lost protective function of the mucous membrane after resection of the gastrin-producing antrum with the potentially damaging action of the contents of small intestine.

Topics: Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Postgastrectomy Syndromes; Stomach Ulcer; Time

Topics: Animals; Anura; Bombesin; Dogs; Duodenal Ulcer; Gastrins; Gastritis; Gastrointestinal Diseases; Humans; Peptic Ulcer; Peptides; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Adolescent; Adult; Aged; Duodenal Ulcer; Female; Gastric Juice; Gastrins; Gastritis; Humans; Male; Middle Aged; Monoamine Oxidase; Pylorus; Stomach Ulcer

Forty eight patients were evaluated to ascertain a correlation (if any) between gastric acid secretion, fasting and post prandial serum gastrin levels, gastric biopsy (antrum and fundus) and gastric emptying time after a standard test meal. The following conclusions were obtained: a) 57.8% of patients with atrophic gastritis and achlorhydria had evaluated serum gastrin levels; b) most patients with high gastrin levels had normal antrum on biopsy or showed only minimal inflamatory changes, while those with normal gastrin levels disclosed more pronounced histological changes; c) patients with achlorhydria had slower gastric emptying rates, and this was more evident among those with higher gastrin levels (though differences were not statistically significant). Further studies are required for a better understanding of the relationship between gastric emptying rate and gastrin levels in patients with chronic gastritis.

Topics: Achlorhydria; Adult; Aged; Chronic Disease; Female; Gastric Emptying; Gastric Juice; Gastrins; Gastritis; Humans; Indium; Male; Middle Aged; Pyloric Antrum; Radioisotopes

Topics: Adult; Duodenal Ulcer; Esophagitis, Peptic; Gastrins; Gastritis; Humans; Middle Aged

Topics: Duodenitis; Esophagitis, Peptic; Female; Gastrins; Gastritis; Humans; Male; Peptic Ulcer; Postgastrectomy Syndromes; Stomach Diseases; Stomach Neoplasms

The distribution and numbers of G cells and of parietal cells were related to the distribution and severity of histopathological alterations (inflammatory cell infiltration, atrophy and intestinal metaplasia) in corresponding mucosal tissue blocks from resected stomachs (12 patients with gastric ulcer, 11 with duodenal ulcer, and 14 with duodenal ulcer and uremia). In all patients the histopathological features were more severe in the pyloric antrum than in the body, and the change in severity corresponded well with the disapperance of G cells at the body-antrum border. The transitional body-antrum zone was histopathologically similar to the remaining antrum. A marked individual heterogeneity of the histopathological alterations was observed. An increasing grade of atrophy was associated with increased severity of inflammation, and the presence of intestinal metaplasia was especially associated with atrophy. No significant correlation was found between the antral G-cell number and the grade of antral inflammatory cell infiltration, whereas there was a reduction in cell number with increasing grade of atrophy in all patient categories. The parietal-cell density in the body mucosa was decreased with increasing grade of inflammation as well as with increasing grade of atrophy. The presence of patchy intestinal metaplasia resulted in a complete absence of G cells and of parietal cells from the corresponding part of the mucosa in the antrum and body respectively.

Topics: Adult; Aged; Atrophy; Cell Count; Duodenal Ulcer; Female; Fluorescent Antibody Technique; Gastrectomy; Gastrins; Gastritis; Humans; Intestinal Mucosa; Intestines; Male; Metaplasia; Middle Aged; Pyloric Antrum; Pylorus; Staining and Labeling; Stomach Ulcer; Uremia

In order to study the development of atrophic gastritis, gastric secretory function was examined by a standard pentagastrin test 24 to 78 months after a previous examination (Ex I). The study included 12 patients with dermatitis herpetiformis (DH), 6 patients with functional signs of atrophic gastritis previously, and 8 healthy controls. The surrent examination (Ex II) also included microbiological culture of gastric juice and estimation of gastrin(s), parietal cell and thyroidal antibodies. Most of the controls had increased their maximum acidity and maximum acid output (MAO) between the examinations. This may indicate an altered potency of pentagastrin in recent years. Conversely, 5 of the 6 patients with atrophic gastritis showed a further reduction of maximum acidity and MAO, indicating progressive parietal cell atrophy. In the DH-group, two tendencies were observed: 6/12 patients had an increased MAO at Ex II. They had had lower mean age and higher mean MAO at Ex I, as compared with the remaining 6 patients who had a decreased MAO at Ex II. The latter group more often had parietal cell antibodies.

Topics: Adult; Aged; Dermatitis Herpetiformis; Female; Gastric Juice; Gastrins; Gastritis; Humans; Male; Middle Aged

In the course of an ultrastructural study on peroral gastric biopsy specimens that were obtained from patients with chronic atrophic gastritis, peculiar pathological changes of endocrine cells were observed and correlated with functional and hormonal data on the patients. An increased number of G (gastrin) cells was found in hypergastrinemic patients. These cells could be divided into a "light" (probably hyperfunctioning) and a "dark" (probably exhausted) type. The light type of cell was prominent regardless of the concomitant gastrin blood levels. The G cells found within the fundic region were always localized within the areas of pyloric metaplasia. Focal micronodular proliferation of antral enterochromaffin cells (EC) was often seen. A proliferation of the closed type of endocrine cells of the fundic mucosa was observed only in patients with elevated gastrin concentrations. In the present study, these cells were identified as enterochromaffin-like cells (ECL). No substantial changes were found in the D and D1 cells. The endocrine cells seen in metaplastic intestinal epithelium exhibited ultrastruct characteristics of at least three different types of intestinal endocrine cells (EC, L, and S cells).

Topics: Adult; Aged; Atrophy; Biopsy; Chronic Disease; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Pylorus; Stomach

In 32 subjects, the HCl secretion, the histological state of the antral and fundic mucosa and the gastrin response to a liquid meal extract were studied. Atrophy of the antrum was associated with normal gastrin concentration in the fasting state and after the test meal, in the presence of normal fundic mucosa and HCl secretion. In achlorhydria and atrophic gastritis, fasting gastrinemia was significantly elevated in subjects with a normal antrum, and only moderately increased in subjects with an atrophic antrum. The gastrin response to feeding was correlated to the fasting gastrin concentration in achlorhydric subjects with normal antral mucosa, in contrast to a uniformly reduced output in achlorhydric subjects with atrophic lesions of the antral mucosa.

Topics: Achlorhydria; Adult; Aged; Atrophy; Dyspepsia; Fasting; Female; Food; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged

34 subjects including 5 probands with pernicious anemia, 3 probands with severe atriphic body gastritis and 26 of their first-degree relatives were studied gastroscopically, bioptically, functionally and immunologically. In general, members of the same family revealed a trend to behave similarly with respect to the parameters studied. Signs of A-gastritis (severe atrophy of gastric body glands with a normal or almost normal antrum, achlorhydria, hypergastrinemia and parietal cell antibodies), with intrinsic factor antibodies in the gastric juice and diminished intrinsic factor secretion without anemia were found both in families of probands with atrophic gastritis and pernicious anemia. This suggests a close etiopathogenetic relation of this type of mucosal lesion to overt pernicious anemia. Determination of HCl output and serum gastrin level enabled us to distinguish two differently behaving subgroups in the series, one of them with characteristics of overt adult pernicious anemia. Very low intrinsic factor secretion was found almost exclusively in connection with the presence of intrinsic factor antibodies in the gastric juice and always with severe atrophy of gastric body glands.

Topics: Anemia, Pernicious; Autoantibodies; Gastric Juice; Gastrins; Gastritis; Gastroscopy; Humans; Intrinsic Factor

Topics: Adult; Aged; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Secretory Rate; Stomach

A patient with atrophic gastritis and excessively raised serum gastrin concentrations (4000 to 5000 pg/ml) was found to have multiple polypous tumors of the gastric corpus mucosa. Following gastrectomy, serum gastrin concentrations decreased to undetectable levels. The tumors consisted of a mixed population of endocrine cells. The majority of tumor cells were of the ECL type, but, in addition, enterochromaffin cells of various subtypes as well as agranular cells were found. The tumors were locally invasive and invaded the walls of submucosal blood vessels. The surrounding mucosa showed a severe atrophic gastritis with intestinalization and contained numerous goblet cells, enterochromaffin cells, and cholecystokinin cells. Cholecystokinin cells do not occur in the normal oxyntic mucosa. Hence, the observation of this cell type in intestinalized gastric epithelium suggests that "intestinalization also is associated with changes in endocrine cell populations. Gastrin has been shown to affect the function of the ECL cells. Indications for a trophic action of gastrin on these cells have been obtained. It is discussed whether greatly raised serum gastrin levels in patients with atrophic gastritis may be associated with increased risks for the development of certain types of gastric tumors.

Topics: Diabetes Complications; Enterochromaffin Cells; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Middle Aged; Stomach; Stomach Diseases; Stomach Neoplasms

Topics: Achlorhydria; Adult; Aged; Atrophy; Chronic Disease; Gastric Mucosa; Gastrins; Gastritis; Humans; Middle Aged

In an attempt to confirm the reported high incidence of raised serum gastrin levels in patients with rheumatoid arthritis (RA), gastrin concentrations were estimated in 54 patients. Only three patients (6%) had basal hypergastrinaemia. The heptadecapeptide (G17) and total carboxyl-terminal immunoreactive gastrin responses to a standard protein meal were measured by specific radioimmunoassay in these three patients and in nine normogastrinaemic RA patients displaying the same age range. The three hypergastrinaemic patients showed significantly greater and more prolonged G17 and total carboxylterminal immunoreactive gastrin responses to the meal compared with the normogastrinaemic RA patients (P less than 0.02). Two of these three patients agreed to have an acid output study (pentagastrin 6 microg/kg subcutaneously) and gastric mucosal biopsies taken for histology. Both were found to be achlorhydric and to have atrophic gastritis. This study suggests that basal hypergastrinaemia in RA patients is considerably less common than previously reported and, when present, is associated with achlorhydria. In addition, the incidence of achlorhydria in rheumatoid arthritis is similar to that found in a normal age-matched population.

Topics: Adult; Arthritis, Rheumatoid; Dietary Proteins; Female; Gastric Juice; Gastrins; Gastritis; Humans; Male; Middle Aged

The influence of a coffee-antazid-mixture was investigated at 30 patients with diseases of the stomach (17 with duodenal ulcer, 6 with gastric ulcer and 7 with chronic gastritis) in comparison to a commercial coffee. The parameters measured were the gastric basal acid output, the continuous registration of the pH by an intragastric electrode and the serum gastrin concentration before and after the application of the tests substances. 75% of the patients with duodenal ulcer showed a positive effect by means of a greater elevation of the intragastric pH after application of the mixture in comparison to coffee. The effect was strongly correlated to the basal acid ouptput. In the group with gastric ulcer and that with duodenal ulcer under the influence of the mixture the pH after the initial rise decreased to less deeper values. There was a close relationship to the patterns of gastric ulcer as well with chronic gastritis there was an additional facourable effect on the symptoms of abdominal pain which occured after coffee and not after the mixture. The group with chronic gastritis showed no difference between the pure coffee and the coffee-antacid-mixture. A possible relationship of the products of coffee roasting and the adsorptive properties of the antacid is discussed.

Topics: Adult; Aged; Antacids; Chronic Disease; Coffee; Fasting; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Peptic Ulcer; Stomach Diseases

Topics: Carbohydrates; Gastric Juice; Gastrins; Gastritis; Glycoproteins; Humans; Pepsin A; Stomach Diseases; Stomach Ulcer

A patient is presented with Zollinger-Ellison syndrome, in whom spontaneous disappearance of gastric hypersecretion and peptic ulcer disease occurred subsequent to an intercurrent illness causing acute nonspecific inflammation of the gastric mucosal lining. The dramatic clinical improvement after subsiding of the intercurrent illness was obviously linked to pronounced failure of the parietal cell mass for acid secretion and not to infarction of the gastrinoma because gastrin secretion by the tumor was unchanged.

Topics: Adenoma, Islet Cell; Adult; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Pancreatic Neoplasms; Remission, Spontaneous; Secretory Rate; Zollinger-Ellison Syndrome

Forty-five patients with achlorhydria due to severe atrophic corpus gastritis or gastric atrophy were studied by determination of serum gastrin, histological examination of multiple biopsy from the antrum, and quantitation of gastrin cells revealed by an indirect immunofluorescence technique. In a reference group of 12 persons with normal gastric secretion and without atrophic antral gastritis the mean number of gastrin cells per field of vision was 52 +/- 6.5 (S.E.M.). In a group of achlorhydric patients having normal antral mucosa (n = 24), the serum gastrin levels was 324 +/- 56 pmol/l and the number of gastrin cells was 79.6 +/- 7.5 cells/field of vision. The corresponding values for a group of achlorhydric patients with chronic superficial antral gastritis (n = 11) were 361 +/- 186 pmol/l and 88.0 +/- 14.4 cells/field of vision. In a group of achlorhydric patients with atrophic antral gastritis (n = 10) serum gastrin was 15.0 +/- 3.3 pmol/l, and the number of gastrin cells was 6.2 +/- 3.3 cells/field of vision. Compared to the subjects in the reference group, the number of gastrin cells was significantly higher in the groups of achlorhydric patients with normal or superficially inflamed antral mucosa and significantly lower in achlorhydric patients with atrophic antral gastritis. It is concluded that serum gastrin in general is a good indicator for the presence or absence of antral atrophic gastritis in achlorhydria.

Topics: Achlorhydria; Adult; Aged; Atrophy; Chronic Disease; Female; Fluorescent Antibody Technique; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Pyloric Antrum

Antral gastrin-producing cell (G-cells) were counted by an immunofluorescence technique in the antral biopsies obtained at endoscopy from 67 subjects; they included patients with duodenal ulcer, gastritis, and individuals with a normal gastric mucosa. The G-cell count was significantly lower (P less than 0.01) in patients with duodenal ulcer (142 G cells per mm2) in comparison to normal subjects (327 G cells per mm2). No statistically significant correlation was found between the G-cell number and any of the other parameters tested (pentagastrin test, basal serum gastrin and its response to a standard meal).

Topics: Adolescent; Adult; Aged; Biopsy; Cell Count; Duodenal Ulcer; Female; Fluorescent Antibody Technique; Gastrins; Gastritis; Gastroscopy; Humans; Male; Middle Aged; Pyloric Antrum

Sheep and calves prepared with separated, innervated pouches made from the acid secreting region of the abomasum were given single or multiple infections of Ostertagia spp and comparisons were made of the secretory changes of parasitised and non-parasitised mucosa by means of cannulas placed in the abomasum and pouch. Contrary reactions of the parasite-free pouches and infected main part of the abomasum are described and explained in terms of a two-part hypothesis. The inhibitory effect on acid secretion of the abomasum (resulting in its contents being pH 5 to 7) was postulated to be due to the direct suppressive effects of substances released locally by parasites or injured host tissues, whereas increased secretion of the hormone, gastrin, was thought to account for the stimulatory effects of infection on acid secretion from the pouches. In sheep treated with anthelmintic and then reinfected the inhibitory effects on abomasal pH were not obtained. The hypersecretion from the pouches still persisted.

Topics: Abomasum; Animals; Cattle; Gastric Juice; Gastrins; Gastritis; Ostertagiasis; Sheep; Sheep Diseases; Trichostrongyloidiasis

The morphological changes of gastric mucosa taken from different areas has been studied in patients of approximately the same age with achlorhydria, extreme hypochlorhydria and normochlorhydria. The serum gastrin level and parietal cell antibodies were determined in the achlorhydric parietal cell antibodies were determined in the achlorhydric patients. In the latter the diffuse gastritis was localized in the corpus-fundic area, while the changes in the antral region were few and occurred mostly in the superficial zone. In normochlorhydric patients however, the diffuse gastritis was localized in the antral region, with only few changes at the corpus-fundic area. In patients with extreme hypochlorhydira either the fundic or the antral region was involved. Besides the diffuse gastritis intestinal metaplasia, pseudopyloric metaplasia, and atrophy of mucosa were also observed, although much less commonly. The increase of gastrin level could not be related to a definite morphological pattern in the gastric mucosa. It can be assumed that each of the two types of gastritis has a different natural history; the antral site of gastrititis cannot be transformed into the fundic site, nor can the fundic site be transformed into the antral site.

Topics: Achlorhydria; Aged; Atrophy; Biopsy; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Metaplasia; Middle Aged; Pyloric Antrum

Antral gastrin concentration (AGC) was measured in prepyloric mucosa specimens obtained by forceps biopsy during endoscopic examination of 174 clinic and hospital patients. AGC in 32 patients who had normal endoscopic findings, the control group, varied widely from 2 to 38.6 ng gastrin/mg tissue. The mean AGC of the control patients was 14.2 +/- 1.4 (mean +/- 1 SE) ng gastrin/mg tissue. AGC was similar to control values in 18 patients with duodenal ulcer, 14.7 +/- 2.1; 12 patients with a pyloric channel or antral ulcer, 16.4 +/- 3.5; and 48 patients with miscellaneous diagnoses, 14.3 +/- 1.5. AGC was significantly less than control values in 13 patients with a ulcer in the body or fundus of the stomach, 5.9 +/- 1.5, and 4 patients with the Zollinger-Ellison syndrome, 4.9 +/- 2.4. AGC was significantly greater than in control values in 16 patients with gastritis, 25.8 +/- 4.3;22 patients with esophagitis, 23.2 +/- 3.0; and 9 patients with gastric atrophy and fasting serum hypergastrinemia 44.6 +/- 12.3. In group of 77 of these patients with heterogeneous diagnoses, meal-stimulated 3-hr integrated gastrin output was directly related to AGC (r = 0.47, P less than 0.001). In a group of 106 patients AGC was inversely related to histalogstimulated maximum acid output. The correlation was very weak (r = -0.20) but significant (P less than 0.05).

Topics: Atrophy; Biopsy; Duodenal Ulcer; Esophagitis; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Pyloric Antrum; Stomach; Stomach Ulcer; Zollinger-Ellison Syndrome

1. Prostaglandin A-, prostaglandin E- and prostaglandin F-like substances were determined radioimmunologically in antral biopsy material obtained by endoscopy. 2. In patients with gastritis, the concentrations of prostaglandin (E+A)-like substances were six times as high and of prostaglandin F-like substances twice as high as in normal subjects. In chronic atrophic gastritis, the concentrations of prostaglandin (E+A)-like material was four times as high as in normal subjects whereas prostaglandin-F like material remained unchanged. In acute gastric ulcer, prostaglandin (E+A)-like material reached concentrations four times times higher than in normal subjects, accompanied by a fivefold increase of prostglandin F-like substances. After healing of the gastric ulcer, prostaglandins returned to normal values. 3. There was no correlation between gastrin and prostaglandins in all biopsy specimens.

Topics: Adult; Aged; Duodenal Ulcer; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Prostaglandins; Prostaglandins A; Prostaglandins E; Prostaglandins F; Stomach Diseases; Stomach Ulcer

Topics: Child; Duodenal Diseases; Enteritis; Gastrins; Gastritis; Humans

Topics: Adult; Aged; Female; Food; Gastrins; Gastritis; Humans; Male; Middle Aged; Peptic Ulcer

In patients with gastric cancer who were to undergo gastrectomy, the fasting serum gastrin concentration in the peripheral vein was estimated by radioimmunoassay. The blood samples were also collected from the gastric veins and artery during the time of operations. These gastrin values were compared with morphological findings in the resected stomach. No significant differences in serum gastrin concentration was found between the patients of gastric cancer and normal subjects. In the patients with mucosal atrophy in the oxyntic gland area but with no atrophy in the pyloric gland area, however, significant increase in serum gastrin concentration was observed. In cases where fundal atrophy was accompanied by atrophy in the pyloric gland area, the increase was not observed. The amount of gastrin content in cancer tissue was negligible. These results indicate that the increase in serum gastrin concentration in some patients with gastric cancer might be due to the accompanied atrophy of oxyntic glands in the stomach.

Topics: Adult; Aged; Atrophy; Female; Gastrectomy; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Male; Middle Aged; Radioimmunoassay; Stomach Neoplasms; Stomach Ulcer

Fasting serum gastrin was determined in 35 Chinese patients with various types of chronic gastritis and in 23 Chinese control subjects. The mean (+/- S.D.) fasting serum gastrin levels for 13 patients with chronic atrophic gastritis, 16 patients with chronic gastritis and six patients with acute-on-chronic gastritis were 32.1 (+/- 38.9) pg./ml., 36.1 (+/- 23.2) pg./ml. and 33.7 (+/- 19.4) pg./ml., respectively. The mean (+/- S.D.) fasting serum gastrin levels for the whole gastritis group (35 patients) and the control group were 34.2 (+/- 28.8) pg./ml. and 24.6 (+/- 13.7) pg./ml., respectively. Statistical analysis showed that the mean basal serum gastrin levels of the three gastritis groups did not differ significantly from control subjects and with each other.

Topics: Adult; China; Chronic Disease; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Singapore

Topics: Anemia, Pernicious; Gastrins; Gastritis; Humans; Pyloric Antrum

Topics: Antacids; Duodenal Ulcer; Gastric Juice; Gastrins; Gastritis; Histamine Release; Humans; Hydrogen-Ion Concentration; Parasympatholytics; Pentagastrin; Pepsin A; Peptic Ulcer; Stomach Ulcer

Seventeen patients with dermatitis herpetiformis were tested for gastric hydrochloric acid secretion. Seven were found to be achlorhydric. Atrophic gastritis in these patients probably had an auto-immune pathogenesis, as judged by elevated serum gastrin level, high prevalence of antibodies against gastric parietal cells and antrum sparing of the gastric atrophy. This type of atrophic gastritis is considered to indicate a precursor state to pernicious anemia.

Topics: Adult; Aged; Autoantibodies; Autoimmune Diseases; Bile Acids and Salts; Dermatitis Herpetiformis; Female; Gastric Juice; Gastrins; Gastritis; Humans; Male; Middle Aged; Secretory Rate; Stomach

Topics: Acute Kidney Injury; Anemia, Pernicious; Duodenal Ulcer; Gastrins; Gastritis; Gastrointestinal Diseases; Humans; Kidney Failure, Chronic; Zollinger-Ellison Syndrome

Correlation between the gastrin cell number of delineated by immunohistological staining and the gastrin content in blood and antral mucosa has been studied in biopsies from the antral region of the human stomach. With a semiquantitative score system of the antral gastrin cells, we found correlation between the number of cells and the gastrin content in mucosa and serum and the grade of atrophic pyloric gastritis in 52 patients with different gastric diseases. It is concluded that further studies will be necessary before it is possible to estimate the total mass of gastrin cells and thereby compare different clinical groups.

Topics: Adult; Aged; Cell Count; Female; Fluorescent Antibody Technique; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Pilot Projects; Pyloric Antrum; Stomach Diseases

Topics: Animals; Gastrins; Gastritis; Ostertagiasis; Sheep; Sheep Diseases; Trichostrongyloidiasis

The mean concentration of gastrin in serum was determined in healthy fasting persons (n = 27), it amounted to 56.8 pg/ml (SD = 19.8 PG/ML). The values of gastrin in serum of patients, who were grouped by endoscopicbioptic criteria of antral mucosa and who exceptionally showed diffuse inflammation of gastric mucosa, amounted to 73.2 pg/ml in patients with mild superficial gastritis (n = 24), to 73.4 pg/ml in those with severe superficial gastritis (n = 55), to 82.3 pg/ml in patients with chronic atrophic gastritis (n = 11) and to 70.7 pg/ml in those with chronic atrophic gastritis and intestinal metaplasia (n = 17). The concentration of serum gastrin in patients with additional pathological processes of gastric or duodenal mucosa was also determined. Patients with gastric resection according to Billroth II (n = 15) revealed gastrin values of 47.8 pg/ml, those with duodenal ulcer (n = 5) of 58.5 pg/ml, with gastric ulcer (n = 50) of 61.3 pg/ml, with polyps in stomach (n = 10) of 109.6 pg/ml and with neoplasms of the stomach (n = 27) of 77.7 pg/ml. Gastrin values were not correlated to age or sex. The difference between the mean gastrin concentrations of the mentioned groups of patients however is not marked enough and the range of values is too wide to characterize those groups by specific gastrin levels. The determination of gastrin in serum of fasting patients is not helpful for diagnosis of gastritis without antibodies to intrinsic factor or for diagnosis of certain localized pathological conditions in stomach or duodenum obviously.

Topics: Adolescent; Adult; Aged; Duodenal Ulcer; Female; Gastrectomy; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Metaplasia; Middle Aged; Polyps; Stomach Diseases; Stomach Neoplasms; Stomach Ulcer

Topics: Achlorhydria; Anemia, Pernicious; Diet; Esophagogastric Junction; Gastrectomy; Gastrins; Gastritis; Humans; Lymphatic Metastasis; Methods; Stomach Neoplasms

Topics: Adult; Female; Food; Gastrins; Gastritis; Humans

A pathophysiological role of gastrin has been established only in the Zollinger-Ellison-Syndrome. Hypergastrinemia may be found in cases with prenicious anemia, atrophic gastritis and after all forms of vagotomy; furthermore in the excluded antrum syndrome, the short bowel syndrome, in renal insufficiency, pyloric stenoses and after oral or parenteral administration of calcium. The role of gastrin in the pathogenesis of duodenal ulcer is unknown.

Topics: Anemia, Pernicious; Duodenal Ulcer; Gastrins; Gastritis; Humans; Postgastrectomy Syndromes; Zollinger-Ellison Syndrome

The effect of short-term infusion of a large dose of pentagastrin and a small dose of synthetic human gastrin I (SHG) on the rate of cell proliferation in gastric mucosa was studied in normal human subjects. Moreover, the kinetic parameters were compared with the serum gastrin concentrations in fasting patients. Endoscopic biopsies were labelled in vitro with 3H-thymidine and autoradiographs were prepared. The percentage of DNA-synthesising cells in the progenitor cell region was estimated. In healthy volunteers infusion of a large dose of pentagastrin (10 mug/kg per hour) was followed by a marked increase in the labelling index in fundic mucosa. The antral mucosa was not responsive to this effect. In the same subjects, infusion of a low dose of SHG (8 ng/kg per min) did not affect the rate of cell proliferation, either in fundic or in antral mucosa. In 46 patients with different gastric diseases no correlation between the serum gastrin concentrations and the labelling indices was found. The results suggest that human fundic mucosa is responsive to a trophic action of pentagastrin. If it exists, however, a physiological action of gastrin as a trophic hormone for human gastric mucosa must be considerably more complex than previously believed.

Topics: Adult; Aged; Autoradiography; Cell Division; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Pentagastrin; Peptic Ulcer; Stomach Ulcer

Mucosal biopsies from multiple sites in the stomachs of 21 patients with pernicious anaemia have been examined. The histological changes almost always involved the entire gastric mucosa, including that of the pyloric antrum. Metaplastic changes were almost universal and consisted of intestinal metaplasia in the body and antrum and pyloric metaplasia in the body. The severity of the pyloric metaplasia was such as to make the distinction between body and antrum on biopsy impossible. No relationship was found between serum gastrin activity and the histological appearances of the gastric antrum or body.

Topics: Adult; Aged; Anemia, Pernicious; Antibodies; Atrophy; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Hyperplasia; Intrinsic Factor; Male; Metaplasia; Middle Aged; Pyloric Antrum

Biopsy specimens have been taken from five standard sites in the stomach and from the duodenal bulb in order to investigate the association of gastritis and duodenitis with duodenal ulcer. Twenty patients with chronic duodenal ulcer were investigated in this manner and in addition had gastric secretion tests and a radio-immune assay of serum gastrin under differing conditions. The patients were then treated either by a truncal vagotomy and pyloroplasty (TVP) or by a highly selective vagotomy without a drainage procedure (HSV). All the investigations were repeated three months postoperatively. Duodenal ulcer was usually associated with gastriitis, although this varied in extent and severity from patient to patient. In nearly all the patients, gastritis was present at the pyloric end of the stomach and along the lesser curve. In more than half of the patients, gastritis was also present in the body of the stomach but the fundus was usually spared. Chronic duodenitis was found in the duodenal bulb in all these patients. After vagotomy there was a marked increase in both the extent and severity of the proximal gastritis in both treatment groups but the distal gastritis remain almost unchanged. There was little change in the incidence of duodenitis after vagotomy but its severity was lessened. No correlation was found between the peak acid output (PAO) in response to Histalog and the severity of the gastritis or the duodenitis either before or after operation, with one exception. The postoperative PAO was significantly less in those patients who developed a severe proximal gastritis after vagotomy. No relationship was found between the severity of the distal gastritis and the levels of serum gastrin. No correlation was found between either the basal or peak acid output and the corresponding serum gastrin levels before or after vagotomy.

Topics: Biopsy; Duodenal Diseases; Duodenal Ulcer; Duodenum; Enteritis; Female; Gastric Juice; Gastrins; Gastritis; Humans; Male; Stomach; Vagotomy

Forty-two patients with pernicious anemia (PA) and 35 patients with achlorhydria but without PA were investigated by means of serum gastrin determination and estimation of circulating parietal cell and thyroidal autoantibodies. In 38 of the 77 patients, gastroscopic and histopathological examinations of the antral and corpus mucosa were performed. The patient groups were similar with regard to distribution of high and normal serum gastrin levels, the frequencey of autoantibodies and antrum-sparing atrophic gastritis. In the present selection of patients, therefore, the achlorhydria group was supposed to represent a precursor state of the group with PA. A minor proportion of patients with severe atrophic gastritis of the antrum as well as of the corpus mucosa was found in the two groups.

Topics: Achlorhydria; Adult; Aged; Anemia, Pernicious; Autoantibodies; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Vitamin B 12

Fasting and after meals serum gastrin levels were determined in healthy subjects and patients with different gastroenterological diseases (duodenal and gastric ulcer, hiatal hernia with gastroesophageal reflux, Billroth II gastric resection, atrophic gastritis, Zollinger-Ellison, Ménétrier, chronic calcifying pancreatitis, gastric carcinoma and lymphoma). The results pointed to the usefulness of evaluating both fasting levels and "gastrin curve" after meals as an expression of the rapidity of response of hormone-secreting gastric cells. Calculation of the I.G.O. (Integrated Gastrin Output) must also be carried out to provide a parameter from which the overall ability of G cells to secrete in response to feeding can be assessed.

Topics: Duodenal Ulcer; Gastrins; Gastritis; Gastroesophageal Reflux; Gastrointestinal Diseases; Hernia, Hiatal; Humans; Pancreatitis; Stomach Neoplasms; Zollinger-Ellison Syndrome

Elevation in fasting serum gastrin levels was found in three patients being evaluated for persistent upper abdominal pain without radiographic evidence of peptic ulcer disease. Fiberoptic endoscopy of the upper gastrointestinal tract in each patient revealed characteristic changes of chronic atrophic gastritis. Gastric biopsies showed diffuse chronic inflammation in the lamina propria, a decrease in the number of parietal cells, and "intestinalization" of gastric mucosa. Total achlorhydria was demonstrated after a maximal histalog stimulus; however, serum levels of vitamin B12 and Schilling test values were normal in all three patients. Parietal cell antibodies were found in the serum in all patients in a dilution of 1:20 to 1:80. These cases represent autoimmune (type A) chronic atrophic gastritis and should be distinguished from chronic simple (type B) gastritis, in which serum gastrin levels are normal and no parietal cell antibodies are found in the serum. Patients with autoimmune gastritis should be observed at frequent intervals for the occurrence of pernicious anemia or gastric carcinoma.

Topics: Achlorhydria; Adult; Antacids; Atrophy; Autoantibodies; Autoimmune Diseases; Chronic Disease; Female; Gastrectomy; Gastrins; Gastritis; Humans; Middle Aged

Topics: Achlorhydria; Aged; Biopsy; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Stomach

Alterations in gastric physiology caused by selective embolization and vasopressin infusion of the left gastric artery were evaluated in 29 dogs. Gastric acidity was not significantly altered following Gelfoam embolization but decreased sharply with vasopressin infusion. These results suggest that the segmental occlusion caused by Gelfoam embolization permits significant collateral blood flow to the gastric mucosa, while the arteriolar and capillary constriction caused by vasopressin effectively decreases mucosal blood flow. These findings are consistent with the clincal observation that embolization is more effective in controlling bleeding ulcers, while vasopressin infusion is more effective for controlling hemorrhagic gastritis.

Topics: Angiography; Animals; Dogs; Embolization, Therapeutic; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Histamine; Models, Biological; Peptic Ulcer Hemorrhage; Stomach; Vasopressins

The consequences of exposure of the intact stomach to intestinal contents were examined in six dogs. Diversion of duodenal contents through the stomach lead to the following changes: histologic gastritis in both antrum and corpus, increase in resting and postprandial serum gastrin levels, increased parietal cell density in four of six animals, and enhanced maximal acid secretory capacity in three of six animals. No significant changes were seen in insulin-stimulated acid secretion, insulin-stimulated pepsin secretion, antral gastrin levels, or G cell numbers. We conclude that chronic exposure of the intact stomach to duodenal contents results in gastritis and an amplified gastrin response to food. Parietal cell numbers and maximal acid secretory capacity are increased in some animals.

Topics: Animals; Bile; Dogs; Duodenum; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Hyperplasia; Pepsin A

Serial morphological, secretory, and serological observations of a patient with Ménétrier's disease disclosed hypergastrinemia, antibodies to parietal cells and dietary substances, and an acute reduction of gastrointestinal protein loss after atropine administration. Transformation of the gastric mucosa from hypertrophy to atrophic gastritis was associated with disappearance of the protein-losing gastroenteropathy and serum antibodies and reduction of the serum gastrin concentration.

Topics: Antibodies; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Hypertrophy; Male; Middle Aged; Protein-Losing Enteropathies

Hypergastrinemia occurs in achlorhydric states if the antrum is not diseased, and evidence has been presented that suggests that antral gastritis diminishes gastrin levels in achlorhydric patients. There is a dramatic gastrin response to calcium challenge in patients with pernicious anemia. Only minimal response was observed in patients with atrophic gastritis. Unlike the response observed in the Zollinger-Ellison syndrome, secretin challenge suppresses gastrin in achlorhydric states. These findings add a new dimension to the utility of serum gastrin determinations.

Topics: Achlorhydria; Anemia, Pernicious; Atrophy; Calcium; Female; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Infusions, Parenteral; Male; Middle Aged; Pyloric Antrum; Secretin

Topics: Atrophy; Biopsy; Chronic Disease; Gastric Mucosa; Gastrins; Gastritis; Humans; Sodium; Stimulation, Chemical

Topics: Achlorhydria; Anemia, Pernicious; Atrophy; Fasting; Gastrins; Gastritis; Humans; Intrinsic Factor; Radioimmunoassay

Topics: Adult; Aged; Chronic Disease; Fasting; Gastrins; Gastritis; Humans; Middle Aged

38 patients were found to have achlorhydria after maximal stimulation with pentagastrin and on multiple biopsies (atrophy of gastric mucosa). It was demonstrated that the sequence pH-antroreceptors-G cells-parietal cells-pH antroreceptors was interrupted already in mild or moderately severe superficial gastritis of the antral mucosa involving more than half of the antral surface. Reduction of specific functional epithelium is unlikely in this form of inflammation so that it is probably an effect of the pH receptors.

Topics: Achlorhydria; Adult; Aged; Atrophy; Biopsy; Female; Gastric Juice; Gastrins; Gastritis; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Pentagastrin; Pyloric Antrum

A women had hypergastrinaemia associated with the variety of gastritis (Type A) that is associated usually with pernicious anaemia, together with recurring bouts of severe abdominal pain. Fasting serum gastrin levels ranged between 600 and 2750 pg/ml. There was a rise in serum gastrin levels after a standard protein meal, indicative of a large G cell mass, and a fall after intragastric HCI, which led to a trial of treatment with HCI; this gave some symptomatic relief. After surgical antrectomy there was a profound fall of serum gastrin from a pre-operative level of 2500 pg/ml to constant values of 16--25 pg/ml, and complete and lasting relief from the bouts of abdominal pain.

Topics: Achlorhydria; Female; Gastrins; Gastritis; Humans; Hydrochloric Acid; Middle Aged; Pyloric Antrum

Topics: Aged; Cell Division; Chromaffin System; Enterochromaffin Cells; Female; Gastrins; Gastritis; Humans; Middle Aged

Topics: Animals; Chromaffin System; Digestive System; Dogs; Endocrine Glands; Enterochromaffin Cells; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Diseases; Gastrointestinal Hormones; Humans; Intestinal Mucosa; Intestines; Microscopy, Electron; Peptic Ulcer; Rabbits; Serotonin; Stomach; Zollinger-Ellison Syndrome

Topics: Alcoholism; Amylases; Anemia, Pernicious; Atrophy; Bicarbonates; Gastrins; Gastritis; Humans; Pancreas; Pancreatic Juice; Pancreatic Neoplasms; Pancreatitis; Secretin; Zollinger-Ellison Syndrome

Topics: Gastric Mucosa; Gastrins; Gastritis; Humans; Hypertrophy; Male; Middle Aged

Using immunoperoxidase technique a considerable variation in the number of antral gastrin cells was demonstrated in patients with atrophic gastritis. This variation must be taken in consideration when the number of gastrin cells is to be estimated on the basis of gastric biopsies.

Topics: Gastric Mucosa; Gastrins; Gastritis; Humans; Pyloric Antrum

Topics: Anemia, Pernicious; Atrophy; Duodenal Ulcer; Gastrins; Gastritis; Humans; Radioimmunoassay

Gastrin is released by food rich in proteins and by vagal mechanisms. HCI and possibly secretin and glucagon inhibit gastrin release. In the wide range of actions of gastrin, stimulation of gastric acid secretion is the most important. With the advent of radioimmunochemical methods for the determination of gastrinaemia, it has been shown that gastrin exists in a number of forms of different molecular weight. To estimate the validity of gastrin radioimmunoassay it is necessary to demonstrate that decrease in antibody-bound labelled antigen is unrelated to non-specific interference by unknown substances present in serum samples, and that the antiserum reacts with endogenous hormone in an identical manner. Heterogeneity of gastrin in serum may affect the validity of the radioimmunoassay. Hypergastrinaemia associated with hyper-normochlorhydria occures in gastrinoma, hyperplasia of antral gastrin cells, diseases with delayed gastric emptying, retained antrum, short bowel syndrome,renal failure. Hypergastrinaemia associated with hypo-achlorhydria occurs in atrophic gastritis without extensive antral lesion and after vagotomy. Gastrin radioimmunoassay can be used for the mass screening of subjects with atrophic gastritis, a high risk group for gastric cancer.

Topics: Antibody Formation; Antigens; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Molecular Weight; Radioimmunoassay

Topics: Adult; Age Factors; Aged; Gastrins; Gastritis; Humans; Middle Aged; Vitiligo

Topics: Achlorhydria; Adolescent; Adult; Age Factors; Aged; Anemia, Pernicious; Antibodies; Gastrins; Gastritis; Humans; Middle Aged; Vitiligo

Topics: Duodenal Ulcer; Gastrins; Gastritis; Histamine H1 Antagonists; Humans; Metoclopramide; Peptic Ulcer; Pyloric Antrum; Stomach Ulcer; Vagotomy

Topics: Digestion; Gastrins; Gastritis; Heart; Hormones, Ectopic; Humans; Peptic Ulcer; Structure-Activity Relationship; Zollinger-Ellison Syndrome

Topics: Animals; Chronic Disease; Gastrins; Gastritis; Humans; Mice

Topics: Cholecystokinin; Cholelithiasis; Duodenal Ulcer; Esophageal Achalasia; Gastrins; Gastritis; Gastrointestinal Hormones; Humans; Pancreatic Diseases; Peptic Ulcer; Secretin; Stomach Neoplasms; Stomach Ulcer

Topics: Adult; Calcium; Diagnosis, Differential; Duodenal Ulcer; Female; Gastrectomy; Gastric Acidity Determination; Gastrins; Gastritis; Humans; Infusions, Parenteral; Male; Middle Aged; Peptic Ulcer; Pyloric Stenosis; Radioimmunoassay; Vagotomy; Zollinger-Ellison Syndrome

Topics: Aged; Antibodies; Atrophy; Biopsy; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis; Humans; Intestinal Polyps; Intrinsic Factor; Male; Metaplasia; Middle Aged; Pyloric Antrum; Stomach; Stomach Diseases; Stomach Neoplasms

Topics: Achlorhydria; Adult; Age Factors; Aged; Anemia, Pernicious; Autoantibodies; Biopsy; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Radioimmunoassay; Stomach

Topics: Anemia, Pernicious; Autoantibodies; Gastric Mucosa; Gastrins; Gastritis; Humans; Stomach

Topics: Adolescent; Adult; Anemia, Pernicious; Animals; Biopsy; Cytoplasmic Granules; Fluorescent Antibody Technique; Gastric Mucosa; Gastrins; Gastritis; Humans; Immune Sera; Male; Methods; Microscopy, Electron; Microscopy, Fluorescence; Rabbits

Topics: Anemia, Pernicious; Chronic Disease; Duodenal Ulcer; Epithelial Cells; Fluorescence; Gastric Mucosa; Gastrins; Gastritis; Humans; Immune Sera; Metaplasia; Methods; Stomach Neoplasms; Stomach Ulcer

Topics: Adult; Aged; Anemia, Pernicious; Duodenal Ulcer; Ethylamines; Female; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Insulin; Male; Middle Aged; Postoperative Complications; Pyrazoles; Recurrence; Stomach Neoplasms; Stomach Ulcer; Vagotomy; Zollinger-Ellison Syndrome

Patients with atrophic gastritis but normal antral mucosa and achlorhydria were divided into three groups according to age-under 40, 40 to 70, and over 70 years. Serum gastrin, both basal and following a standard protein meal, was estimated in all patients by radioimmunoassay. There was a significant correlation between the magnitude of the gastrin response and age, the older the patient the greater the response. These results suggest that with increasing duration of gastritis and continued stimulation of a normal antrum in the absence of inhibition by acid, the functional G (gastrin) cell mass increases. However the possibility exists that each cell may secrete more gastrin in response to the same stimulus with age. This may be resolved by counting the number of G cells in the stomachs of subjects with atrophic gastritis and different ages.

Topics: Achlorhydria; Adult; Age Factors; Aged; Atrophy; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Radioimmunoassay

Topics: Atrophy; Biopsy; Duodenal Ulcer; Evaluation Studies as Topic; Follow-Up Studies; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastroenterostomy; Gastroscopy; Humans; Metaplasia; Stomach; Vagotomy

Topics: Chronic Disease; Gastrins; Gastritis; Zollinger-Ellison Syndrome

Topics: Antacids; Gastric Mucosa; Gastrins; Gastritis; Humans; Hydrogen-Ion Concentration; Osmosis; Stomach Ulcer

Topics: Achlorhydria; Circadian Rhythm; Fasting; Gastrins; Gastritis; Humans; Stomach; Time Factors

The serum gastrin response to a standard protein meal has been determined in achlorhydric patients with atrophic gastritis and contrasted with the response in normal subjects whose gastric contents were kept continuously neutral by intragastric bicarbonate instillation. Five normal subjects showed a significant increase in serum gastrin from a mean (+/- SEM) of 17 +/- 3 pg/ml to 119 +/- 10 pg/ml but their response did not approach that of four patients with atrophic gastritis and antral sparing (605 +/- 133 pg/ml to 1418 +/- 186 pg/ml). By contrast, in four patients with antral gastritis, there was no significant change in gastrin levels (24 +/- 13 pg/ml to 55 +/- 19 pg/ml). These studies indicate that the gastrin-secreting cell mass is increased in atrophic gastritis with antral sparing and decreased in atrophic gastritis with antral involvement, as compared to the normal state. They provide further evidence for the existence in man of two distinct forms of atrophic gastritis.

Topics: Achlorhydria; Aged; Bicarbonates; Dietary Proteins; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Stomach

Topics: Adult; Anemia, Hypochromic; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Methods; Middle Aged

Topics: Antibodies; Fluorescent Antibody Technique; Gastric Mucosa; Gastrins; Gastritis; Histocytochemistry; Humans; Metaplasia

Topics: Achlorhydria; Adult; Digestion; Gastrins; Gastritis; Gelatin; Humans; Proline

Topics: Adult; Aged; Caffeine; Female; Gastric Acidity Determination; Gastrins; Gastritis; Humans; Male; Middle Aged; Stomach Neoplasms; Stomach Ulcer

The gastric antral mucosa was studied histologically in 22 patients with atrophic gastritis, of whom 11 had high levels and 11 had normal levels of serum gastrin. The antrum was graded histologically from normal to grade 3 gastritis. All patients with hypergastrinaemia (nine seropositive and two seronegative for parietal cell antibody) had either a normal antrum or minimal (grade 1) antral gastritis. In contrast all but one patient without raised serum gastrin (nine seronegative and two seropositive for parietal cell antibody) had severe (grades 2-3) antral gastritis. Thus circulating gastrin levels observed in patients with gastritis and achlorhydria can be directly related to the presence or absence of antral mucosal damage.Comparison of the histological appearances of the antral mucosa with serum gastrin and parietal cell antibody status has provided a basis for the separation of two distinctive forms of atrophic gastritis.

Topics: Achlorhydria; Anemia, Pernicious; Antibodies; Atrophy; Chronic Disease; Gastric Mucosa; Gastrins; Gastritis; Humans; Middle Aged; Postgastrectomy Syndromes; Radioimmunoassay; Stomach

Topics: Adult; Duodenal Ulcer; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastritis; Gastrointestinal Diseases; Humans; Male; Middle Aged; Pyrazoles; Stomach Ulcer

Topics: Anemia, Aplastic; Animals; Antibodies; Chronic Disease; Gastrins; Gastritis; Guinea Pigs; Humans; Liver Diseases; Peptic Ulcer; Rabbits; Radioimmunoassay

Fasting gastrin levels in serum were measured in 49 patients with different types of chronic gastritis and in matched controls. In 15 patients with established pernicious anaemia the mean (+/- S.E. of mean) level of gastrin was greatly raised (699 +/- 99 pg/ml). In 17 patients with chronic atrophic gastritis, seropositive for parietal cell antibody but with adequate vitamin-B(12) absorption, the level was also raised (476 +/- 74 pg/ml). By contrast, in "simple" atrophic gastritis seronegative for parietal cell antibody the gastrin levels were significantly lower for both diffuse atrophic gastritis (129 +/- 31 pg/ml) and multifocal gastritis (14 +/- 4 pg/ml). These levels were similar to those in the controls (46 +/- 7 pg/ml).The mechanism of the raised gastrin levels remains uncertain, but neither achlorhydria nor in vivo action of the parietal cell antibody wholly accounted for the hypergastrinaemia.We conclude that hypergastrinaemia is characteristic of gastritis associated with autoimmune reactions to gastric antigens and pernicious anaemia and that a raised serum gastrin is a useful marker of the type of gastritis that tends to progress to the gastric lesion of pernicious anaemia. The findings suggest that this type of gastritis is an essentially different disease from "simple" atrophic gastritis, and the differences in gastrin levels may be due to sparing of the antral mucosa in the autoimmune type but not in "simple" gastritis.

Topics: Achlorhydria; Aged; Anemia, Pernicious; Antibodies; Antigens; Autoimmune Diseases; Chronic Disease; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Vitamin B 12

Topics: Achlorhydria; Chronic Disease; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Histamine; Humans; Hydrogen-Ion Concentration; Hypertrophy; Insulin; Intubation, Gastrointestinal; Protein-Losing Enteropathies; Stimulation, Chemical; Stomach; Stomach Diseases; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Atrophy; Biopsy; Chromium Isotopes; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Motility; Humans; Peptides; Stomach; Stomach Neoplasms

Topics: Adolescent; Adult; Aged; Chronic Disease; Female; Gastric Juice; Gastrins; Gastritis; Humans; Injections, Intramuscular; Male; Middle Aged

Topics: Adult; Aged; Animals; Dogs; Duodenal Ulcer; Female; Gastric Juice; Gastrins; Gastritis; Humans; Male; Middle Aged; Pepsin A; Stimulation, Chemical; Stomach Ulcer

Topics: Achlorhydria; Antacids; Gastric Juice; Gastrins; Gastritis; Humans; Pepsin A

Topics: Adult; Carcinoma; Computers; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastritis; Humans; Male; Middle Aged; Peptides; Pyrazoles; Statistics as Topic; Stimulation, Chemical; Stomach Neoplasms; Stomach Ulcer

Topics: Biopsy; Chronic Disease; Duodenal Ulcer; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Injections, Subcutaneous; Time Factors

Topics: Bicarbonates; Cholecystokinin; Enteritis; Gallbladder Diseases; Gastric Acidity Determination; Gastrins; Gastritis; Pancreas; Pancreatitis; Pyrazoles; Secretin; Stimulation, Chemical; Stomach Ulcer

Topics: Adult; Aged; Biopsy; Chronic Disease; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Stomach Diseases

Topics: Adult; Chronic Disease; Duodenal Ulcer; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastritis; Humans; Male; Methods; Middle Aged; Nausea; Succinates

Topics: Adolescent; Adult; Biopsy; Child; Gastric Juice; Gastrins; Gastritis; Hepatitis A; Humans

Topics: Achlorhydria; Adult; Aged; Biopsy; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Stomach Diseases

Topics: Adult; Biopsy; Diabetes Mellitus; Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Histamine; Histological Techniques; Humans; Injections, Intravenous; Peptides; Stimulation, Chemical; Stomach; Stomach Ulcer

Topics: Blood Glucose; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Histamine; Humans; Insulin; Methods; Pepsin A; Peptic Ulcer; Proteins; Time Factors; Zollinger-Ellison Syndrome

Topics: Biopsy; Diabetes Mellitus; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Histamine; Humans; Peptic Ulcer

Topics: Biopsy; Celiac Artery; Congo Red; Cytodiagnosis; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Histamine; Humans; Peptides; Phosphorus Isotopes; Pyrazoles; Radiography; Stomach Neoplasms; Technetium; Zollinger-Ellison Syndrome

Topics: Adult; Aged; Biopsy; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Metaplasia; Middle Aged; Pylorus

Topics: Adult; Aged; Amides; Cholecystitis; Dicarboxylic Acids; Female; Gastrins; Gastritis; Gastroenteritis; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Amides; Dicarboxylic Acids; Gastric Juice; Gastrins; Gastritis; Gastroenteritis; Humans; Peptic Ulcer

Topics: Adult; Aged; Amides; Dicarboxylic Acids; Female; Gastric Juice; Gastrins; Gastritis; Gastroenteritis; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Adult; Amides; Dicarboxylic Acids; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Adult; Aged; Amides; Dicarboxylic Acids; Gastric Juice; Gastrins; Gastritis; Humans; Middle Aged; Peptic Ulcer

Topics: Achlorhydria; Anemia, Pernicious; Gastric Juice; Gastrins; Gastritis; Histamine; Humans; Intrinsic Factor; Radioimmunoassay; Schilling Test; Vitamin B 12

Topics: Age Factors; Chronic Disease; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Glycyrrhiza; Humans; Male; Plants, Medicinal; Regeneration; Stomach Ulcer; Terpenes

Topics: Adolescent; Adult; Aged; Female; Gastric Juice; Gastrins; Gastritis; Histamine; Humans; Male; Middle Aged; Peptic Ulcer; Pyrazoles; Stimulation, Chemical

Topics: Adolescent; Adult; Child; Chronic Disease; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastritis; Histamine; Humans; Middle Aged; Pyrazoles

Topics: Adult; Aged; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastritis; Heart Diseases; Histamine; Humans; Injections, Subcutaneous; Male; Melena; Middle Aged; Neurotic Disorders; Nitrogen; Oral Hemorrhage; Peptic Ulcer; Proteins; Sclerosis; Secretory Rate; Stomach Neoplasms

Topics: Adult; Anemia, Pernicious; Duodenal Ulcer; Female; Gastrectomy; Gastric Juice; Gastrins; Gastritis; Humans; Male; Middle Aged; Stimulation, Chemical; Stomach; Stomach Diseases

Topics: Duodenal Ulcer; Female; Gastrectomy; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastroenterostomy; Humans; Middle Aged; Pylorus; Stomach Ulcer; Vagotomy

Topics: Biliary Dyskinesia; Cholecystitis; Cholecystokinin; Duodenum; Fats; Gastrins; Gastritis; Gastrointestinal Motility; Hepatitis A; Humans; Stomach

Topics: Anemia, Pernicious; Antibodies; Biopsy; Diagnosis; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Histamine; Humans; Immunochemistry; Intestinal Absorption; Intrinsic Factor; Pharmacology; Vitamin B 12

Topics: Diarrhea; Duodenal Ulcer; Gastrins; Gastritis; Humans; Postoperative Complications; Secretory Rate; Vagotomy

Topics: Gastrins; Gastritis; Humans

Topics: Amino Acids; Autonomic Nervous System Diseases; Cholecystitis; Duodenal Ulcer; Fatty Liver; Gastric Acidity Determination; Gastrins; Gastritis; Humans; Pancreatitis; Proctitis; Stomach Ulcer