gastrins and Gastritis--Atrophic

Autoimmune atrophic gastritis (AAG) is a persistent, corpus-restricted immune-mediated destruction of the gastric corpus oxyntic mucosa with reduced gastric acid and intrinsic factor secretion, leading to iron deficiency and pernicious anemia as a consequence of iron and cobalamin malabsorption. Positivity toward parietal cell (PCA) and intrinsic factor (IFA) autoantibodies is very common. AAG may remain asymptomatic for many years, thus making its diagnosis complex and often delayed. Due to the increased risk of gastric neoplasms, a timely diagnosis of AAG is clinically important.. The gold standard for AAG diagnosis is histopathological assessment of gastric biopsies obtained during gastroscopy, but noninvasive, preendoscopic serological screening may be useful in some clinical scenarios. Serum biomarkers for AAG may be divided into 2 groups: gastric autoimmunity-related biomarkers, such as PCA and IFA, and gastric corpus atrophy/reduced gastric acid secretion-related biomarkers, such as serum gastrin and pepsinogens. The present review focuses on the clinical significance and pitfalls of serum biomarkers related to gastric autoimmunity and gastric corpus atrophy, including some discussion of analytical methods.. Serum assays for PCA, IFA, gastrin, and pepsinogen I show good diagnostic accuracy for noninvasive diagnostic work-up of AAG. Diagnostic performance may increase by combining >1 of these tests, overcoming the problem of seronegative AAG. However, appropriately designed, comparative studies with well-characterized patient cohorts are needed to better define the reliability of these biomarkers in the diagnosis of patients with AAG. Currently, positive serum tests should always be followed by the state-of-art diagnostic test, that is, histopathological assessment of gastric biopsies obtained during gastroscopy to definitively confirm or rule out AAG and eventually neoplastic complications.

Topics: Atrophy; Biomarkers; Gastrins; Gastritis, Atrophic; Helicobacter pylori; Humans; Intrinsic Factor; Reproducibility of Results

Autoimmune diseases, characterized by an alteration of the immune system which results in a loss of tolerance to self antigens often coexist in the same patient. Autoimmune atrophic gastritis, characterized by the development of antibodies agains parietal cells and against intrinsic factor, leads to mucosal destruction that affects primarily the corpus and fundus of the stomach. Autoimmune atrophic gastritis is frequently found in association with thyroid disease, including Hashimoto's thyroiditis, and with type 1 diabetes mellitus, Other autoimmune conditions that have been described in association with autoimmune atrophic gastritis are Addison's disease, chronic spontaneous urticaria, myasthenia gravis, vitiligo, and perioral cutaneous autoimmune conditions, especially erosive oral lichen planus. Interestingly, however, celiac disease, another frequent autoimmune condition, seems to play a protective role for autoimmune atrophic gastritis. The elevated prevalence of autoimmune disease clustering should prompt the clinicial to exclude concomitant autoimmune conditions upon diagnosis of any autoimmune disease.

Topics: Autoantibodies; Autoantigens; Autoimmune Diseases; Biomarkers; Comorbidity; Disease Susceptibility; Gastrins; Gastritis, Atrophic; Humans; Intrinsic Factor; Parietal Cells, Gastric; Pepsinogens; Prevalence; Sensitivity and Specificity

The combination of pepsinogen, gastrin-17 and anti-H. pylori antibodies serological assays (panel test) is a non-invasive tool for the diagnosis of atrophic gastritis. However, the diagnostic reliability of this test is still uncertain.. To assess the diagnostic performance of the serum panel test for the diagnosis of atrophic gastritis.. Medline via PubMed, Embase, Scopus, Cochrane Library databases and abstracts of international conferences proceedings were searched from January 1995 to December 2016 using the primary keywords "pepsinogens," "gastrin," "atrophic gastritis," "gastric precancerous lesions." Studies were included if they assessed the accuracy of the serum panel test for the diagnosis of atrophic gastritis using histology according to the updated Sydney System as reference standard.. Twenty studies with a total of 4241 subjects assessed the performance of serum panel test for the diagnosis of atrophic gastritis regardless of the site in the stomach. The summary sensitivity was 74.7% (95% confidence interval (CI), 62.0-84.3) and the specificity was 95.6% (95%CI, 92.6-97.4). With a prevalence of atrophic gastritis of 27% (median prevalence across the studies), the negative predictive value was 91%. Few studies with small sample size assessed the performance of the test in detecting the site of atrophic gastritis.. The combination of pepsinogen, gastrin-17 and anti-H. pylori antibodies serological assays appears to be a reliable tool for the diagnosis of atrophic gastritis. This test may be used for screening subjects or populations at high risk of gastric cancer for atrophic gastritis; however, a cost-effectiveness analysis is needed.

Topics: Cost-Benefit Analysis; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Hematologic Tests; Humans; Pepsinogen A; Prevalence; Reproducibility of Results; Sensitivity and Specificity; Stomach Neoplasms

A meta-analysis was performed to assess the diagnostic value of gastrin-17 (G-17) for the early detection of chronic atrophic gastritis (CAG).An extensive literature search was performed, with the aim of selecting publications that reported the accuracy of G-17 in predicting CAG, in the following databases: PubMed, Science Direct, Web of Science, Chinese Biological Medicine, Chinese National Knowledge Infrastructure, Wanfang, and VIP. To assess the diagnostic value of G-17, the following statistics were estimated and described: sensitivity, specificity, diagnostic odds ratios (DOR), summary receiver operating characteristic curves, area under the curve (AUC), and 95% confidence intervals (CIs).Thirteen studies that met the inclusion criteria were included in this meta-analysis, comprising 894 patients and 1950 controls. The pooled sensitivity and specificity of these studies were 0.48 (95% CI: 0.45-0.51) and 0.79 (95% CI: 0.77-0.81), respectively. The DOR was 5.93 (95% CI: 2.93-11.99), and the AUC was 0.82.G-17 may have potential diagnostic value because it has good specificity and a moderate DOR and AUC for CAG. However, more studies are needed to improve the sensitivity of this diagnostic tool in the future.

Topics: Area Under Curve; Biomarkers; Gastrins; Gastritis, Atrophic; Humans; ROC Curve

Gastric carcinoids (GCs) or neuroendocrine tumours (NETs) are increasingly identified at endoscopy, and account for 0.6-2% of all gastric polyps identified. The SEER database in the US has demonstrated a rising incidence of gastric NETs amongst all NETs; from 2.2% between 1950 and 1969 to 6.0% between 2000 and 2007.. To review the literature and assist clinicians in managing patients with GCs.. A literature search was conducted through MEDLINE using search terms: gastric, carcinoid, neuroendocrine tumour, therapy, endoscopy, mucosal resection, submucosal dissection. Relevant articles were identified through manual review. The reference lists of these articles were reviewed to include further appropriate articles.. There are three types of GCs with important epidemiological, pathophysiological, histological and endoscopic differences that affect prognosis and management. Type 1 and 2 GCs develop in the context of hypergastrinaemia that originates from achlorhydria in atrophic gastritis and a gastrinoma, respectively. Type 3 GCs occur sporadically and independent of gastrin. The histological type, grade and Ki67 index are used to determine prognosis and direct clinical management. Type 1 GCs >1 cm in size and type 2 GCs should be assessed for invasion beyond the submucosa with EUS prior to endoscopic resection with EMR or ESD. Type 3 GCs should be managed as per recommendations for gastric adenocarcinoma. The treatment of advanced disease is multimodal.. Patients with gastric carcinoids should be discussed in a specialist neuroendocrine tumour multidisciplinary meeting to ensure all treatment options are explored in localised and advanced disease. Areas of controversy exist that need further research.

Topics: Dissection; Endoscopy; Gastrins; Gastritis, Atrophic; Humans; Neuroendocrine Tumors; Polyps; Prognosis; Stomach Neoplasms

Atrophic gastritis (AG) results most often from Helicobacter pylori (H. pylori) infection. AG is the most important single risk condition for gastric cancer that often leads to an acid-free or hypochlorhydric stomach. In the present paper, we suggest a rationale for noninvasive screening of AG with stomach-specific biomarkers.. The paper summarizes a set of data on application of the biomarkers and describes how the test results could be interpreted in practice.. In AG of the gastric corpus and fundus, the plasma levels of pepsinogen I and/or the pepsinogen I/pepsinogen II ratio are always low. The fasting level of gastrin-17 is high in AG limited to the corpus and fundus, but low or non-elevated if the AG occurs in both antrum and corpus. A low fasting level of G-17 is a sign of antral AG or indicates high intragastric acidity. Differentiation between antral AG and high intragastric acidity can be done by assaying the plasma G-17 before and after protein stimulation, or before and after administration of the proton pump inhibitors (PPI). Amidated G-17 will rise if the antral mucosa is normal in structure. H. pylori antibodies are a reliable indicator of helicobacter infection, even in patients with AG and hypochlorhydria.. Stomach-specific biomarkers provide information about the stomach health and about the function of stomach mucosa and are a noninvasive tool for diagnosis and screening of AG and acid-free stomach.

Topics: Achlorhydria; Antibodies, Bacterial; Biomarkers; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Mass Screening; Pepsinogen A; Pepsinogen C; Stomach Neoplasms; Vitamin B 12

Chronic atrophic gastritis, a precancerous change for gastric cancer, shows a loss of appropriate glands, Helicobacter pylori infection and autoimmune gastritis being the two main etiologic factors. While H. pylori eradication is the mandatory treatment for the former, no etiologic treatment is available for the latter, in which a Th1-type response, modulated by Tregs and Th17 cells, is involved. H. pylori-related atrophic gastritis is a risk factor for gastric adenocarcinoma, while autoimmune atrophic gastritis is also linked to a substantial risk of gastric type I carcinoid, related to the chronic stimulus exerted by hypergastrinemia on enterochromaffin-like cells. Several studies have been published on gastric cancer treatment through an active specific immunotherapy, aimed at improving the immunoregulatory response and increasing the circulating tumor-specific T cells. No study on immunotherapy of carcinoids is available but, in our experience, the administration of an antigastrin 17 vaccine induced carcinoid regression in two out of three patients treated.

Topics: Adenocarcinoma; Animals; Antineoplastic Combined Chemotherapy Protocols; Cancer Vaccines; Enterochromaffin-like Cells; Gastrins; Gastritis, Atrophic; Humans; Immunotherapy; Precancerous Conditions; Risk; 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

Gastric carcinoid tumors comprise 7% of all gastrointestinal carcinoids and have significantly increased in incidence over the past few decades. Seventy to 80% of gastric carcinoids are type I, which usually are clinically asymptomatic and found incidentally at endoscopic evaluation for abdominal pain or anemia. In this review, advances in understanding the pathophysiology of type I gastric carcinoid are highlighted. In addition, various current diagnostic and treatment options are discussed. Although type I carcinoids generally hold a benign course, rigorous investigation is needed to ensure accurate diagnosis and optimal treatment. This includes appropriate diagnostic procedures and imaging and accurate staging of tumor. Tumor size, depth of invasion, presence of metastasis, and the tumor's gastrin dependency dictate treatment options. Appropriate treatments can consist of endoscopic resection, antrectomy, medical management, or frequent follow-up. This article provides a systematic method of evaluating and treating type I gastric carcinoid.

Topics: Carcinoid Tumor; Enterochromaffin Cells; Gastrectomy; Gastric Acidity Determination; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Neoplasm Staging; Polyps; Prognosis; Pyloric Antrum; Radionuclide Imaging; Risk Factors; Stomach Neoplasms

Topics: Anti-Ulcer Agents; Biomarkers, Tumor; Chromogranin A; Disease Progression; Enterochromaffin-like Cells; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Histamine Release; Humans; Hyperplasia; Metaplasia; Middle Aged; Neuroendocrine Tumors; Parietal Cells, Gastric; Stomach Neoplasms; Synaptophysin; Vesicular Transport Proteins

In addition to regulating acid secretion, the gastric antral hormone gastrin regulates several important cellular processes in the gastric epithelium including proliferation, apoptosis, migration, invasion, tissue remodelling and angiogenesis. Elevated serum concentrations of this hormone are caused by many conditions, particularly hypochlorhydria (as a result of autoimmune or Helicobacter pylori (H pylori)-induced chronic atrophic gastritis or acid suppressing drugs) and gastrin producing tumors (gastrinomas). There is now accumulating evidence that altered local and plasma concentrations of gastrin may play a role during the development of various gastric tumors. In the absence of H pylori infection, marked hypergastrinemia frequently results in the development of gastric enterochromaffin cell-like neuroendocrine tumors and surgery to remove the cause of hypergastrinemia may lead to tumor resolution in this condition. In animal models such as transgenic INS-GAS mice, hypergastrinemia has also been shown to act as a cofactor with Helicobacter infection during gastric adenocarcinoma development. However, it is currently unclear as to what extent gastrin also modulates human gastric adenocarcinoma development. Therapeutic approaches targeting hypergastrinemia, such as immunization with G17DT, have been evaluated for the treatment of gastric adenocarcinoma, with some promising results. Although the mild hypergastrinemia associated with proton pump inhibitor drug use has been shown to cause ECL-cell hyperplasia and to increase H pylori-induced gastric atrophy, there is currently no convincing evidence that this class of agents contributes towards the development of gastric neuroendocrine tumors or gastric adenocarcinomas in human subjects.

Topics: Adenocarcinoma; Animals; Cell Movement; Cell Proliferation; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Humans; Mice; Mice, Transgenic; Models, Biological; Neoplasm Invasiveness; Neovascularization, Pathologic; Neuroendocrine Tumors; Stomach Neoplasms; Zollinger-Ellison Syndrome

The gastrointestinal peptide hormone gastrin is responsible for initiating the release of gastric acid in the stomach in response to the presence of food and/or humoral factors such as gastrin releasing peptide. However, it has a role in the growth and maintenance of the gastric epithelium, and has been implicated in the formation and growth of gastric cancers. Hypergastrinemia resulting from atrophic gastritis and pernicious anemia leads to hyperplasia and carcinoid formation in rats, and contributes to tumor formation in humans. Additionally, gastrin has been suspected to play a role in the formation and growth of cancers of the colon, but recent studies have instead implicated gastrin processing intermediates, such as gastrin-17-Gly, acting upon a putative, non-cholecystokinin receptor. This review summarizes the production and chemical structures of gastrin and of the processing intermediate gastrin-17-Gly, as well as their activities in the gastrointestinal tract, particularly the promotion of colon cancers.

Topics: Animals; Cholecystokinin; Gastric Acid; Gastrins; Gastritis, Atrophic; Gastrointestinal Neoplasms; Gastrointestinal Tract; Humans; Rats; Receptor, Cholecystokinin B; Signal Transduction

Although the gastric cancer incidence is decreasing, this neoplasia remains one of the major causes of oncological mortality. Because of an insidious development, gastric cancer is often diagnosed in an advanced stage and consequently with a poor prognosis. Accurate non-invasive tests should be extremely useful in order to detect gastric neoplasm in an early phase. In clinical practice, there is no reliable bio-marker for detecting this malignant disease. However, intestinal as well as diffuse types of gastric cancer are preceded by gastric mucosa inflammation. Furthermore, the intestinal type of the neoplasia is, generally, related to chronic atrophic gastritis, especially if associated with intestinal metaplasia. In particular, the risk of the neoplasm is linked to both extension and severity of gastric atrophy. Serological parameters such as serum pepsinogens I (PGI) and II (PGII), gastrin-17 (G-17) cytokines (e.g. IL-8), antiparietal cells, IgG anti-Hp and CagA antibodies and lastly ghrelin supply information about either atrophic or inflammatory conditions characterising gastric mucosa. Low PGI and PGI/PGII ratio levels, especially if combined with high G-17 levels, are recognised bio-markers of corpus atrophic gastritis. Low G-17 levels could be, also, suggestive of antral atrophic gastritis. Furthermore, plasmatic ghrelin levels seem to be also a bio-marker of corpus atrophy. Anti-Hp IgG and CagA antibodies as well as PGII levels are able to detect gastric inflammation. Serological parameters could select subjects at risk for gastric mucosa alterations such as inflammation or atrophy, rather than gastric cancer itself. This review analyses the information derived from serological bio-markers as well as the involved clinical studies.

Topics: Biomarkers; Cytokines; Diagnosis, Differential; Evidence-Based Medicine; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Ghrelin; Humans; Interleukin-8; Pepsinogens; Stomach Diseases; Stomach Neoplasms

Topics: Biomarkers; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Pepsinogens; Risk Factors; Stomach Neoplasms

The hormone gastrin plays 2 important roles in gastrointestinal physiology--1 as a major factor in meal-stimulated gastric acid secretion and the other as a trophic hormone for epithelial and enterochromaffin cells. These roles are exaggerated to the point of pathology under conditions of chronic hypergastrinemia as exemplified by the Zollinger-Ellison syndrome and pernicious anemia. More recently, the concern about the potential risk of chronic hypergastrinemia has risen because of the widespread use of proton pump inhibitors for maintenance therapy in reflux esophagitis. For this reason, we present a concise overview of the origin, causes, and potential risks of chronic hypergastrinemia.

Topics: Animals; Enzyme Inhibitors; Gastric Acid; Gastrinoma; Gastrins; Gastritis, Atrophic; Humans; Peptic Ulcer; Proton Pump Inhibitors; Risk Factors; Zollinger-Ellison Syndrome

The most frequent conditions of hypergastrinemia in man are the Zollinger-Ellison syndrome with autonomous gastrin hypersecretion by the tumour cell and reactive hypergastrinemia in type A autoimmune chronic atrophic gastritis with achlorhydria causing unrestrained gastrin release from the gastrin-producing antral G-cells. Both entities differ with respect to the pH in the gastric fluid, which is < 2 in patients with Zollinger-Ellison syndrome and neutral in type A gastritis. Other conditions with moderate hypergastrinemia as treatment with proton pump inhibitors, gastric outlet obstruction, previous vagotomy, chronic renal failure or short bowel syndrome are of minor clinical importance.

Topics: Autoimmune Diseases; Carcinoid Tumor; Diagnosis, Differential; Duodenal Neoplasms; Enterochromaffin-like Cells; Gastric Mucosa; Gastrinoma; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Pancreatic Neoplasms; Stomach Neoplasms; Zollinger-Ellison Syndrome

Gastric neuroendocrine tumours (NET) are rare. Clinically they are classified in tumours type 1 to 3. The histological classification is according to the WHO 2000 classification for endocrine tumours. NET type 1 occur in coincidence with chronic atrophic gastritis, as single or multiple small tumours. The prognosis of type 1 tumours is excellent, with no tumour related death reported during follow-up. NET type 2 are part of the MEN-1 syndrome. These tumours may be more aggressive and even develop metastasis. However, in most patients with MEN-1 the prognosis is due to other manifestations of the disease as duodenal or pancreatic neuroendocrine tumours. Gastric neuroendocrine tumours type 3 are sporadic tumours without relationship to other gastric pathology. They tend to occur earlier, without sex preference. These tumours may develop an aggressive course, with metastatic disease and an overall poor prognosis. Thus, aggressive surgical therapy is recommended.

Topics: Biopsy; Chronic Disease; Diagnosis, Differential; Duodenal Neoplasms; Enterochromaffin-like Cells; Gastric Mucosa; Gastrinoma; Gastrins; Gastritis, Atrophic; Humans; Multiple Endocrine Neoplasia Type 1; Neuroendocrine Tumors; Pancreatic Neoplasms; Prognosis; Stomach Neoplasms

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

Topics: Biomarkers; Diagnostic Techniques, Endocrine; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Hyperparathyroidism; Radioimmunoassay; Reagent Kits, Diagnostic; Reference Values; Zollinger-Ellison Syndrome

Topics: Gastric Acid; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Polyps; Stomach Neoplasms

Gastric carcinoids are rare neuroendocrine tumors, usually classified as type I, if associated with atrophic body gastritis; type II, if associated with Zollinger-Ellison syndrome and multiple endocrine neoplasia type I, and type III, in the absence of any gastric pathology (sporadic tumors). The pathological features, as well as the prognosis of the tumor and the patient's survival strictly depend on this classification. The correct management of the patient with gastric carcinoid can only be proposed when the tumor has been classified by an accurate pathological and clinical evaluation of the patient. While the therapeutic approach in types I and II is based on a conservative strategy, including endoscopic resection, an adequate follow-up program, and the possible use of somatostatin analogues, an aggressive surgical approach is required in type III.

Topics: Enterochromaffin Cells; Gastrins; Gastritis, Atrophic; Humans; Neuroendocrine Tumors; Stomach Neoplasms

Helicobacter pylori (Hp) infection represents a crucial factor in pathogenesis of gastric cancer (GC). Factors emanating from bacterium as well as from environmental contributions such as salt diet and inadequate supply of antioxidants, affect the risk for GC development.. Atrophic gastritis is considered to be a precursor lesion of intestinal type GC that is accompanied by hypergastrinemia with subsequent induction of cyclooxygenase-2 (COX-2), whose products are responsible for slowing apoptosis and for angiogenesis in GC tumor. The involvement of proinflammatory cytokines (especially IL-1 and IL-8) and reactive oxygen species (ROS) due to NF kappa B activation, increased cell proliferation combined with inhibition of apoptosis as well as upregulation of peroxisome proliferation activated receptor gamma (PPAR gamma) and inducible nitric oxide synthase (iNOS) appear to be major molecular biology alterations in pathogenesis of GC.. These results suggest the therapeutic usefulness of inhibitors of gastrin expression and release such as powerful somatostatin analogs (Sandostatin) or blockers of COX-2 (coxibs) in the control of GC development and progression as chemopreventive agents. Comparative genomic and proteomic is the key in identifying biomarkers in host and bacterium for the prediction of gastric cancer in Hp-infected patients.

Topics: Animals; Apoptosis; Bacterial Proteins; Cyclooxygenase 2; Cytokines; Gastrins; Gastritis, Atrophic; Gene Expression Regulation, Neoplastic; Helicobacter Infections; Helicobacter pylori; Humans; Isoenzymes; Membrane Proteins; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; Prostaglandin-Endoperoxide Synthases; Receptors, Cytoplasmic and Nuclear; Stomach Neoplasms; Survival Rate; Transcription Factors

On the basis of the levels of serum pepsinogen I (S-PGI) and gastrin-17 (S-G-17) as well as Helicobacter pylori - antibodies assayed from a blood sample it is possible to establish with high sensitivity and specificity whether the patient has gastritis, whether the gastritis is atrophic or not and in which part of the stomach the atrophic changes are located. The test enables the identification of patients whose risk of gastric cancer, of the consequences of vitamin B12 deficiency (e.g. elevated levels of homocysteine) or of peptic ulcer is considerably increased and who can then undergo gastroscopy. It also facilitates the diagnosis of non-atrophic Helicobacter gastritis enabling treatment before endoscopy.

Topics: Finland; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Humans; Pepsinogen A; Peptic Ulcer; Stomach Neoplasms; Vitamin B 12 Deficiency

Topics: Duodenal Ulcer; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-1; Methylhistamines; Somatostatin; Tumor Necrosis Factor-alpha

Topics: Animals; Cell Division; Chronic Disease; Duodenal Ulcer; Enterochromaffin-like Cells; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Histamine Release; Humans; Somatostatin

Gastric epithelial dysplasia is the earliest visible stage of neoplasia. Most histopathologists can recognize or at least suspect it, and a set of established clinical responses follow its detection. In contrast, proliferations and dysplastic changes of gastric endocrine cells are difficult to identify and generally neglected. Such changes are known to predispose to the development of carcinoid tumours and usually arise in patients with corpus-predominant atrophic gastritis and elevated gastrin levels. A report in this issue suggests that patients with dysplasia of the enterochromaffin-like cells have a much greater risk of developing carcinoid tumours than previously suspected. These carcinoids (known as type I) tend to have an indolent course, are almost never functional and have a favourable prognosis; nevertheless, they need to be detected and excised endoscopically. Because of the small numbers of patients in this series and the relatively short follow-up time of the study, it would be premature to issue guidelines on the long-term management of patients with atrophic gastritis and hypergastrinaemia. However, it is incumbent on clinical researchers with access to well-defined cohorts, such as the one studied here, to continue the follow-up studies that will lead to a more precise definition of risk and to the development of usable evidence-based clinical strategies.

Topics: Enterochromaffin-like Cells; Epithelium; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastrointestinal Neoplasms; Humans; Intestinal Mucosa; Precancerous Conditions; Prognosis; Risk Factors

The role of gastrin in the pathophysiology of two diseases affecting the human stomach, the Zollinger Ellison syndrome (ZES) and the pernicious anemia (PA), is reviewed. Both diseases present chronic hypergastrinemia but from different origins. The ZES is characterized by the occurrence of ectopic endocrine gastrin-secreting tumors and PA by a fundic atrophic gastritis leading to complete atrophy of fundus and resulting in achlorhydria. In PA, the lack of acid induces continuous gastrin cell activation and is responsible for the subsequent gastrin hypersynthesis and secretion. In ZES, hypergastrinemia causes hypertrophy of the oxyntic mucosa, which, in addition, displays hyperplasia of parietal and mucus cells. In both diseases, hypergastrinemia also induces the hyperproliferation of enterochromaffin-like endocrine cells in the fundic mucosa, which can offer all aspects from hyperplasia, then dysplasia, until true carcinoid tumor. The influence of antisecretory treatments and MEN 1 in the ZES as well as that of several other factors and antrectomy in PA on the behavior of the different gastric cells is evoked. Finally, the role that gastrin and its receptor play in the maintenance of the normal development of gastric mucosa and gastric acid secretion is emphasized by results observed in gene knockout models.

Topics: Anemia, Pernicious; Animals; Atrophy; Autoimmune Diseases; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Hypertrophy; Mice; Mice, Knockout; Multiple Endocrine Neoplasia Type 1; Zollinger-Ellison Syndrome

The safety of proton-pump inhibitors (PPIs) for long-term use is reviewed. PPIs are being used with increasing frequency to inhibit secretion of gastric acid in order to treat acid-related disorders such as gastroesophageal reflux disease and peptic ulcer disease. Some patients may require long-term acid suppressive treatment to control the symptoms of their disease, which raises questions about the long-term safety of PPIs. A thorough literature search was conducted, and the clinical consequences of sustained hypergastrinemia induced by all antisecretory therapy, the consequences of atrophic gastritis in patients infected with Helicobacter pylori, the effects of hypochlorhydria on bacterial overgrowth and nutrient absorption, and possible interactions of PPIs with other drugs were identified as areas of concern with long-term use of PPIs. Short- and long-term studies showed that PPIs have a wide safety margin and a favorable adverse-event profile with few drug interactions. Available data support the short- and long-term safety of PPIs.

Topics: Anti-Ulcer Agents; Colonic Neoplasms; Drug Interactions; Enterochromaffin Cells; Gastric Acid; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Proton Pump Inhibitors; Stomach Neoplasms

Topics: Chronic Disease; Duodenal Ulcer; Gastric Acid; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Stomach Ulcer; Virulence

The enterochromaffin-like (ECL) cell of the oxyntic, acid-secreting mucosa is at present the most extensively studied endocrine cell type in the gastrointestinal tract. It is functionally related to acid secretion through paracrine release of histamine. Its ability to undergo proliferation in response to the trophic stimulus of hypergastrinemia has important implications in pathology, being involved in the development of ECL-cell carcinoid tumors of rodents treated with powerful inhibitors of acid secretion as well as in that of most human gastric carcinoids which, with rare exceptions, are composed of ECL cells. The various aspects of the ECL-cell response to hypergastrinemia in humans are discussed in this review. The trophic effect of gastrin is specific for ECL cells and its sensitivity is enhanced by the female sex and by the genetic background of the multiple endocrine neoplasia type 1 (MEN-1) syndrome. Exposure of ECL cells to hypergastrinemia induces peculiar changes in the structure of cytoplasmic granules and triggers the phenotypic expression of a novel protein, the alpha subunit of glycoprotein hormones, absent in normal cells. The ECL-cell hyperplasia driven by hypergastrinemia may influence the hypersecretory gastric state of patients with Zollinger-Ellison syndrome (ZES) by inappropriate intramucosal secretion of histamine and may contribute to the high circulating levels of basic fibroblast growth factor (bFGF), an ECL-cell product responsible for parathyroid mitogenic effects in MEN-1 patients. However, hypergastrinemia per se cannot promote evolution of hyperplasia into carcinoid tumors, for which additional unknown factors, particularly associated with atrophic gastritis or MEN-1 syndrome, are required. ECL-cell carcinoids developing within these backgrounds have a strikingly more favorable course than their gastrin-independent counterpart. Suppression of hypergastrinemia, either by antrectomy or treatment with somatostatin analogues, may induce regression of both ECL-cell hyperplasia and gastrin-sensitive ECL-cell carcinoids.

Topics: Carcinoid Tumor; Enterochromaffin Cells; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Stomach Neoplasms; Zollinger-Ellison Syndrome

Gastric carcinoid tumors were previously believed to be rare lesions, representing less than 2% of all carcinoid tumors and less than 1% of all stomach neoplasms. More recent studies have demonstrated that they may constitute as much as 10-30% of carcinoid tumors. Patients with conditions associated with hypergastrinemia, such as chronic atrophic gastritis, Zollinger-Ellison syndrome with multiple endocrine neoplasia type 1 (ZES-MEN-1), and pernicious anemia, display a markedly elevated incidence of gastric carcinoid tumor formation. A classification system distinguishing three types of gastric carcinoid tumor has been proposed: 1) tumors associated with chronic atrophic gastritis, 2) tumors associated with Zollinger-Ellison syndrome, and 3) sporadic lesions. Tumors that develop in association with hypergastrinemia are usually composed of enterochromaffin-like (ECL) cells, in contrast to sporadic lesions that contain a variety of endocrine cell types (enterochromaffin, ECL, X). In both intact animal models such as the rat and Praomys (mastomys) natalensis and in isolated purified ECL cell preparations, gastrin has been demonstrated to exert a powerful trophic effect on ECL cells, in addition to stimulating histamine secretion. It is apparent that hypergastrinemia-associated gastric carcinoids display relatively benign biological behavior. Sporadic lesions require aggressive surgical management on diagnosis. Type I and type II (hypergastrinemia-associated) lesions can be managed initially by endoscopic excision of accessible tumors, followed by endoscopic surveillance. If tumors recur, antrectomy and local excision may be used to remove the source gastrin, resulting in cure in the vast majority of patients.

Topics: Animals; Carcinoid Tumor; Decision Trees; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Incidence; Multiple Endocrine Neoplasia Type 1; Stomach Neoplasms; Zollinger-Ellison Syndrome

Topics: Achlorhydria; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Histamine; Humans; Hyperplasia; Pyloric Antrum; Stomach

Topics: Achlorhydria; Carcinoid Tumor; Gastrectomy; Gastrins; Gastritis, Atrophic; Humans; Stomach Neoplasms

Topics: Adenocarcinoma; Carcinoid Tumor; Enterochromaffin Cells; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Omeprazole; Stomach Neoplasms; Zollinger-Ellison Syndrome

Three cases of gastric carcinoid polypi associated to atrophic gastritis and high levels of seric gastrin, are presented. One of the cases was a multiple micropolyposis the literature regarding this association is reviewed and the therapy discussed. Tumors of greater than 2 cm have to be considered potentially malignant and be treated likewise. The treatment of the micropolyposis is not well established.

Topics: Achlorhydria; Adult; Autoimmune Diseases; Carcinoid Tumor; Female; Follow-Up Studies; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Neoplasms, Multiple Primary; Polyps; Pyloric Antrum; Stomach Neoplasms

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

Topics: Anemia, Pernicious; Gastric Acid; Gastric Emptying; Gastrins; Gastritis, Atrophic; Genetic Markers; Humans; Pepsinogens; Peptic Ulcer

The past 20 years have seen gastrin attain true hormonal status. Its structure has been characterized, it has been synthesized, radioimmunoassays for its measurement in blood and tissues have been developed and its physiology and metabolism elucidated. Of much interest to clinicians has been the association between gastrin and tumours of the pancreas (gastrinomas) and atrophic gastritis. The advent of gastrin measurement has facilitated the diagnosis of gastrinoma and the availability of powerful acid suppressants has altered the therapy of gastrinoma.

Topics: Duodenal Ulcer; Gastrins; Gastritis, Atrophic; Humans; Kidney Failure, Chronic; Radioimmunoassay; Zollinger-Ellison Syndrome

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

We aim to investigate the therapeutic effect of self-made

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

Topics: Anti-Inflammatory Agents; Brassica; Cytokines; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-17; Interleukin-18; Interleukin-8; Pepsinogen A; Tumor Necrosis Factor-alpha; Urea

Develop a program to identify, treat, and prevent severe atrophic gastritis to reduce gastric cancer incidence and mortality.. In total, 2,847 people aged > 40 years old underwent serological noninvasive screening for atrophic gastritis by identifying postprandial gastrin-17 and pepsinogen-1 in the fasting state. Anti-H pylori IgG was found in 2,134 patients. Seven years later, 2,220 patientswho had undergone serological noninvasive screening were asked to fill out a questionnaire survey (were interviewed). We could not find any information on 627 of 2,847 patients. Next, 75 patients with multifocal atrophic gastritis who underwent gastroscopy and biopsies (the Updated Sydney System (USS)) were selected. To study gastrin-17 production, morpho-functional correlation was studies in 75 patients with multifocal atrophic gastritis.. During seven years, no reported case of gastric cancer was done among 2,220 persons who underwent serological screening and treatment. In the same population, 4.3 persons who did not receive screening during the same period, developed gastric cancer and died of it. In this study, we can say that 4.3 lives were saved out of 2,220 tested persons. The cost for screening this number of people amounted to €23,750. A comparison of the prevalence rate of the four stages of multifocal atrophic gastritis based on the data of the histopathology tests and noninvasive serologic screening in accordance with OLGA classification showed a strong correlation (the correlation coefficient is 0.812). This finding suggested that using this classification not only for histopathology tests for atrophic gastritis but also for serologic markers of antral mucosa and corpus ventriculi atrophy: gastrin-17 and pepsinogen-1.. Complex pathogenetic treatment of atrophic gastritis significantly reduced gastric cancer risk and incidence for such patients.
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Topics: Adult; Antineoplastic Combined Chemotherapy Protocols; Biomarkers; Case-Control Studies; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Mass Screening; Pepsinogen A; Precancerous Conditions; Prognosis; Prospective Studies; Stomach Neoplasms

Helicobacter pylori (Hp) infection affects a substantial proportion of the world population and is a major risk factor of gastric cancer (GC). The caveats of common Hp-tests can be evaded by a serological biomarker test (GastroPanel®, Biohit Oyj, Helsinki), the most comprehensive Hp-test on the market. The clinical validation of Helicobacter pylori IgG ELISA of the new-generation GastroPanel® test is reported. The aim of the study is to validate the clinical performance of the Helicobacter pylori IgG ELISA test in diagnosis of biopsy-confirmed Hp-infection in gastroscopy referral patients.. A cohort of 101 patients (mean age=50.1 years) referred for gastroscopy at the outpatient Department of Gastroenterology (SM Clinic, St. Petersburg) were examined by two test versions to validate the new-generation GastroPanel®. All patients were examined by gastroscopy and biopsies, which were stained with Giemsa for specific identification of Hp in the antrum (A) and corpus (C).. Biopsy-confirmed Hp-infection was found in 64% of patients, most often confined to antrum. The overall agreement between Hp IgG ELISA and gastric biopsies in Hp-detection was 91% (95%CI=84.1-95.8%). Hp IgG ELISA diagnosed biopsy-confirmed Hp (A&C) with sensitivity (SE) of 92.3%, specificity (SP) of 88.6%, positive predictive value (PPV) of 93.8% and negative predictive value (NPV) of 86.1%, with AUC=0.904 (95%CI=0.842-0.967). In ROC analysis for Hp detection (A&C), Hp IgG ELISA shows AUC=0.978 (95%CI=0.956-1.000).. The Hp IgG ELISA test successfully concludes the clinical validation process of the new-generation GastroPanel® test, which retains the unrivalled diagnostic performance of all its four biomarkers, extensively documented for the first-generation test in different clinical settings.

Topics: Adolescent; Adult; Antibodies, Bacterial; Biopsy; Enzyme-Linked Immunosorbent Assay; Female; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Referral and Consultation; Stomach; Stomach Neoplasms; Young Adult

Netazepide, a gastrin/cholecystokinin 2 receptor antagonist, once daily for 12 weeks reduced the number of tumours and size of the largest one in 16 patients with autoimmune chronic atrophic gastritis (CAG), achlorhydria, hypergastrinaemia and multiple gastric neuroendocrine tumours (type 1 gastric NETs), and normalized circulating chromogranin A (CgA) produced by enterochromaffin-like cells, the source of the tumours. The aim was to assess whether longer-term netazepide treatment can eradicate type 1 gastric NETs.. After a mean 14 months off netazepide, 13 of the 16 patients took it for another 52 weeks. Assessments were: gastroscopy; gene-transcript expression in corpus biopsies using quantitative polymerase chain reaction; blood CgA and gastrin concentrations; and safety assessments.. While off-treatment, the number of tumours, the size of the largest one, and CgA all increased again. Netazepide for 52 weeks: cleared all tumours in 5 patients; cleared all but one tumour in one patient; reduced the number of tumours and size of the largest one in the other patients; normalized CgA in all patients; and reduced mRNA abundances of CgA and histidine decarboxylase in biopsies. Gastrin did not increase further, confirming that the patients had achlorhydria. Netazepide was safe and well tolerated.. A gastrin/cholecystokinin 2 receptor antagonist is a potential medical and targeted treatment for type 1 gastric NETs, and an alternative to regular gastroscopy or surgery. Treatment should be continuous because the tumours will regrow if it is stopped. Progress can be monitored by CgA in blood or biomarkers in mucosal biopsies.

Topics: Achlorhydria; Aged; Autoimmune Diseases; Benzodiazepinones; Chromogranin A; Gastrins; Gastritis, Atrophic; Histidine Decarboxylase; Humans; Middle Aged; Neuroendocrine Tumors; Phenylurea Compounds

Helicobacter-induced atrophic gastritis with a hypochlorhydric milieu is a risk factor for gastric cancer. Microbes colonising acid-free stomach oxidise ethanol to acetaldehyde, a recognised group 1 carcinogen.. To assess gastric production of acetaldehyde and its inert condensation product, non-toxic 2-methyl-1,3-thiazolidine-4-carboxylic acid (MTCA), after alcohol intake under treatment with slow-release L-cysteine or placebo.. Seven patients with biopsy-confirmed atrophic gastritis, low serum pepsinogen and high gastrin-17 were studied in a cross-over single-blinded design. On separate days, patients randomly received 200 mg slow-release L-cysteine or placebo with intragastric instillation of 15% (0.3 g/kg) ethanol. After intake, gastric concentrations of ethanol, acetaldehyde, L-cysteine and MTCA were analysed.. Administration of L-cysteine increased MTCA (p < .0004) and decreased gastric acetaldehyde concentrations by 68% (p < .0001). The peak L-cysteine level was 7552 ± 2687 μmol/L at 40 min and peak MTCA level 196 ± 98 μmol/L at 80 min after intake. Gastric L-cysteine and MTCA concentrations were maintained for 3 h. The AUC for MTCA was 11-fold higher than acetaldehyde, indicating gastric first-pass metabolism of ethanol. With placebo, acetaldehyde remained elevated also at low ethanol concentrations representing 'non-alcoholic' beverages and food items.. After gastric ethanol instillation, slow-release L-cysteine eliminates acetaldehyde to form inactive MTCA, which remains in gastric juice for up to 3 h. High acetaldehyde levels indicate a marked gastric first-pass metabolism of ethanol resulting in gastric accumulation of carcinogenic acetaldehyde. Local exposure of the gastric mucosa to acetaldehyde can be mitigated by slow-release L-cysteine capsules.

Topics: Acetaldehyde; Adult; Carbolines; Carcinogenesis; Cross-Over Studies; Cysteine; Delayed-Action Preparations; Ethanol; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter; Humans; Male; Middle Aged; Single-Blind Method; Stomach Neoplasms; Sweden

Autoimmune chronic atrophic gastritis (CAG) causes hypochlorhydria and hypergastrinaemia, which can lead to enterochromaffin-like (ECL) cell hyperplasia and gastric neuroendocrine tumours (type 1 gastric NETs). Most behave indolently, but some larger tumours metastasise. Antrectomy, which removes the source of the hypergastrinaemia, usually causes tumour regression. Non-clinical and healthy-subject studies have shown that netazepide (YF476) is a potent, highly selective and orally-active gastrin/CCK-2 receptor antagonist. Also, it is effective in animal models of ECL-cell tumours induced by hypergastrinaemia.. To assess the effect of netazepide on tumour biomarkers, number and size in patients with type I gastric NETs.. We studied 8 patients with multiple tumours and raised circulating gastrin and chromogranin A (CgA) concentrations in an open trial of oral netazepide for 12 weeks, with follow-up 12 weeks later. At 0, 6, 12 and 24 weeks, we carried out gastroscopy, counted and measured tumours, and took biopsies to assess abundances of several ECL-cell constituents. At 0, 3, 6, 9, 12 and 24 weeks, we measured circulating gastrin and CgA and assessed safety and tolerability.. Netazepide was safe and well tolerated. Abundances of CgA (p<0.05), histidine decarboxylase (p<0.05) and matrix metalloproteinase-7(p<0.10) were reduced at 6 and 12 weeks, but were raised again at follow-up. Likewise, plasma CgA was reduced at 3 weeks (p<0.01), remained so until 12 weeks, but was raised again at follow-up. Tumours were fewer and the size of the largest one was smaller (p<0.05) at 12 weeks, and remained so at follow-up. Serum gastrin was unaffected.. The reduction in abundances, plasma CgA, and tumour number and size by netazepide show that type 1 NETs are gastrin-dependent tumours. Failure of netazepide to increase serum gastrin further is consistent with achlorhydria. Netazepide is a potential new treatment for type 1 NETs. Longer, controlled trials are justified.. European Union EudraCT database 2007-002916-24 https://www.clinicaltrialsregister.eu/ctr-search/search?query=2007-002916-24ClinicalTrials.gov NCT01339169 http://clinicaltrials.gov/ct2/show/NCT01339169?term=yf476&rank=5.

Topics: Aged; Antineoplastic Agents; Benzodiazepinones; Biomarkers; Biopsy; Chromogranin A; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Male; Middle Aged; Neuroendocrine Tumors; Phenylurea Compounds; Receptor, Cholecystokinin B; Stomach Neoplasms; Treatment Outcome; Tumor Burden

Serological biomarkers can be used for non-invasive diagnosis of gastritis and atrophic gastritis. The aim of this study was to compare the validity of serum levels of pepsinogen I (PGI) and II (PGII), gastrin-17 (G-17) and Helicobacter pylori antibodies (Hpab) with that of the gold standard histology for diagnosis of atrophic gastritis in a population sample from Northern Sweden.. In all, 1000 subjects underwent endoscopies with biopsies. Serum biomarkers were available in 976 subjects for independent diagnosis of gastric mucosal status using a predetermined diagnostic algorithm.. Overall agreement between histology and serological biomarkers in diagnosing corpus atrophy was 96% (CI 95%: 95-97%). Sensitivity and specificity of markers for atrophic gastritis were 71% (CI 68-74%) and 98% (CI 97-99%) respectively, corresponding to 69% (CI 95%: 66-72%) and 98% (95% CI 97-99%) positive and negative predictive values. The positive likelihood ratio was 35.5 (95% CI: 35.0-36.0%). In subgroups with normal stomachs, H. pylori non-atrophic gastritis and H. pylori-negative gastritis by histology, the prevalence of corpus atrophy diagnosed with the biomarkers was 0.8% and 4.9%, respectively. In total, 6.6% of subjects in the study population had corpus atrophy according to the serological biomarkers. CONCLUSIONS. Serological biomarkers show a high degree of accuracy as a non-invasive method to diagnose corpus atrophy, which is common in the general population.

Topics: Antibodies, Bacterial; Biomarkers; Female; Gastrins; Gastritis, Atrophic; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Reproducibility of Results; Sensitivity and Specificity

The aim of this study was to assess the gastric histopathology and serum gastrin-17 and pepsinogens profiles in patients with duodenal ulcer before and after Helicobacter pylori eradication in a population with a very high prevalence of H. pylori. At the same time we assessed the role of H. pylori density on these variables.. Eighty Caucasian patients with H. pylori-associated duodenal ulcer before treatment and 1 year after randomized eradication were studied. Among patients with unsuccessful eradication two groups were distinguished according to the data obtained after treatment: the group with negative rapid urease test and decreased bacterial density according to morphological score (partial elimination group); the group with positive rapid urease test and high bacterial density (failed eradication group).. One year after successful eradication, serum levels of gastrin-17, pepsinogen I and pepsinogen II decreased. Similar changes of serum pepsinogen I and pepsinogen II levels were observed in patients with partial elimination of H. pylori infection. In the group with successful eradication, inflammation, activity, atrophy and number of lymphoid follicles in the antral mucosa fell. In the group with partial elimination, antral mucosa activity and H. pylori score reduced. Other morphological changes were statistically non-significant.. Patients with duodenal ulcer after successful eradication have improvement of morphological and functional characteristics of gastric mucosa.

Topics: Adolescent; Adult; Anti-Bacterial Agents; Antibodies, Bacterial; Biomarkers; Down-Regulation; Drug Therapy, Combination; Duodenal Ulcer; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Proton Pump Inhibitors; Time Factors; Treatment Failure; Treatment Outcome; Urease; Young Adult

Noninvasive diagnosis of atrophic gastritis would help to identify individuals at increased risk of gastric carcinoma. In the present study, we evaluated the utility of a serological panel combining pepsinogen I and II, gastrin-17, and anti-Helicobacter pylori antibodies (Gastropanel) as a screening method for atrophic gastritis.. The serological panel was evaluated in 56 patients divided in two groups: group 1 consisted of 47 patients with uninvestigated dyspepsia and group 2 was composed of nine consecutive patients with gastric carcinoma. In all patients, we performed endoscopy with biopsies of the gastric antrum and body. Levels of pepsinogen I and II, gastrin-17, and anti-H. pylori antibodies were determined through a specific EIA test (Biohit plc, Helsinki, Finland) in fasting serum samples.. Atrophic gastritis was significantly more frequent in patients with gastric carcinoma than in those with dyspepsia (56 vs 6%; p = 0.0015). Agreement between the Gastropanel and gastric histology was good (kappa = 0.68). The sensitivity and specificity of the Gastropanel in the diagnosis of atrophic gastritis was 87.5% and 100%, respectively. However, the Gastropanel would not have detected four of the nine cases of gastric carcinoma, since these tumors arose in stomachs with nonatrophic mucosa.. Gastropanel is a useful noninvasive method for the diagnosis of atrophic gastritis. However, its utility as a screening method is limited by cases of gastric carcinoma that arise in stomachs without atrophic mucosa.

Topics: Adult; Aged; Antibodies, Bacterial; Female; Gastrins; Gastritis, Atrophic; Helicobacter pylori; Humans; Male; Pepsinogen A; Pepsinogen C; Serologic Tests

Gastrin and pentagastrin stimulate thyroid C cells and elevate serum calcitonin levels. Gastrin levels may be elevated when histamine-2 receptor blockers (H2RB) and/or proton pump inhibitors (PPI) are used, or in patients with pernicious anemia (PA). This study was designed to investigate the long-term effects of elevated gastrin levels on serum calcitonin levels. We conducted a pentagastrin stimulation test to evaluate C cell reserves in patients who had been using PPI and/or H2RB for an extended period, as well as in patients with PA. We compared the results with a healthy control group of similar age and sex. A total of 40 controls (26 women, 24 men) and 25 patients (15 women, 10 men) using H2RB and/or PPI, and 37 patients (24 women, 13 men) with PA were enrolled. The groups were similar in terms of mean age and sex distribution. Mean fasting gastrin levels, and mean baseline and pentagastrin-stimulated calcitonin levels were significantly higher in the H2RB+PPI and PA groups than in controls. No significant differences were observed between the H2RB+PPI and PA groups. There was no correlation between gastrin and calcitonin levels. However, mean calcitonin levels were significantly higher in subjects with high baseline gastrin levels than in controls. The prevalence of autoimmune thyroid disease was 32% in the PA group. Patients with PA and thyroiditis had significantly higher baseline gastrin levels than patients with PA only (p<0.01). PA with autoimmune thyroid disease had also significantly higher baseline and pentagastrin-stimulated calcitonin levels than did PA patients without autoimmune thyroid disease. In conclusion, chronic elevated gastrin levels led to elevated calcitonin levels. Further histopathological studies showing C cell hyperplasia are needed to confirm the mechanism of this relationship.

Topics: Adult; Anemia, Pernicious; Calcitonin; Female; Gastric Juice; Gastrins; Gastritis, Atrophic; Hematologic Tests; Histamine Antagonists; Humans; Male; Middle Aged; Pentagastrin; Proton Pump Inhibitors; Thyroid Gland; Time

The aim of this study was to determine the effect of 6-12 months of treatment with esomeprazole on the histopathology of the gastric mucosa.. Two identically designed, randomized, placebo-controlled trials of esomeprazole 40, 20, or 10 mg daily for up to 6 months, as well as a noncomparative, multicenter trial of esomeprazole 40 mg daily for up to 12 months, were conducted in 1326 patients with healed erosive esophagitis (1294 negative for Helicobacter pylori [H. pylori]). Gastric biopsy samples were obtained before treatment and on completion of (or discontinuation from) the trials. Samples were evaluated for the presence of H. pylori, characteristics of acute gastritis or atrophic gastritis, and enterochromaffin-like cell pathology.. During treatment with esomeprazole, the number of patients with an improvement in gastric histological scores was typically greater than or equal to the number who worsened. Gastric histological scores worsened for each corporal or antral characteristic of gastritis in <6.2% of patients. Histological scores with esomeprazole and placebo were similar throughout the 6-month trials. Only one among 1326 patients treated with esomeprazole (H. pylori negative) had evidence of treatment-emergent atrophic gastritis. On final biopsy, 5-12% of patients had abnormal enterochromaffin-like cell scores (simple, linear, or micronodular hyperplasia). There were no instances of enterochromaffin-like cell dysplasia, carcinoids, or neoplasia.. Patients with healed erosive esophagitis receiving esomeprazole for up to 12 months had minor fluctuations in gastric histological scores, similar to those experienced in untreated populations. Use of esomeprazole did not raise any safety concerns with respect to the development of atrophic gastritis, or cause clinically significant changes in enterochromaffin-like cells.

Topics: Adult; Anti-Ulcer Agents; Enterochromaffin-like Cells; Esomeprazole; Esophagitis; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Metaplasia

: To investigate the effect of the eradication of Helicobacter pylori on histological gastritis.. : Twenty-six patients with moderate to severe atrophy received successful eradication therapy of H.pylori. Four patients dropped out and 22 were followed up prospectively for 5 years. The grades of gastritis were estimated from gastric biopsy specimens. The grade of intestinal metaplasia was also evaluated by dye-endoscopy using methylene blue (methylthioninium chloride). The serum levels of pepsinogen, gastrin and anti-parietal cell antibody were also determined.. : The grades of atrophy decreased in patients with successful eradication therapy in the gastric corpus (before vs. 5 years after eradication, 2.09 +/- 0.15 vs. 0.91 +/- 0.17; P < 0.01) and in the antrum (2.14 +/- 0.17 vs. 1.36 +/- 0.17; P < 0.01). The levels of intestinal metaplasia were also decreased in the corpus (0.91 +/- 0.24 vs. 0.50 +/- 0.16; P < 0.05) and in the antrum (1.41 +/- 0.20 vs. 1.00 +/- 0.16; P < 0.05), which was also demonstrated by the methylene blue (methylthioninium chloride) staining method (33.4 +/- 8.2% vs. 23.0 +/- 6.5%; P < 0.05). The improvement of corpus atrophy correlated well with the high serum level of pepsinogen I (P = 0.005), but showed no correlation with the levels of anti-parietal cell antibody.. : These results suggest that gastric atrophy and intestinal metaplasia are reversible events in some patients.

Topics: Adult; Aged; Anti-Bacterial Agents; Biomarkers; Drug Therapy, Combination; Female; Follow-Up Studies; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Intestines; Male; Metaplasia; Methylene Blue; Middle Aged; Pepsinogens; Precancerous Conditions; Prognosis; Prospective Studies; Stomach Neoplasms

Helicobacter pylori infection induces atrophic body gastritis, but the long-term effect of its cure on body atrophy is unclear.. To investigate the long-term effects of H. pylori cure on gastric morpho-functional parameters in patients with atrophic body gastritis.. Forty patients with atrophic body gastritis were cured of H. pylori infection. Gastroscopy with biopsies, gastrin and pepsinogen I levels and basal and stimulated acid secretion were evaluated before and 6-12 months after treatment.. At eradication assessment (6-12 months), in eight of the 40 patients, body atrophy was no longer observed, whereas in 32 of the 40 it remained substantially unchanged (2.03 +/- 0.12 vs. 1.83 +/- 0.15). In the eight patients with reversed body atrophy, gastrinaemia decreased significantly with respect to pre-treatment values (265 +/- 59.9 pg/mL vs. 51.8. +/- 6.04 pg/mL), and basal and stimulated acid secretion increased significantly after cure. In the 32 patients still presenting body atrophy, gastrinaemia was similar topre-treatment values (457 +/- 76.04 pg/mL vs. 335.1 +/- 58.8 pg/mL). At follow-up (21-25 and 32-70 months), the eight patients with reversed body atrophy continued with normal gastrinaemia (35.3 +/- 10.1 pg/mL vs. 38.5 +/- 8.8 pg/mL), but in the 19 patients with continued atrophy, both corporal atrophy and intestinal metaplasia remained substantially unchanged.. Following successful treatment in patients with atrophic body gastritis and H. pylori infection, long-term histological investigations are crucial in order to detect reversed body damage or to confirm continued body atrophy.

Topics: Adult; Aged; Anti-Bacterial Agents; Female; Follow-Up Studies; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Prospective Studies

Helicobacter pylori causes gastric adenocarcinoma. We assessed the success of H. pylori eradication therapy in a medically underserved population in Chiapas, Mexico, that is at high risk for gastric cancer risk.. Healthy volunteers with both antibodies to CagA and gastrin levels > or = 25 ng/ml were randomly assigned to receive either a combination of omeprazole, amoxicillin, and clarithromycin or matched placebo for 1 wk. Endoscopy with seven biopsies was performed at baseline, at 6 wk, and 1 yr after treatment. Treatment success was defined as loss of H. pylori by histological analysis. Cure was assessed using change in serology based on the standardized absorbance of a H. pylori ELISA.. H. pylori eradication rates were high (intent-to-treat analysis: 76.3% [95% CI = 68.7-84.0%] after 6 wk and 76.1% [95% CI = 67.7-84.6%] after 1 yr; per protocol analysis: 77.8% [95% CI = 70.1-85.4%] after 6 wk and 75.2% [95% CI = 66.5-84.0%] after 1 yr). Nine subjects on active treatment and one subject on placebo who were without H. pylori at 6 wk were infected at 1 yr (recurrence rates 10.7% and 33.3%, respectively, p = 0.31). Median changes in standardized absorbance at 1 yr were 47% and 1% for successfully and unsuccessfully treated patients, respectively. A 10% decline in standardized absorbance after 1 yr had 84% sensitivity and 100% specificity for H. pylori eradication.. Even with a short course of treatment against H. pylori, a high rate of eradication rate can be achieved in populations at high risk for stomach cancer. Serum antibodies are useful in assessing efficacy of therapy.

Topics: Adenocarcinoma; Adult; Amoxicillin; Anti-Bacterial Agents; Anti-Ulcer Agents; Antibodies, Bacterial; Antigens, Bacterial; Bacterial Proteins; Clarithromycin; Drug Therapy, Combination; Enzyme-Linked Immunosorbent Assay; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Omeprazole; Penicillins; Precancerous Conditions; Recurrence; Risk Factors; ROC Curve; Stomach Neoplasms

Intestinal-type gastric adenocarcinomas usually are preceded by chronic atrophic gastritis. Studies of gastric cancer prevention often rely on identification of this condition. In a clinical trial, we sought to determine the best serological screening method for chronic atrophic gastritis and compared our findings to the published literature. Test characteristics of potential screening tests (antibodies to Helicobacter pyloni or CagA, elevated gastrin, low pepsinogen, increased age) alone or in combination were examined among consecutive subjects enrolled in a study of H. pylori and preneoplastic gastric lesions in Chiapas, Mexico; 70% had chronic atrophic gastritis. English-language articles concerning screening for chronic atrophic gastritis were also reviewed. Sensitivity for chronic atrophic gastritis was highest for antibodies to H. pylori (92%) or CagA, or gastrin levels >25 ng/l (both 83%). Specificity, however, was low for these tests (18, 41, and 22%, respectively). Pepsinogen levels were highly specific but insensitive markers of chronic atrophic gastritis (for pepsinogen I <25 microg/l, sensitivity was 6% and specificity was 100%; for pepsinogen I:pepsinogen II ratio <2.5, sensitivity was 14% and specificity was 96%). Combinations of markers did not improve test characteristics. Screening test characteristics from the literature varied widely and did not consistently identify a good screening strategy. In this study, CagA antibodies alone had the best combination of test characteristics for chronic atrophic gastritis screening. However, no screening test was both highly sensitive and highly specific for chronic atrophic gastritis.

Topics: Adult; Age Distribution; Aged; Biomarkers; Biopsy, Needle; Chronic Disease; Confidence Intervals; Female; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Incidence; Male; Mass Screening; Mexico; Middle Aged; Pepsinogen A; Predictive Value of Tests; Risk Factors; Sensitivity and Specificity; Sex Distribution

Body-predominant atrophic gastritis is considered a risk factor for gastric cancer and carcinoid. Timing of follow-up for patients with this disorder has not been defined. This study was undertaken to determine the optimal time for the first endoscopic/histologic follow-up in patients with body-predominant atrophic gastritis.. Forty-two patients with body-predominant atrophic gastritis were randomly assigned to 1 of 2 follow-up intervals: group A (n = 22) at 24 months and group B (n = 20) at 48 months. At baseline and follow-up patients underwent gastroscopy at which biopsies were obtained from the antrum and body for histopathology and evaluation for enterochromaffin-like cells.. In group A patients, 2 antral hyperplastic polyps (9.1%) were present at baseline and 4 antral hyperplastic polyps (18.2%) were found at follow-up. In group B patients, baseline gastroscopy revealed 2 antral hyperplastic polyps (10%) and follow-up 2 antral hyperplastic polyps (10%) and 1 carcinoid tumor (5%) in the body. Atrophy and intestinal metaplasia scores in gastric body and antral mucosa in both groups did not change significantly between baseline and follow-up, except an increase in antral mucosa atrophy in group B patients (p = 0.02) was revealed.. The results of this study indicate that performing the first follow-up in patients with body-predominant atrophic gastritis need not be earlier than at 4 years after diagnosis. This interval is satisfactory for detection of potential neoplastic lesions.

Topics: Adult; Aged; Anemia, Pernicious; Biopsy; Carcinoid Tumor; Enterochromaffin-like Cells; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Polyps; Prospective Studies; Pyloric Antrum; Random Allocation; Stomach Neoplasms; Time Factors

The effects of H. pylori eradication on atrophic body gastritis are controversial.. To investigate the effect of triple therapy on atrophic body gastritis in H. pylori-positive patients and its effect on morpho-functional gastric parameters.. Thirty-five consecutive atrophic body gastritis patients with histological/serological evidence of H. pylori infection were treated. Before and 6 and 12 months after H. pylori eradication the patients were evaluated for fasting gastrinemia and pepsinogen I, basal and peak acid output, and detailed histological assessment including the ECL cell proliferative patterns.. Six months after treatment, 25 out of 32 patients were cured (78%). Cure of infection was associated with improvement in both basal (basal acid output mean 0.23 +/- 0.14 mmol/h vs. 1.75 +/- 0.7 mmol/h, P < 0.005) and stimulated acid secretion (peak acid output mean 3.0 +/- 1.06 mmol/h vs. 16.6 +/- 4.1 mmol/h, P=0.0017) as well as with reduction in hypergastrinemia (mean gastrin levels 444.1 +/- 110.7 pg/mL vs. 85.3. +/- 28 pg/mL; P < 0.005). In contrast, the eradication had no effect on body corporal atrophy and intestinal metaplasia, or pepsinogen I levels (mean 16.6 +/- 2.9 ng/mL vs. 14.2 +/- 2.1 ng/mL, N.S.). These results were confirmed at 12 months after eradication. A statistical inverse correlation was obtained (r=-0.3635, P < 0.05) between the corporal chronic infiltrate score and peak acid output values. A total of 53% of atrophic body gastritis patients showed a regression in severity of body ECL cell hyperplastic change.. Cure of H. pylori infection in patients with atrophic gastritis reverses some adverse effects on gastric function and ECL cell hyperplasia. H. pylori infection may be cured in atrophic body gastritis patients with partial reversion of its negative consequences on acid secretion and body ECL cell hyperplasia.

Topics: Adult; Aged; Enterochromaffin Cells; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Hyperplasia; Male; Middle Aged; Pepsinogen A; Prospective Studies; Treatment Outcome

A cross sectional study was designed to elucidate the factors influencing the argyrophil cell population in patients with gastroesophageal reflux disease treated with omeprazole (N = 201) or H2-receptor antagonists (N = 118) and in control patients (N = 215). Fasting gastrinemia and Helicobacter pylori serology were determined. Gastritis, Helicobacter pylori infection, and argyrophil cell density and hyperplasia were evaluated in gastric biopsies. The argyrophil cell density was higher in both treatment groups than in controls (P = 0.002 and P = 0.051), whereas argyrophil cell hyperplasia was similar in the three groups. According to multivariate analysis, positive Helicobacter pylori serology was an independent parameter that decreased both density and grade of hyperplasia of argyrophil cells. Female gender and hypergastrinemia were independent factors increasing argyrophil cell density and hyperplasia, whereas antisecretory therapy, age and active gastritis were not. In addition, atrophic gastritis independently increased argyrophil cell hyperplasia. The prevalence of atrophic gastritis was significantly higher in Helicobacter pylori-positive than in negative patients and lower in the patients treated long-term with omeprazole than in the other groups.

Topics: Adult; Aged; Aged, 80 and over; Anti-Ulcer Agents; Cell Count; Cross-Sectional Studies; Enterochromaffin-like Cells; Esophagitis, Peptic; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Histamine H2 Antagonists; Humans; Hyperplasia; Male; Middle Aged; Multivariate Analysis; Omeprazole; Sex Factors

To evaluate the response of endocrine cells of the gastric oxyntic mucosa in hypergastrinaemic patients to either antrectomy or treatment with the somatostatin analogue octreotide.. (a) Two patients with enterochromaffin-like (ECL) cell carcinoid and chronic atrophic gastritis, treated with antrectomy; (b) four patients with Zollinger-Ellison syndrome, treated with octreotide.. Oxyntic endocrine cells were examined by ultrastructural morphometry on full thickness biopsy specimens taken: (a) before and four months after antrectomy, (b) before and after three months' treatment with octreotide 200 micrograms daily.. Both treatments induced prompt, significant reduction of gastrinaemia and a significant decrease of the volume density of the whole endocrine cell mass and of the cross sectional area of all nucleated endocrine cell profiles (antrectomy: -38%, p < 0.04 and -31%, p < 0.04, respectively; octreotide: -59%, < 0.007 and -26%, < 0.04, respectively). Assessment of the relative proportion of individual endocrine cell types showed a different response to antrectomy or octreotide. After antrectomy, in fact, only the volume fraction of ECL cells was significantly reduced, from 56.5% to 22.5% (-60%, p < 0.04). After octreotide treatment, in contrast, the proportion of all endocrine cell types remained remarkably constant, showing that all cell types took part in the observed overall decrease.. Postantrectomy reduction of oxyntic endocrine cells mostly reflects the withdrawal of the specific trophic stimulus of hypergastrinaemia on ECL cells. In contrast, the inhibitory response to octreotide seems to be exerted on virtually all types of oxyntic endocrine cells, probably reflecting a universal occurrence of somatostatin receptors.

Topics: Adult; Aged; Carcinoid Tumor; Female; Gastrins; Gastritis, Atrophic; Gastrointestinal Agents; Humans; Male; Microscopy, Electron; Middle Aged; Octreotide; Parietal Cells, Gastric; Pyloric Antrum; Stomach Diseases; Stomach Neoplasms; Zollinger-Ellison Syndrome

Gastric abnormalities are more common in diabetics than in the normal population. They seem to be related to gastric parietal cell autoantibodies (GPCA). We have studied 168 patients affected with non-insulin-dependent diabetes mellitus (NIDDM), and assessed the GPCA in the serum and haematologic disorders. We have also assessed the endoscopic and histological findings of atrophic gastritis in patients with GPCA. GPCA were found in 15.74% of diabetic patients and in 2% of a control group of blood donors. 80% of GPCA positive patients showed signs of atrophic gastritis. Such presence of GPCA seems to be a good marker to identify patients affected by atrophic gastritis and its complications.

Topics: Adult; Autoantibodies; Diabetes Mellitus, Type 2; Female; Ferritins; Gastrins; Gastritis, Atrophic; Humans; Iron; Islets of Langerhans; Male; Middle Aged; Parietal Cells, Gastric

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

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

Serum pepsinogen (PG) testing is recommended by the European guidelines for diagnosis of chronic atrophic gastritis (CAG). However, wide variations in diagnostic performances are observed, due to the differences in the extent of gastric atrophy, and possibly in its origin (Helicobacter pylori-, autoimmune (AIG)).. To analyze the diagnostic performances of PGs testing according to these different parameters, using enzyme-linked-immunosorbent serologic assay (ELISA) and chemiluminescent immunoassay (CLEIA).. Serum samples from patients having undergone gastroscopy with biopsies in five French centers were collected prospectively. Sensitivity (Se), specificity (Sp), and Area Under Curve were analyzed according to the extent and origin of CAG.. Overall, 344 patients (156 males [45%]; mean age 58.8 [±14.2] years) were included, among whom 44 had AIG. Diagnostic performances of PG I for the detection of corpus CAG were excellent, with Se and Sp of 92.7% and 99.1% for ELISA and 90.5% and 98.2% for CLEIA, respectively. For AIG, corresponding values were 97.7% and 97.4% for ELISA, and 95.6% and 97.1% for CLEIA. In multivariate analysis, PG levels were associated with the auto-immune origin (p<0.001) but not with the extent of the atrophic gastritis.. Pepsinogens are highly efficient for the diagnosis of corpus-limited CAG and allow to discriminate AIG from H. pylori-induced gastritis.

Topics: Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Prospective Studies

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

Simple objective modalities are required for evaluating suspected autoimmune gastritis (AIG). This cross-sectional study aimed to examine whether pepsinogen, gastrin, and endoscopic findings can predict AIG. The diagnostic performance of endoscopic findings and serology in distinguishing AIG was evaluated. AIG was diagnosed in patients (N = 31) with anti-parietal cell antibody and/or intrinsic factor antibody positivity and histological findings consistent with AIG. Non-AIG patients (N = 301) were seronegative for anti-parietal cell antibodies. Receiver operating characteristic curve analysis of the entire cohort (N = 332) identified an endoscopic atrophic grade cutoff point of O3 on the Kimura-Takemoto classification (area under the curve [AUC]: 0.909), while those of pepsinogen-I, I/II ratio, and gastrin were 20.1 ng/mL (AUC: 0.932), 1.8 (AUC: 0.913), and 355 pg/mL (AUC: 0.912), respectively. In severe atrophy cases (≥ O3, N = 58, AIG/control; 27/31), the cutoff values of pepsinogen-I, I/II ratio, and gastrin were 9.8 ng/mL (AUC: 0.895), 1.8 (AUC: 0.86), and 355 pg/mL (AUC: 0.897), respectively. In conclusion, endoscopic atrophy is a predictor of AIG. High serum gastrin and low pepsinogen-I and I/II ratio are predictors even in the case of severe atrophy, suggesting their usefulness when the diagnosis of AIG is difficult or as serological screening tests.

Topics: Atrophy; Autoantibodies; Autoimmune Diseases; Cross-Sectional Studies; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Humans; Pepsinogen A

To analyze and test the effect of. Rats with chronic atrophic gastritis that were modeled successfully were randomly divided into control and study groups and were treated with conventional western medicine or Rhizoma phragmitis and Rhizoma curcumae, respectively. The pharmacological mechanism of action and efficacy were evaluated.. The treatment efficiency was 76.32% and 97.37% in the control and study group, respectively. After treatment, the serum tumor necrosis factor-. Based on the network pharmacological results,

Topics: Animals; Gastrins; Gastritis, Atrophic; Internet; Rats; Rhizome; Signal Transduction

In Mongolia, gastric cancer morbidity and mortality are high, and more than 80 percent of cases are diagnosed at an advanced stage. This study aimed to evaluate pepsinogens (PGIs) and gastrin-17 (G-17) levels and to determine the diagnostic performances for gastric cancer and chronic atrophic gastritis among Mongolian individuals. We enrolled a total of 120 subjects, including gastric cancer (40), atrophic gastritis (40), and healthy control (40), matched by age (±2) and sex. Pepsinogen I (PGI), Pepsinogen II (PGII), G-17, and H. pylori IgG levels were measured using GastroPanel ELISA kit (Biohit, Helsinki, Finland). Also, PGI to PGII ratio (PGR) was calculated. For atrophic gastritis, when the optimal cut-off value of PGI was ≤75.07 ng/ml, the sensitivity and specificity were 75% and 50%, respectively; when the optimal cut-off value of PGR was ≤6.25, sensitivity and specificity were 85% and 44.7%, respectively. For gastric cancer, when the optimal cut-off value of PGI was ≤35.25 ng/ml, the sensitivity and specificity were 47.2% and 86.8%, respectively; when the optimal cut-off value of PGR was ≤5.27, sensitivity and specificity were 75% and 60.5%, respectively. Combinations of biomarkers with risk factors could improve diagnostic accuracy (AUC for atrophic gastritis 74.8, 95% CI 64.0-85.7, p<0.001; AUC for gastric cancer 75.5, 95% CI 64.2-86.8, p<0.001). PGI, PGR biomarkers combined with the risk of age, family history of gastric cancer, and previous gastric disease could not be an alternative test for upper endoscopy but might be a supportive method which is identifying individuals at medium- and high risk of gastric cancer and precancerous lesions who may need upper endoscopy.

Topics: Biomarkers; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Pepsinogen A; Pepsinogen C; Stomach Neoplasms

Prompted by the increasing demand of non-invasive diagnostic tools for screening of gastric cancer (GC) risk conditions, i.e., atrophic gastritis (AG) and Helicobacter pylori (Hp) infection, the GastroPanel. Altogether, 522 patients were enrolled among the patients referred for gastroscopy at the Gastro Center, Oulu University Hospital (OUH). All patients underwent gastroscopy with biopsies classified using the Updated Sydney System (USS), and blood sampling for GP testing.. The new generation GastroPanel

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Biomarkers; Biopsy; Enzyme-Linked Immunosorbent Assay; Female; Finland; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Host-Pathogen Interactions; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Predictive Value of Tests; Referral and Consultation; Reproducibility of Results; Serologic Tests; Young Adult

Topics: Crohn Disease; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans

A hospital-based cross-sectional study in SIGES project was conducted during 2016.5-2017.5 in West China Hospital. It was aimed to observe the prevalence of atrophic gastritis (AG) in southwest China, and assess the diagnostic strength of serum gastrin-17 (G-17) in predicting AG in Chinese population. Asymptomatic healthy controls from health check-up, cancer-free patients with unspecific upper gastrointestinal symptoms, and histologically proven gastric cancer patients were eligible, if serum pepsinogen-I (PG-I), PG-II, and G-17 were detected. AG status was classified by the accredited cutoffs of PG-I (<70 ug/L) and PG-I/II ratio (<3). Totally, healthy controls (n = 9,425), symptomatic patients (n = 671) and gastric cancer patients (n = 305) were simultaneously observed, in which the prevalence of AG in southwest China were estimated as 15.9/1,000, 28.3/1,000, and 55.7/1,000 persons, respectively. The age-specific prevalence of AG in healthy controls showed a significantly uphill trend (p for trend <0.001). Higher level of serum G-17 was significantly associated with increased risk of AG in healthy population (15-30 pmol/L, aOR = 20.67, 95% CI 9.17-46.55; >30 pmol/L, aOR = 314.41, 95% CI 166.10-595.12). Throughout the progression of stomach diseases, the diagnostic strength of serum G-17 for AG showed a downhill trend across more advanced situations. In despite of that, serum G-17 displayed a good performance in predicting AG in the entire cross-sectional population (AUC = 0.92, 95% CI 0.89-0.94; SEN = 85.5%; SPE = 93.2%; LR+ = 12.55; LR- = 0.11). Population in southwest China had intermediate prevalence of AG, while the prevalence was increased over age or disease progression. High level of serum G-17 might be a reliable non-invasive measurement to predict AG in southwest Chinese population.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Biomarkers; Cross-Sectional Studies; Female; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Odds Ratio; Prevalence; Prognosis; ROC Curve; Young Adult

Autoimmune atrophic gastritis (AIG) is very rare in children. Despite a better understanding of histopathologic changes and serological markers in this disease, underlying etiopathogenic mechanisms and the effect of Helicobacter pylori (H pylori) infection are not well known. We aimed to investigate the relation between AIG and H pylori infection in children.. We evaluated the presence of AIG and H pylori infection in fifty-three patients with positive antiparietal cell antibody (APCA). Demographic data, clinical symptoms, laboratory and endoscopic findings, histopathology, and presence of H pylori were recorded.. The children were aged between 5 and 18 years, and 28 (52.8%) of them were male. Mean age was 14.7 ± 2.6 years (median: 15.3; min-max: 5.2-18), and 10 (18.8%) of them had AIG confirmed by histopathology. In the AIG group, the duration of vitamin B12 deficiency was longer (P = .022), hemoglobin levels were lower (P = .018), and APCA (P = .039) and gastrin (P = .002) levels were higher than those in the non-AIG group. Endoscopic findings were similar between the two groups. Intestinal metaplasia was higher (P = .018) in the AIG group. None of the patients in the AIG group had H pylori infection (P = .004). One patient in the AIG group had enterochromaffin-like cell hyperplasia.. Our results show that, in children, H pylori infection may not play a role in AIG. AIG could be associated with vitamin B12 deficiency, iron deficiency, and APCA positivity in children. APCA and gastrin levels should be investigated for the early diagnosis of AIG and intestinal metaplasia.

Topics: Adolescent; Anemia, Iron-Deficiency; Autoimmune Diseases; Child; Child, Preschool; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metaplasia; Parietal Cells, Gastric; Retrospective Studies; Stomach; Vitamin B 12 Deficiency

Autoimmune metaplastic atrophic gastritis (AMAG) is an underrecognized entity, especially in its early stage. This study assessed whether the use of gastrin immunohistochemistry would increase sensitivity for diagnosing early AMAG.. Three-hundred gastric biopsies were prospectively stained for gastrin by immunohistochemistry. Inclusion criteria included well-oriented gastric mucosa with mucus glands and minimal plasma cell infiltrate not suspected to represent pyloric metaplasia. Patient age, sex, designated location of biopsy, presence or absence of intestinal metaplasia, and clinical information were not criteria. Any case with absence of gastrin-positive endocrine cells reflexed to chromogranin immunohistochemistry. Maloriented biopsies or cases with current Helicobacter infection were excluded.. The 298-patient study cohort comprised 222 females (mean age, 47 years; range, 16-80 years) and 76 males (mean age, 49 years; range, 7-80 years). Biopsies were designated as "antral/antral nodules" (61%), and the rest were labeled "gastric/random stomach" (39%). Nine cases (3%) exhibited absence of gastrin-positive endocrine cells; one of those showed endocrine cell hyperplasia by chromogranin staining.. Pathologists should be aware of the histologic features of early AMAG and meticulously analyze tissue regardless of specimen labeling. Gastrin immunostain is a supplemental diagnostic tool when encountering inflamed antral-appearing specimens.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Autoimmune Diseases; Biopsy; Child; Diagnosis, Differential; False Negative Reactions; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Immunohistochemistry; Male; Middle Aged; Prospective Studies; Pyloric Antrum; Young Adult

Analysis of serum biomarkers for the assessment of atrophic gastritis (AG), considered as gastric precancerous lesion, is of growing interest and recommended by current guidelines. Our aim was to evaluate the diagnostic performance of a panel of biomarkers (GastroPanel®) for the detection of AG in France, a country of a low gastric cancer (GC) incidence.. In this prospective, multicenter, cross-sectional study, consecutive patients considered at increased risk of GC and undergoing upper endoscopy with gastric biopsies were included. Blood samples were collected for the analysis of GastroPanel® (association of Pepsinogens I and II, Gastrin-17, and Helicobacter pylori serology) using ELISA. The results of GastroPanel® were compared to the results of histology considered as the reference.. Between 2016 and 2019, 344 patients (148 cases with AG, 196 controls without AG) were included. Sensitivity, specificity, positive, and negative predictive values for the detection of AG by GastroPanel® were of 39.9% (95% CI 31.9; 48.2), 93.4% (95% CI 88.9; 96.4), 81.9 (95% CI 71.1; 90.0), and 67.3 (95% CI 61.4; 72.8), respectively. The sensitivity was significantly higher for the detection of severe AG [60.8% (95% CI 46.1; 74.6) P = .015] and corpus AG [61.0% (95% CI 49.2; 72.0), P = .004]. Diagnostic performances of GastroPanel® tended to be better than those of Pepsinogen I alone, but the difference did not reach statistical significance (P = .068).. Serum pepsinogen and GastroPanel® tests show promising results for the detection of AG, especially of corpus AG and severe AG, in patients at high risk of GC in France.

Topics: Adult; Aged; Antibodies, Bacterial; Biomarkers; Cross-Sectional Studies; Enzyme-Linked Immunosorbent Assay; Female; France; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Humans; Incidence; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Prospective Studies; Sensitivity and Specificity; Stomach Neoplasms

Proton pump inhibitor (PPI) therapy causes hypergastrinemia, which could promote the development and progression of neuroendocrine tumors (NETs). Concerns have been raised about the safety of long-term PPI use due to a possible increased risk of NETs. This study aimed to investigate the association between hypergastrinemia and the risk of NETs. Twenty outpatients presenting with serum gastrin levels greater than 400 pg/mL after long-term PPI treatment were registered in this study. Immunohistochemical analyses for chromogranin A (CgA), Ki67, gastrin and CCK/B gastrin receptor (CCKBR) were performed, and positive cell numbers were counted. There were no NET or gastric epithelial neoplasia cases observed among any of the 20 patients examined throughout the PPI treatment period. Histologically, ECL cell hyperplasia were shown in all patients. However, no relationship was found between serum gastrin levels and the number of CgA positive ECL cells. There was also no relationship between serum gastrin levels and the proportion of Ki67 positive cells or the density of CCKBR positive cells. The data indicate no relationship may exist between NETs and hypergastrinemia secondary to PPI treatment in patients having no, or mild, atrophic gastritis.

Topics: Aged; Aged, 80 and over; Carcinogenesis; Enterochromaffin-like Cells; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Neuroendocrine Tumors; Proton Pump Inhibitors; Stomach Neoplasms

Chronic atrophic autoimmune gastritis (CAAG) can lead to the development of gastric neuroendocrine tumors (gNETs) and can be accompanied by other autoimmune diseases. This study aimed to determine, in CAAG patients, the association of gNET development, the prevalence of autoimmune diseases other than CAAG, the association of autoimmunity, and gNET development with pepsinogen I, II, gastrin-17, and Helicobacter pylori infection analysis.. We determined the prevalence of gNETs and other autoimmune diseases and analyzed pepsinogen I and II, gastrin-17 serum levels, and H. pylori infection in all patients diagnosed with CAAG at our hospital between 2013 and 2017.. A total of 156 patients were studied and in 15.4% was observed concomitant gNET. Approximately 68.6% had at least 1 other autoimmune disease at diagnosis of CAAG. Approximately 60.9% had autoimmune thyroiditis, followed by diabetes (19.9%) and autoimmune polyendocrine syndrome (12.8%). CAAG patients with and without gNET had similar rates of comorbidity with other autoimmune diseases, but the pepsinogen I/II ratio was lower in patients with gNET (1.6 vs 4.5, P = 0.018). Receiver operating characteristic curve analyses identified a pepsinogen I/II ratio <2.3 and gastrin-17 levels >29.6 pmol/L as cutoffs distinguishing CAAG patients with gNET from those without. The combined use of these cutoff correctly identified 16 of the 18 CAAG patients with gNET (P = 0.007). H. pylori infection was observed in 28.7% of cases tested but did not associate with gNET.. This study suggests that a low pepsinogen I/II ratio and high gastrin-17 levels characterize patients with CAAG and gNET and confirms the frequent coexistence of CAAG with other autoimmune diseases.

Topics: Adolescent; Adult; Aged; Autoimmune Diseases; Biomarkers; Diagnosis, Differential; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Neuroendocrine Tumors; Pepsinogen A; Pepsinogen C; Prevalence; Retrospective Studies; ROC Curve; Stomach Neoplasms; Young Adult

The aim: To study the gastrin level dynamics in patients with diabetes mellitus (DM) 2 type and chronic gastritis (CG) on the background of antihelicobacter therapy (AHT).. Materials and methods: 60 patients with DM type 2 and HP-associated CG underwent examination. Patients were divided into two groups of 30 patients each: group 1 included patients who received only standard AHT, group 2 - patients who in addition to standard AHT received the drug SB (Normagut, company Mega) 2 capsules 2 times/day.. Results: According to our study results yeast SB, not only increase the HP eradication rate but together with the standard AHT contribute to the serum gastrin reduction, which is a gastric acid stimulator, which in turn leads to an improvement in the CG clinical course.. Conclusions: Patients with DM type 2 and CG associated with HP should include yeast SB to standard AHT as they reduce side effects from this treatment (by an average of 20%), increase the eradication frequency (by 10%), and also lead to significant decrease in serum gastrin (up to 82.15 ± 2.47 pg/ml).A decrease in serum gastrin levels in patients with HP-associated CG and DM type 2 leads to an improvement in the clinical course of the diseases, namely a decrease in nausea, diarrhea, abdominal pain, and discomfort incidence.

Topics: Diabetes Mellitus, Type 2; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans

Autoimmune atrophic gastritis (AAG) is an immune-mediated disorder characterised by destruction of gastric oxyntic mucosa AIM: To explore gastric histopathological evolution in a cohort of AAG patients over a prolonged follow-up METHODS: Single centre prospective study enrolling consecutive patients with histologically confirmed AAG between 2000 and 2018. All AAG patients undergoing endoscopic follow-up every 1-3 years were classified as having stages 1, 2 or 3 according to atrophy severity (mild, moderate and severe). AAG patients with either glandular or neuroendocrine dysplasia/neoplasia were classified as having stage 4. Disease stage progression, and changes in serum anti-parietal cell antibody (PCA), chromogranin A and gastrin-17 were assessed.. In total, 282 AAG patients (mean age 60.3 years; F:M ratio 2.4:1; median follow-up 3 years, interquartile range 1-7) were enrolled. All patients with stages 1 or 2 progressed to stage 2 or 3 over time with a steady trend (P = .243) and regression from a severe to a milder stage was never noticed. Disease progression of patients with stages 1 or 2 occurred within the first 3 years. PCA positivity rate did not change over time. Stage 3 patients had higher gastrin-17 levels compared to patients with stages 1 and 2 (median 606 vs 295 pg/mL; P < .001). In stage 3, the hazard ratio for the risk of developing stage 4 was 6.6 (95% CI 1.5-29; P = .001).. AAG is a steadily progressive disease, in which stages 1 and 2 always progress to stage 3. The risk of developing a complicated disease stage is greater in patients with more severe gastric lesions.

Topics: Adult; Aged; Autoimmune Diseases; Disease Progression; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Neuroendocrine Tumors; Prospective Studies; Severity of Illness Index; Stomach Neoplasms

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

Our group observed the first case of synchronous gastric neuroendocrine tumor (NET) and duodenal gastrinoma with autoimmune chronic atrophic gastritis (CAG), in the absence of Helicobacter pylori infection. Demographic, clinical, endoscopic, and pathologic data were abstracted from the electronic medical record at Mount Sinai Hospital from 2013 to 2015. The patient's anonymity was carefully protected, and informed consent was obtained for publication of protected health information. A 53-year-old woman with hypertension presented to Mount Sinai Hospital in June 2013 for a second opinion for management of gastric and duodenal NETs. After evaluation by gastroenterology and surgery, repeat upper endoscopy with ultrasound and fine-needle aspiration revealed multiple diminutive type I gastric NETs and 2 duodenal NETs, against a background of autoimmune CAG, with biopsy pathology negative for H. pylori. She subsequently underwent a transduodenal resection of the duodenal NETs, confirming low-grade, gastrin-positive, stage T2 duodenal NET. On routine follow-up over the next 2 years, clinical, radiographic, and endoscopic surveillance revealed no recurrent or metastatic gastric or duodenal disease. This first report of synchronous duodenal gastrinoma and gastric NET in the setting of autoimmune CAG can broaden our understanding of gastric NET pathophysiology.

Topics: Autoimmune Diseases; Chronic Disease; Duodenal Neoplasms; Female; Gastrinoma; Gastrins; Gastritis, Atrophic; Humans; Hypertension; Middle Aged; Neuroendocrine Tumors; Stomach Neoplasms

BACKGROUND This study investigated the effect and mechanism of notoginsenoside R1 (NGR1) on chronic atrophic gastritis (CAG) in a rat model. MATERIAL AND METHODS To perform our investigation, a rat model of CAG was established, and then rats were treated with various doses of NGR1. After treatment, hematoxylin-eosin (HE) staining was used for histopathological observation and further scoring. Enzyme-linked immunosorbent assay (ELISA) was used to determine the contents of gastrointestinal hormones, inflammatory factors, gastric mucosal destruction factors, and gastric mucosal-protective factors. Gene and protein expressions were measured using quantitative real-time PCR and Western blot assay, respectively. RESULTS Results indicated that NGR1 relieved rat CAG. NGR1 treatment significantly increased the levels of gastrin (GAS) and somatostatin (SS) and reduced motilin (MTL) in the serum of CAG rats. The serum levels of interleukin (IL)-1β and IL-6 were significantly reduced by NGR1 treatment in CAG rats in a dose-dependent manner. Additionally, the increased levels of prostaglandin (PG)E2, nitric oxide synthase (NOS), and endothelin (ET) in CAG rats were significantly decreased by NGR1 administration. Moreover, the decreased level of secretory IgA (sIgA) and glutathione (GSH) in rats caused by MNNG was notably increased by NGR1 treatment. No significant changes were found in glutathione disulfide (GSSG) secretion. Finally, we found that the increased Bcl-2 expression and reduced Bax expression in the stomach tissues of rats caused by MNNG were eliminated by NGR1 treatment. CONCLUSIONS NGR1 exerts a protective effect on CAG, and it is a multi-target, multi-linked, comprehensive process.

Topics: Animals; Chronic Disease; Disease Models, Animal; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Ginsenosides; Male; Rats; Rats, Sprague-Dawley; Signal Transduction; Somatostatin

The use of proton pump inhibitors (PPIs) is known to lead to hypergastrinemia; however, the data in patients with atrophic gastritis is still lacking. The aim of this study was to investigate the effects of long-term PPIs use on the gastrin levels in patients with atrophic gastritis and to determine factors affecting hypergastrinemia in long-term users of PPIs.. Serum Helicobacter pylori IgG, gastrin and pepsinogen levels were measured. Atrophic gastritis was assessed by upper gastrointestinal endoscopies based on the Kimura-Takemoto classification and pepsinogen levels. CYP2C19 polymorphisms were assessed using DNA extracted from peripheral blood.. A total number of 382 patients (275 men and 107 women) were enrolled. Median serum gastrin levels were higher in PPI users than in non- users (234 vs. 113 pg/mL, p < 0.001) and in women than in men (252 vs. 155 pg/mL, p = 0.006). Gastrin levels were significantly associated with corpus atrophy only in the subgroup of non-users of PPIs. Multivariate analysis revealed that hypergastrinemia (over 150 pg/mL) was significantly associated with PPI use (OR 5.30; 95% CI 3.32-8.47), women (OR 2.22; 95% CI 1.33-3.72) and corpus atrophy (OR 1.82; 95% CI 1.14-2.90).. PPI use, women and corpus atrophy were risk factors for hypergastrinemia. Gender, but not corpus atrophy, affected the gastrin levels in long-term users of PPIs.

Topics: Aged; Antibodies, Bacterial; Atrophy; Cross-Sectional Studies; Cytochrome P-450 CYP2C19; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Polymorphism, Genetic; Proton Pump Inhibitors; Sex Factors; Time Factors

The long-term administration of proton pump inhibitors (PPIs) is useful for preventing recurrent reflux esophagitis. On the other hand, several adverse reactions, such as an increase in the blood gastrin level, have been reported. The aim of the present study was to examine the increase in the blood gastrin level due to the long-term administration of conventional PPIs compared with vonoprazan.. A prospective cross-sectional study was conducted. We examined the blood gastrin levels of patients taking vonoprazan or conventional PPIs in whom the grade of atrophic gastritis had been endoscopically evaluated in the last year.. The blood gastrin level was significantly higher in the vonoprazan group than that in the PPI group in patients with milder or no atrophic gastritis, irrespective of the administration periods. However, no significant difference was observed between the groups in patients with severe atrophic gastritis.. Vonoprazan more markedly increased the blood gastrin level compared with conventional PPIs in patients with milder or no atrophic gastritis. This indicates that vonoprazan may have stronger acid-suppressing effects in such patients than conventional PPIs. Key Message: We should be aware of the potential development of hypergastrinemia during the long-term administration of vonoprazan, especially in patients with mild or no atrophic gastritis.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Aged, 80 and over; Cross-Sectional Studies; Esophagitis, Peptic; Female; Gastrins; Gastritis, Atrophic; Humans; Long-Term Care; Male; Middle Aged; Prospective Studies; Proton Pump Inhibitors; Pyrroles; Sulfonamides; Treatment Outcome; Young Adult

Methods for the measure of gastric acid secretion include invasive and non-invasive tests. The gold-standard to measure the acid output is the collection of gastric after in basal condition (Basal Acid Output, B.A.O.) and after an i.m. injection of pentagastrin (Maximal Acid Output, M.A.O.). However, direct measurement of gastric acid production is out of order in clinical practice, but many GI symptoms are claimed to be related with acid disorders and empirically cured. Hypochlorhydria is associated with precancerous conditions such as chronic atrophic gastritis (CAG). Acid measurement with non-invasive methods (pepsinogens) is supported by international guidelines.

Topics: Achlorhydria; Biomarkers; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastritis, Atrophic; Humans; Pentagastrin; Pepsinogens; Peptic Ulcer; Precancerous Conditions

Neuroendocrine tumors (NETs) represent uncommon tumors arising from the excessive proliferation of enterochromaffin-like (ECL) cells (so-called Kulchitsky cell). Gastric NETs (GNET) represent less than 2% of all NETs and less than 1% of all stomach neoplasms. In particular, gastric NETs type 1 (associated to chronic atrophic gastritis and hypergastrinaemia) is the more frequent one, accounting for 70-80% of all GNET. A macrocytic anemia is a frequent manifestation of GNET type 1. The possibility that macrocytic anemia appear during therapy with methotrexate (MTX) is widely documented. Similarly, MTX can determine gastric atrophy. We describe the case of a patient with rheumatoid factor-positive early arthritis (EA) in which the appearance of macrocytic anemia during treatment with MTX led to the recognition of a GNET type 1, until then asymptomatic. The endoscopic eradication of polypoid formations forming the GNET, the immediate suspension of MTX and therapy with octreotide long-action determined the complete remission of arthritis. This remission is maintained until today. According to our knowledge, the possibility that an EA may represent a paraneoplastic manifestation of GNET has never been described.

Topics: Anemia, Macrocytic; Antimetabolites, Antineoplastic; Antineoplastic Agents, Hormonal; Arthritis; Enterochromaffin Cells; Erythrocytes; Gastrins; Gastritis, Atrophic; Humans; Male; Methotrexate; Middle Aged; Neuroendocrine Tumors; Octreotide; Rheumatoid Factor; Stomach Neoplasms

Serum pepsinogen (PG) test, as an indicator of gastric mucosal atrophy, reflects the functional and morphologic status of gastric mucosal and it is suggested to serve as a useful predictive marker for patients with gastric cancer (GC). The available classifications of gastritis, known as the Operative Link on Gastritis Assessment (OLGA) and Operative Link on Gastritis Intestinal Metaplasia (OLGIM), integrating the severity and topography of atrophy/intestinal metaplasia (IM), have been gradually accepted and used in screening for GC in recent years.. To assess whether serum pepsinogen test, including PGI, PGII, PGI/PGII and gastrin-17 (G-17) could reflect the extent and topography of gastric mucosal atrophy/IM. Furthermore, to discuss the relationship between OLGA/OLGIM staging system and serum pepsinogen test in assessment of gastric atrophy/IM.. A total of 177 non-atrophic gastritis and 154 atrophic gastritis were analyzed, among which 40 were antrum atrophy, 32 were corpus atrophy and 82 were pan-atrophy. All patients were assessed applying the OLGA/OLGIM criteria with a mean age of 54.7 ± 10.8 years. Patients among OLGA/OLGIM Stage III-IV were presented with a lower level of serum PGI and PGI/PGII (p < .05), especially for Stage IV (p = .01). For both Hp-positive patients and Hp-negative patients according to OLGA system, PGI/PGII level correlated inversely with the rising stage (p = .022; p = .028). As for OLGIM system, similar difference can be seen in PGI/PGII level in either Hp-positive patients, or Hp-negative patients (p = .036; p = .013). In addition, the percentage of G-17 <1 pmol/L combined with PG-negative in antrum atrophy group was much higher than that of non-atrophy group and corpus atrophy group (25 versus 15.8 versus 6.3%) (p = .029). The proportion of G-17 > 15 pmol/L combined with PG-positive was apparently higher in corpus atrophy group, compared with other two groups (25 versus 11.3 versus 8.1%) (p = .023). Logistic regression modeling showed there exist significant connections between OLGA/OLGIM stages and serum pepsinogen test in patient stratification for gastric mucosal atrophy assessment (p < .001, p < .001).. Serum pepsinogen test has a strong correlation with OLGA/OLGIM gastritis stage and could provide important information in assessment of atrophy/intestinal metaplasia.

Topics: Adult; Aged; Antibodies, Bacterial; Biomarkers; China; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter pylori; Humans; Logistic Models; Male; Metaplasia; Middle Aged; Pepsinogen A; Retrospective Studies; Risk Assessment; Risk Factors; Stomach Neoplasms

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

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

Pernicious anemia (PA) develops from atrophic gastritis due to autoimmune destruction of parietal cells and results in achlorhydria, vitamin B12 and iron deficiencies, anemia, neurologic deficits, and premalignant and malignant stomach lesions. We report the presentation, diagnosis and gastric complications of PA in patients from an endocrinology practice.. Thirty-four patients (31 female, 3 male) with PA who underwent esophagogastroduodenoscopy (EGD) or gastrectomy were identified. Pertinent clinical, laboratory, and pathology findings were reviewed and summarized.. The mean age of patients was 58.6 ± 14.2 years; the onset of PA was age 50.2 ± 15.3 years. Anemia reflected vitamin B12 and/or iron deficiencies. Parietal cell antibodies (PCA) were detected in 97% of patients, and intrinsic factor blocking antibody (IFBA) was found in 52%. Fasting gastrin and chromogranin A levels were elevated (1,518.0 ± 1,588.3 pg/mL, and 504.9.1 ± 1,524.9 ng/mL respectively). Autoimmune or immunologic diseases (AIDs) were present in 32/34 patients. Stomach pathology showed premalignant or malignant lesions in 26 patients, including gastric neuroendocrine tumors (GNETs) in 6 and adenocarcinoma in 1. One patient presented with neurologic symptoms and subacute combined degeneration of the posterior column of the spinal cord.. PA should be suspected in patients with unexplained anemia or neurologic symptoms. The diagnosis of PA relies on fasting gastrin and gastric auto-antibody testing, in addition to hematologic evaluation. EGD with measurement of gastric pH and biopsies of the fundus and antrum identifies patients with achlorhydria, atrophic gastritis, and premalignant and malignant stomach lesions. EGD surveillance of patients with high-risk stomach lesions is recommended.. AID = autoimmune or immunologic disease; EGD = esophagogastroduodenoscopy; GNET = gastric neuroendocrine tumor; IFBA = intrinsic factor blocking antibody; PA = pernicious anemia; PCA = parietal cell antibody; T1D = type 1 diabetes.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Anemia, Pernicious; Autoimmune Diseases; Endoscopy, Digestive System; Female; Gastrectomy; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Retrospective Studies; Young Adult

In patients with adenoma, assessing premalignant changes in the surrounding mucosa is important for surveillance. This study evaluated atrophic and metaplastic progression in the background mucosa of adenoma or early gastric cancer (EGC) cases.. Among 146 consecutive patients who underwent endoscopic resection for intestinal-type gastric neoplasia, the adenoma group included 56 patients with low-grade dysplasia and the ECG group included 90 patients with high-grade dysplasia or invasive carcinoma. For histology, 3 paired biopsies were obtained from the antrum, corpus lesser curvature (CLC), and corpus greater curvature (CGC). Serological atrophy was determined based on pepsinogen A (PGA), progastricsin (PGC), gastrin-17, and total ghrelin levels. Topographic progression of atrophy and/or metaplasia was staged using the operative link on gastritis assessment (OLGA) and operative link on gastric intestinal metaplasia assessment (OLGIM) systems.. Rates of moderate-to-marked histological atrophy/metaplasia in patients with adenoma were 52.7%/78.2% at the antrum (vs. 58.8%/76.4% in EGC group), 63.5%/75.0% at the CLC (vs. 60.2%/69.7% in EGC group), and 10.9%/17.9% at the CGC (vs. 5.6%/7.8% in EGC group). Serological atrophy indicated by PGA and PGC occurred in 23.2% and 15.6% of cases in the adenoma and ECG groups, respectively (p = 0.25). Mean serum gastrin-17 concentrations of the adenoma group and EGC group were 10.4 and 9.0 pmol/L, respectively (p = 0.54). Mean serum total ghrelin levels were 216.6 and 209.5 pg/mL, respectively (p = 0.71). Additionally, between group rates of stage III-IV OLGA and OLGIM were similar (25.9% vs. 25.0%, p = 0.90; 41.8% vs. 44.9%, p = 0.71, respectively).. Atrophic and metaplastic progression is extensive and severe in gastric adenoma patients. A surveillance strategy for metachronous tumors should be applied similarly for patients with adenoma or EGC.

Topics: Adenoma; Aged; Biomarkers; Disease Progression; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Male; Metaplasia; Middle Aged; Neoplasms, Second Primary; Pepsinogen C; Risk Factors; Stomach Neoplasms

We report a case of developing multiple adenocarcinoma foci in multiple hyperplastic polyps in a patient with Helicobacter pylori infection and hypergastrinemia during long-term proton pump inhibitor (PPI) therapy. A 57-year-old man, who was undergoing hemodialysis for chronic renal failure, underwent an upper gastrointestinal endoscopy to elucidate the cause of anemia. Atrophic gastritis with H. pylori infection and multiple adenocarcinoma foci in multiple hyperplastic polyps were found in the endoscopic and histological examinations. Enterochromaffin-like micronests and parietal cell protrusion in the background of the polyps suggested the existence of hypergastrinemia. The serum gastrin level was markedly high-10,206 pg/ml (normal range 37-172 pg/ml). The cause of this marked hypergastrinemia was not autoimmune gastritis and gastrinoma. After discontinuing PPI therapy and successful eradication of H. pylori, the serum gastrin level decreased to normal range. These findings indicate that hypergastrinemia may be caused by long-term PPI therapy in patients with H. pylori infection. This case suggests that hypergastrinemia may mediate gastric carcinogenesis in patients with H. pylori infection.

Topics: Adenocarcinoma; Cocarcinogenesis; Drug Administration Schedule; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Hyperplasia; Male; Middle Aged; Polyps; Proton Pump Inhibitors; Stomach Neoplasms

A man in his 60s was referred to our institution for the evaluation of a gastric neuroendocrine tumor (G-NET) located in the fornix and that measured 13mm in size. Blood test results revealed hypergastrinemia (up to 3376pg/ml). Additional tests, including esophagogastroduodenoscopy, computed tomography, and intragastric pH monitoring, indicated that hypergastrinemia was not associated with type A autoimmune gastritis or gastrinoma. The patient was positive for the immunoglobulin G antibody against Helicobacter pylori, suggesting type B chronic atrophic gastritis as the cause for the condition. This report describes a rare case of G-NET with hypergastrinemia following type B chronic atrophic gastritis. Evaluation of similar cases is necessary to determine if H. pylori-associated chronic atrophic gastritis is frequently associated with G-NET.

Topics: Chronic Disease; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Neuroendocrine Tumors; Stomach Neoplasms

Autoimmune gastritis may be associated with other organ-specific autoimmune disorders, but the prevalence of this association is not entirely quantified. The aims of this study were to investigate the prevalence of autoimmune disorders and evaluate the factors that might affect this association in patients with autoimmune gastritis.. A total of 320 patients with autoimmune gastritis were retrospectively studied and data on concomitant autoimmune diseases, serum gastrin and chromogranin A levels, anti-Hp IgG, antiparietal cell antibodies, presence of enterochromaffin-like cell hyperplasia and gastric atrophy were gathered for each patient and associations between autoimmune gastritis and studied parameters were explored through descriptive statistics and logistic regression analysis.. Of the 320 atrophic body autoimmune gastritis patients, 171 (53.4%) had an associated autoimmune disorder. Autoimmune thyroiditis was the most common concurrent disease, diagnosed in 116 patients (36.2%). Multivariate analysis showed that, presence of enterochromaffin cell hyperplasia (odds ratio [OR] 9.445, 95% confidence [CI]: 4.42-20.22), serum gastrin (OR 3.1, 95% CI: 1.46-6.60) and serum chromogranin A (OR 4.14, 95% CI: 2.01-8.52) levels remained significantly associated with the coexistence of an autoimmune disease.. Concurrent autoimmune diseases are common in patients with autoimmune gastritis. Autoimmune thyroiditis is the most encountered disease. These data suggest that patients with autoimmune gastritis should be investigated for the presence of an autoimmune disease, in particular patients with enterochromaffin cell hyperplasia and those with serum gastrin and chromogranin A levels above cut-off values.

Topics: Adult; Aged; Chromogranin A; Female; Gastrins; Gastritis, Atrophic; Humans; Logistic Models; Male; Middle Aged; Multivariate Analysis; Odds Ratio; Retrospective Studies; ROC Curve; Thyroiditis, Autoimmune; Turkey

Several biomarkers have been proposed for the diagnosis of autoimmune atrophic gastritis (AAG), but at the present there is no appropriate testing strategy for the disease.. The aim of this study was to develop and validate a laboratory score able to address the diagnosis of AAG in a general practice setting.. We prospectively evaluated a number of serum biomarkers (vitamin B12, mean corpuscular volume, hemoglobin, gastrin, and chromogranin A levels) in a case-control population and built 2 biochemical scores, the first with all the parameters [Global Score (GS)], and the second as the best statistical combination of them [Simple Score (SS)]. In the second phase we validated the score that proved to be more efficient on a random population referred to our center (Gastroenterology Outpatient Clinic).. Both models turned out to be reliable in detecting patients with suspected AAG, showing excellent accuracy [area under the receiver operating curve (AUC-ROC) 0.94; 95% confidence interval (CI), 0.91-0.97 for GS and AUC-ROC 0.93; 95% CI, 0.89-0.86 for SS]. The SS proved to be more convenient because of its accessibility and availability in a general setting and its low cost. The validation of the SS showed a sensitivity of 85.7% (95% CI, 57.2-98.2) and a specificity of 83.7% (95% CI, 74.2-90.89).. Herein, we describe 2 nonexpensive and reliable score models, particularly the SS, that can be applied in daily medical practice for identifying patients potentially affected by AAG.

Topics: Adult; Aged; Area Under Curve; Autoimmune Diseases; Biomarkers; Case-Control Studies; Chromogranin A; Erythrocyte Indices; Female; Gastrins; Gastritis, Atrophic; Hemoglobins; Humans; Logistic Models; Male; Middle Aged; Prospective Studies; ROC Curve; Vitamin B 12

Topics: Gastrectomy; Gastrins; Gastritis, Atrophic; Humans; Laparoscopy; Neuroendocrine Tumors; Pyloric Antrum

Although serum pepsinogen tests are useful for predicting the presence of atrophic gastritis, the optimal cut-off values have not been fully evaluated.. To determine the optimal serum pepsinogen cut-off value for predicting atrophic gastritis.. Patients scheduled for upper endoscopy at Severance Hospital, Korea, between August 2012 and October 2013, were recruited prospectively. Endoscopic biopsies for atrophic gastritis were obtained and histologically graded, based on the updated Sydney system.. Ninety-five patients were enrolled in the study. The mean age was 57.7±12.1 years, and 44.2% of the patients were male. Serum pepsinogen I/II ratios were lower in patients with atrophic gastritis than in those without it (antrum, 4.2±1.7 vs. 5.2±2.1, P=0.040; corpus, 3.3±1.9 vs. 5.4±1.9, P<0.001). Serum pepsinogen I/II ratios were significantly correlated with histologic atrophic gastritis (antrum, P=0.030; corpus, P<0.001). Using a cut-off value of 4.9, the sensitivity and specificity of the serum pepsinogen I/II ratio for predicting atrophic gastritis in the antrum were 68.2% and 60.3%, respectively.. The optimal serum pepsinogen I/II ratio cut-off values for atrophic gastritis of the antrum and for the corpus were 4.9 and 3.5, respectively. Serum pepsinogen I/II ratios, with these cut-off values, are useful for screening patients for the presence of atrophic gastritis.

Topics: Aged; Area Under Curve; Biomarkers; Biopsy; Endoscopy, Gastrointestinal; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metaplasia; Middle Aged; Pepsinogen A; Pepsinogen C; Predictive Value of Tests; Pyloric Antrum; Reference Values; ROC Curve

Optimal management and treatment of type-1 gastric carcinoids is under debate.. This prospective study evaluates the outcome of patients with recurrent type-1 gastric carcinoids treated with somatostatin analogues.. From 2000 to 2013, among a population of 107 chronic atrophic gastritis patients, 25 (20% males, median age 62 years) developed type-1 gastric carcinoids and underwent regular clinical and endoscopic follow-up (median 77 months, range 6-165) after the initial treatment. Those patients showing recurrent disease were treated with somatostatin analogues until carcinoid disappearance.. 12/25 patients (33% males, median age 65 years) showed recurrent gastric carcinoids and were treated with somatostatin analogues for a median duration of 12 months. Median gastrin and chromogranin A levels, which were 802 pg/mL and 33 U/L, respectively, decreased to 299 pg/mL (p=0.002) and 15.6 U/L (p=0.001) at the end of the treatment. Gastric carcinoids disappeared after a median length of treatment of 12 months. After a median time of 19.5 months from somatostatin analogues discontinuation, 4/12 patients (25% males, median age 56 years) showed a further recurrence. A new cycle of treatment was performed successfully.. This study confirms that type-1 gastric carcinoids are a recurring disease and somatostatin analogues, administered on 12-month cycles, represent an effective treatment.

Topics: Aged; Aged, 80 and over; Antineoplastic Agents, Hormonal; Autoimmune Diseases; Carcinoid Tumor; Chromogranin A; Cohort Studies; Female; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Neoplasm Recurrence, Local; Octreotide; Peptides, Cyclic; Prospective Studies; Somatostatin; Stomach Neoplasms; Treatment Outcome

Bone marrow-derived mesenchymal stem cells (BM-MSCs) promote gastric cancer in response to gastritis. In culture, BM-MSCs are prone to mutation with continued passage but it is unknown whether a similar process occurs in vivo in response to gastritis.. The purpose of this study was to identify the role of chronic gastritis in the transformation of BM-MSCs leading to an activated cancer-promoting phenotype.. Age matched C57BL/6 (BL/6) and gastrin deficient (GKO) mice were used for isolation of stomach, serum and mesenchymal stem cells (MSCs) at 3 and 6 months of age. MSC activation was assessed by growth curve analysis, fluorescence-activated cell sorting and xenograft assays. To allow for the isolation of bone marrow-derived stromal cells and assay in response to chronic gastritis, IRG/Vav-1(Cre) mice that expressed both enhanced green fluorescent protein-expressing hematopoietic cells and red fluorescent protein-expressing stromal cells were generated. In a parabiosis experiment, IRG/Vav-1(Cre) mice were paired to either an uninfected Vav-1(Cre) littermate or a BL/6 mouse inoculated with Helicobacter pylori.. GKO mice displayed severe atrophic gastritis accompanied by elevated gastric tissue and circulating transforming growth factor beta (TGFβ) by 3 months of age. Compared to BM-MSCs isolated from uninflamed BL/6 mice, BM-MSCs isolated from GKO mice displayed an increased proliferative rate and elevated phosphorylated-Smad3 suggesting active TGFβ signaling. In xenograft assays, mice injected with BM-MSCs from 6-month-old GKO animals displayed tumor growth. RFP+ stromal cells were rapidly recruited to the gastric mucosa of H. pylori parabionts and exhibited changes in gene expression.. Gastritis promotes the in vivo activation of BM-MSCs to a phenotype reminiscent of a cancer-promoting cell.

Topics: Animals; Biomarkers; Cell Proliferation; Cell Transformation, Neoplastic; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Hedgehog Proteins; Helicobacter Infections; Helicobacter pylori; Immunoblotting; Mesenchymal Stem Cells; Mice; Mice, Inbred C57BL; Mice, Transgenic; Parabiosis; Phenotype; Real-Time Polymerase Chain Reaction; Smad3 Protein; Transforming Growth Factor beta

Atrophic gastritis (AG), first step in the cascade leading to gastric adenocarcinoma, is related to Helicobacter pylori (H. pylori) infection. Currently, the gold standard for the diagnosis of AG is esophagogastroduodenoscopy (EGD) with histological examination of the biopsy specimens. However, since the latter are taken in random order and the distribution of AG is often patchy, histology is only representative of mucosal status. Considering this limitation, a test named GastroPanel®, that measures the blood concentrations of pepsinogen I and II, gastrin-17 and H. pylori antibodies, has been developed as a potential non-invasive biopsy. Aim of this study has been to assess the accuracy of GastroPanel® in patients with AG.. Forty-seven dyspeptic patients (24 males, mean age 52.2±9.3 years), in follow-up for antral or diffuse AG, were enrolled. All underwent at least two EGDs with random biopsies and blood collection for GastroPanel® parameters examination.. Of the 47 patients, 16 (34.1%) had histological diagnosis of antral and 31 (65.9%) multifocal AG; 17 (36.2%) patients had mild and 30 (63.8%) had moderate-severe AG. H. pylori was detected in 39 (82.9%) and intestinal metaplasia was found in all patients. GastroPanel® showed 82.9% sensitivity for the diagnosis of AG and 53.8% for the diagnosis of H. pylori infection. The prediction of advanced atrophy was not sufficiently accurate, neither in patients with antral nor in those with multifocal AG.. GastroPanel® can be useful for detecting patients with AG. However, it does not reflect the severity of atrophy.

Topics: Adult; Antibodies, Bacterial; Biomarkers; Biopsy; Dyspepsia; Endoscopy, Digestive System; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Predictive Value of Tests; Sensitivity and Specificity; Severity of Illness Index

Topics: Autoimmune Diseases; Chromogranin A; Female; Gastrectomy; Gastric Mucosa; Gastrin-Secreting Cells; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Middle Aged; Mucin-6; Neuroendocrine Tumors; Stomach; Stomach Neoplasms; Synaptophysin

It has been suggested that GastroPanel might be a useful tool for the diagnosis of chronic atrophic gastritis (CAG) measuring four biomarkers in blood: basal gastrin-17 (G17), pepsinogen I and II (PGI and PGII), and Helicobacter pylori antibodies.. To determine the accuracy of GastroPanel for the diagnosis of CAG.. This was a prospective, blinded, multicenter study that included dyspeptic patients. G17, PGI, and PGII were determined by enzyme immunoassays. Three antrum and two corpus biopsies were obtained for standard histological analysis and rapid urease test. Biopsies were analyzed by a single blinded expert pathologist.. Ninety-one patients were included (77% women, mean age 44 years, 51% H. pylori positive, 17% with CAG). G17 was reduced in patients with antrum CAG (5.4 vs. 13.4 pmol/l; P<0.01) and increased in patients with corpus CAG (11 vs. 24 pmol/l; P<0.05), but its accuracy was only acceptable in the case of corpus localization [area under the receiver operating characteristic curve (AUC), 74%]; PGII difference was almost statistically significant only when testing for corpus atrophy (33 vs. 21 μg/l; P=0.05; AUC=72%). The PGI and PGI/PGII ratio showed no significant differences (AUCs were all unacceptably low). Helicobacter pylori antibody levels were higher in H. pylori-infected patients (251 vs. 109 EIU, P=0.01; AUC=70). The accuracy of GastroPanel for the diagnosis of CAG was as follows: sensitivity 50%; specificity 80%; positive 25% and negative 92% predictive values; and positive 2.4 and negative 0.6 likelihood ratios.. GastroPanel is not accurate enough for the diagnosis of CAG; thus, its systematic use in clinical practice cannot be recommended.

Topics: Adult; Algorithms; Antibodies, Bacterial; Biomarkers; Biopsy; Chronic Disease; Double-Blind Method; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Predictive Value of Tests; Prospective Studies; Pyloric Antrum; Stomach

Fasting serum gastrin-17 (FsG17) is considered as a noninvasive biomarker reflecting the structure and functional status of gastric mucosa, but its clinical utility remains unclear. This study aimed to evaluate FsG17 comprehensively: establish the ranges and cut-off points of FsG17 levels in different gastric diseases, identify their influencing factors, and investigate the accuracy of FsG17 for identifying diseased stomach.. The study included 4064 participants from Northern China between 2008 and 2013. FsG17 and serum Helicobacter pylori IgG antibody levels were measured by enzyme-linked immunosorbent assay. Diagnostic accuracy was assessed by receiver operator characteristic curves. Multivariate logistic regression analysis was performed to determine the best predictors of gastric histopathological conditions.. Median FsG17 levels in healthy, non-atrophic, atrophic, and cancerous stomachs were 1.8, 4.0, 3.8, and 6.1 pmol/l, respectively. Age, smoking status, alcohol consumption, H. pylori infection, and predominant lesion site were factors that affected FsG17 levels. The optimal cut-off values for FsG17 were 3.0 pmol/l (sensitivity of 59.3% and specificity of 67.3%) for discriminating between healthy stomach and diseased stomach and 10.7 pmol/l (sensitivity of 37% and specificity of 83.7%) for discriminating between cancerous stomach and cancer-free stomach; the screening accuracy was higher (sensitivity of 50.0% and specificity of 83.0%) for gastric cancer in the corpus. Multivariate analysis showed that FsG17, gender, age, and H. pylori infection were independent predictors of cancerous stomach.. With the progression from health stomach to malignancy, FsG17 levels significantly increased and were influenced by other factors. FsG17 combined with age, gender, and H. pylori infection could distinguish between cancerous stomach and cancer-free stomach. The results will enhance our understanding of the potential clinical utility of FsG17.

Topics: Age Factors; Alcohol Drinking; Area Under Curve; Biomarkers; China; Fasting; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Predictive Value of Tests; ROC Curve; Smoking; Stomach Neoplasms

Vagotomy causes inhibition of basal and post-prandial acid secretion in humans, but the knowledge about the trophic effect of the vagal nerves is limited. Vagotomy is known to induce hypergastrinemia and we aimed to study the long-term effects of proximal gastric vagotomy (PGV) on the oxyntic mucosa and the enterochromaffin-like (ECL) cell density in particular.. Eleven patients operated with PGV because of duodenal ulcer and age- and sex-matched controls were examined 26 to 29 years postoperatively by gastroscopy with biopsies from the antrum and oxyntic mucosa. Neuroendocrine cell volume densities were calculated after immunohistochemical labeling of gastrin, the general neuroendocrine cell marker chromogranin A (CgA) and the ECL cell marker vesicular monoamine transporter 2 (VMAT2). Gastritis was graded and Helicobacter pylori (H. pylori) status was determined by polymerase chain reaction of gastric biopsies. Fasting serum gastrin and CgA were measured.. Serum gastrin was higher in the PGV group compared to controls (median 21.0 [interquartile range (IQR) = 22.0] pmol/L vs 13.0 [IQR = 4.0] pmol/L, p = 0.04). However, there was neither a significant difference in serum CgA or in CgA (neuroendocrine) nor VMAT2 (ECL cell) immunoreactive cell volume density in the oxyntic mucosa. There was significantly more inflammation and atrophy in H. pylori-positive patients, but PGV did not influence the grade of gastritis.. Despite higher serum gastrin concentrations, patients operated with PGV did not have higher ECL cell mass or serum CgA. Vagotomy may prevent the development of ECL cell hyperplasia caused by a moderate hypergastrinemia.

Topics: Aged; Biopsy; Chromogranin A; Duodenal Ulcer; Enterochromaffin-like Cells; Female; Follow-Up Studies; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pyloric Antrum; Time Factors; Vagotomy, Proximal Gastric; Vesicular Monoamine Transport Proteins

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 article is devoted to the problem of diagnostics of atrophic gastritis. The main principles of morphological diagnostics are presented. The endoscopic findings are discussed. The authors had used the mathematical regression model to reveal groups of patients with some specific signs of atrophic gastritis, such as endoscopic sings, morphological and clinical signs. This model can be used to put a diagnosis and to look after the patients with metaplasia, dysplasia and early cancer.

Topics: Biopsy; Decision Trees; Diagnosis, Differential; Endoscopy, Gastrointestinal; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Metaplasia; Models, Biological; Pepsinogens; Prognosis

Helicobacter pylori-infection associated gastritis is known to be a significant risk factor of gastric cancer. Serum levels of Gastrin-17 and Pepsinogen1which are respectively biomarkers of gastric antral and corpus mucosal activity are well known parameters of atrophic gastritis.. To determine the prevalence of Helicobacter pylori and atrophic gastritis amongst dyspeptic patients and to compare the production of PGI and G-17 in the various atrophic stages.. A total of 139 dyspeptic patients aged 46.68±15.50 years [females 106 aged47.23±15.51years, males 33 aged 44.48±14.62] were included during the one year period, March 2008-april 2009 at the district hospital Tombel. The degree of atrophy was determined by the levels of serum pepsinogen1, and gastrin-17 and the presence of Helicobacter pylori antibodies detected by an enzyme immunoassay.. The prevalence of Helicobacter pylori was 79.82% and that for atrophic gastritis was 6.6%. A decrease in mean serum levels of gastin-17 along with increasing antral atrophy was observed; the mean serum levels of pepsinogen1 were reduced during progression of corpus atrophy.. A weak reverse correlation(r =-0.036) was found between Gastrin-17 and Helicobacter pylori antibodies.

Topics: Adult; Aged; Aged, 80 and over; Algorithms; Antibodies, Bacterial; Cameroon; Cross-Sectional Studies; Dyspepsia; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Male; Middle Aged; Pepsinogen A; Prevalence; Risk Factors; Socioeconomic Factors; Surveys and Questionnaires; Young Adult

Iran is a country with very high incidences of stomach cancer, especially in Northern parts. Here we assessed prognostic value of serum screening biomarkers among people >50 years old for early detection of precancerous lesions in a hot spot for gastric carcinoma in Guilan Province, North Iran.. A cross- sectional population-based survey was conducted on 1,390 residents of Lashtenasha city with the mean age (SD) of 61.8 (9.02) years old (50.8% females) to assess the association of gastrin and the pepsinogen (PG) I/II ratio with premalignant gastric lesions. Blood samples were taken for CBC, blood group, and serologic exams (PGI, PGII, and gastrin 17) from each subject. Expert gastroenterologists performed upper GI endoscopy and ROC curves were generated to determine appropriate cutoff points.. Mean values of PGI, PGII, PGI/PGII and gastrin were significantly different between patients with and without atrophy or metaplasia (P<0.05). To diagnose atrophy and intestinal metaplasia, a significantly higher AUC was observed for the PGI/PGII ratio (70 and 72%, respectively) compared to the PGI (56, 55%), PGII (63, 64%) and gastrin (59, 61%) (all p<0.001).. Biomarker tests such as the PGI/II ratio can be used in the screening and diagnosis of subjects at high gastric cancer risk in our region.

Topics: Aged; Aged, 80 and over; Biomarkers; Biomarkers, Tumor; Cross-Sectional Studies; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Iran; Male; Metaplasia; Middle Aged; Neoplasm Staging; Pepsinogen A; Pepsinogen C; Precancerous Conditions; Prognosis; ROC Curve; Stomach Neoplasms

This study investigated the effect and mechanism of Astragalus polysaccharides (APS) on chronic atrophic gastritis (CAG) induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in rats. Histomorphological, hormone-level, and immunohistochemistry experiments were used to investigate the gastric mucosal injury. Pathological changes were readily found in CAG rats. Compared to the control rats, the CAG rats showed significantly decreased plasma levels of gastrin and somatostatin while their motilin levels increased. Moreover, PGE2 in gastric tissue increased and serum sIgA decreased significantly, while the GSH/GSSG ratio showed no change. Immunohistochemical detection showed that the expression of EGFR, COX-2, and MMP-2 was higher in the gastric tissue of CAG rats. After APS treatment, the gastric morphology of CAG rats improved. APS increased plasma gastrin and somatostatin levels significantly but had no significant effect on the motilin level. APS also decreased tissue PGE2 and increased serum sIgA in CAG rats without affecting the GSH/GSSH ratio. This study suggested that APS had a beneficial effect on CAG rats by deregulating EGFR at its downstream effectors COX-2 and MMP-2.

Topics: Animals; Astragalus Plant; Chronic Disease; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Glutathione; Male; Methylnitronitrosoguanidine; Polysaccharides; Rats; Rats, Sprague-Dawley; Somatostatin

Health authorities of Kazakhstan are seeking for effective measures to interrupt the untoward trend, projected to increase the current number of gastric cancer (GC) cases (n=3,316) by 50% until the year 2030.. Use of a non-invasive blood test with four stomach-specific biomarkers [Pepsinogen-I (PG-I) and -II (PG-II), amidated gastrin-17 (G-17), and Helicobacter pylori (HP) IgG antibodies], to assess for the prevalence of stomach conditions: Helicobacter pylori (HP) infection and atrophic gastritis (AG), both known to increase GC risk of in Kazakhstan.. A cohort of 835 (symptomatic and asymptomatic) cases (473 women and 362 men)(median age 46.8 years; range 13.6-74.8) was examined with a panel of biomarkers. Results were assigned in five categories: 1) Healthy stomach, 2) HP infection, 3) atrophic gastritis (AG) of the antrum, 4) AG of the corpus, and 5) AG of both antrum and corpus (pangastritis).. The distribution in these five categories was identical in both sexes (p=0.259). Healthy stomach was detected only in 196 (23.5%) subjects, whereas the vast majority, 62.3% (n=519) had HP infection (with no AG). In 118 (14.1%) subjects, results were consistent with AG; in antrum (n=72), corpus (n=42) or pangastritis (n=4). Prevalence of AG increased with patient's age in both sexes. There was no age-related pattern in biomarker levels, and only slight differences between the genders.. While capable of detecting the subjects at risk for GC (HP or AG), GP seems to be a cost-effective means to intervene the current ominous trend in GC incidence in Kazakhstan.

Topics: Adolescent; Adult; Aged; Antibodies, Bacterial; Biomarkers; Dyspepsia; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Kazakhstan; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Phenotype; Prevalence; Sex Distribution; Young Adult

The gastric hormone ghrelin is known as an important factor for energy homeostasis, appetite regulation and control of body weight. So far, ghrelin has mainly been examined as a serological marker for gastrointestinal diseases, and only a few publications have highlighted its role in local effects like mucus secretion. Ghrelin can be regarded as a gastroprotective factor, but little is known about the distribution and activity of ghrelin cells in pathologically modified tissues. We aimed to examine the morphological changes in ghrelin expression under several inflammatory, metaplastic and carcinogenic conditions of the upper gastrointestinal tract. In particular, autoimmune gastritis showed interesting remodeling effects in terms of ghrelin expression within neuroendocrine cell hyperplasia by immunohistochemistry. Using confocal laser microscopy, the gastrin/cholecystokinin receptor (CCKB) could be detected on normal ghrelin cells as well as in autoimmune gastritis. Functionally, we found evidence for a physiological interaction between gastrin and ghrelin in a primary rodent cell culture model. Additionally, we gathered serological data from patients with different basic gastrin levels due to long-term autoimmune gastritis or short-term proton pump inhibitor treatment with slightly reactive plasma gastrin elevations. Total ghrelin plasma levels showed a significantly inverse correlation with gastrin under long-term conditions. Autoimmune gastritis as a relevant condition within gastric carcinogenesis therefore has two effects on ghrelin-positive cells due to hypergastrinemia. On the one hand, gastrin stimulates the proliferation of ghrelinpositive cells as integral part of neuroendocrine cell hyperplasia, while on the other hand, plasma ghrelin is reduced by gastrin and lost in pseudopyloric and intestinal metaplastic areas. Ghrelin is necessary for the maintenance of the mucosal barrier and might play a role in gastric carcinogenesis, if altered under these pre neoplastic conditions.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Animals; Autoimmune Diseases; Child; Child, Preschool; Down-Regulation; Duodenum; Esophagus; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Ghrelin; Humans; Infant; Male; Middle Aged; Rats; Rats, Wistar; Receptor, Cholecystokinin B; Stomach Neoplasms; Young Adult

In a prospective study the risk of subsequent gastric cancer (GC) was assessed in persons aged 45-69 over 5 years after the initial testing with a set of serological tests (pepsinogen I, pepsinogen II, gastrin-17, antibodies to Helicobacter pylori). The presence of gastric atrophy markers was a significant predictor of GC in the forthcoming years. Non-invasive techniques may be used in the formation of high-risk groups, followed by GC active surveillance.

Topics: Aged; Antibodies, Bacterial; Biomarkers; Cohort Studies; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Pepsinogens; Retrospective Studies; Serologic Tests; Stomach Neoplasms

Atrophic gastritis of the corporal mucosa is a frequent cause of hypergastrinemia. Hypergastrinemia is implicated in colorectal cancer development.. To assess whether hypergastrinemic atrophic gastritis is associated with a higher risk of neoplastic colorectal lesions.. Among 441 hypergastrinemic atrophic gastritis patients, 160 who were aged >40 and underwent colonoscopy for anaemia, diarrhoea or colorectal cancer-screening were retrospectively selected. Each patient was age- and gender-matched with a normogastrinemic control with healthy stomach. Controls had colonoscopy, gastroscopy with biopsies and gastrin assessment.. 160 hypergastrinemic atrophic gastritis patients and 160 controls were included. 28 atrophic gastritis patients and 36 controls had neoplastic colorectal lesions (p=0.33). Patients and controls did not differ for frequency of colorectal adenomas (10.6% vs. 13.1%, p=0.60) or cancer (6.9% vs. 9.4%, p=0.54). Hypergastrinemic atrophic gastritis was not associated with a higher probability of developing colorectal cancer (OR 1.03, 95% CI 0.34-3.16). Age >50 years (OR 3.86) but not hypergastrinemia (OR 0.61) was associated with colorectal cancer.. Hypergastrinemic atrophic gastritis is not associated with higher risk for colorectal cancer. Atrophic gastritis-related hypergastrinemia is not associated with an increased risk of neoplastic colorectal lesions. Closer surveillance of colonic neoplasia in atrophic gastritis patients seems not appropriate.

Topics: Adenocarcinoma; Adenoma; Adult; Age Factors; Aged; Aged, 80 and over; Case-Control Studies; Colorectal Neoplasms; Confidence Intervals; Female; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Odds Ratio; Retrospective Studies; Risk Factors; Statistics, Nonparametric

Serum gastrin levels exceeding 1000pg/ml (normal, <100) usually raise the suspicion for a neuroendocrine tumor (NET) that secretes gastrin. Rarely, such elevated gastrin levels are seen in patients with pernicious anemia which most commonly is associated with autoimmune gastritis (AG). AG can occur concomitantly with other autoimmune disorders including lymphocytic colitis (LC). Gastrin stimulates enterochromaffin-like cells which increase histamine secretion. Histamine excess can cause diarrhea as can bacterial overgrowth or LC. We present a 57-year-old woman with diarrhea, sporadic epigastric pain, and bloating. She also had a history of interstitial cystitis and took pentosan polysulfate and cetirizine. She had no history of ulcers, renal impairment or carcinoid syndrome. Fasting serum gastrin was 1846pg/ml. Esophagoduodenal gastroscopy and biopsies revealed chronic gastritis and a pH of 7 with low stomach acid. Serum gastrin and plasma chromogranin A were suggestive of a gastrinoma or NET. Pernicious anemia was unlikely. Imaging studies did not reveal any tumor. Random colonic biopsy was compatible with LC, possibly explaining her diarrhea, although we also considered excessive histamine from elevated gastrin, bacterial overgrowth, and pentosan polysulfate which can cause diarrhea and be misleading in this setting, pointing to the diagnosis of gastrinoma. At 4year follow-up in 2012, fasting serum gastrin was 1097pg/ml and the patient asymptomatic taking only cetirizine for nasal allergies. This case illustrates that diarrhea may be associated with very high serum gastrin levels in the setting of chronic gastritis, LC, and interstitial cystitis (pentosan use), without clear evidence for a gastrinoma or NET. If no history of ulcers or liver metastases is present in such cases, watchful observation rather than an extensive/invasive and costly search for a NET may be justified. Considering the various forms of polyglandular syndrome, this may represent a variant and we here provide an algorithm for working up such patients, while also reviewing literature on the intertwined relationship between the immune and endocrine systems.

Topics: Autoimmune Diseases; Chronic Disease; Colitis, Lymphocytic; Diagnosis, Differential; Digestive System Neoplasms; Female; Gastrinoma; Gastrins; Gastritis, Atrophic; Humans; Middle Aged; Neuroendocrine Tumors

To assess the predictive value for chronic autoimmune gastritis (AIG) of the combined assay of anti-parietal-cell antibodies (PCA), anti-intrinsic-factor antibodies (IFA), anti-Helicobacter pylori (Hp) antibodies, and measurement of blood gastrin.. We studied 181 consecutive patients with anemia, due to iron deficiency resistant to oral replacement therapy or to vitamin B12 deficiency.. 83 patients (45.8%) tested positive for PCA and underwent gastroscopy with multiple gastric biopsies. On the basis of the histological diagnosis, PCA-positive patients were divided into 4 groups: (1) 30 patients with chronic atrophic gastritis; they had high concentrations of PCA and gastrin and no detectable IFA; (2) 14 subjects with metaplastic gastric atrophy; they had high PCA, IFA, and gastrin; (3) 18 patients with nonspecific lymphocytic inflammation with increased PCA, normal gastrin levels, and absence of IFA; (4) 21 patients with multifocal atrophic gastritis with "borderline" PCA, normal gastrin, absence of IFA and presence of anti-Hp in 100% of the cases.. The assay of four serological markers proved particularly effective in the diagnostic classification of gastritis and highly correlated with the histological profile. As such, this laboratory diagnostic profile may be considered an authentic "serological biopsy."

Topics: Aged; Antibodies; Autoimmune Diseases; Biopsy; Female; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Intrinsic Factor; Lymphocytes; Male; Middle Aged; Parietal Cells, Gastric; Serologic Tests

We investigated whether corpus atrophic gastritis worsens in Mongolian gerbils (MGs) after long-term administration of proton pump inhibitor (PPI). MGs are an excellent model for studying Helicobacter pylori-related gastritis and adenocarcinoma.. MGs were separated into four groups (n =15/group); H pylori (ATCC43504) was inoculated into the OPZ(omeprazole)+Hp (H pylori) and Hp groups, a PPI (OPZ) was administered to the OPZ+Hp and OPZ groups and the control group received no treatment. MGs had access to food containing omeprazole (100 mg/kg body weight/day) for 6 months, after which their stomachs were removed and cut into nine sections (six sections in the fundus and three sections in the antrum). Corpus atrophy was evaluated by the absence of parietal cells in the six sections in the fundus. First, we calculated a percentage of the area devoid of parietal cells in each haematoxylin and eosin-stained section, and then we scored the degree of atrophy by adding the percentages of the six sections. A full score was 600.. Neutrophilic and lymphoid infiltrates were greater in the OPZ+Hp group than in the other groups. The corpus atrophy score in the OPZ+Hp group was significantly higher than that in the Hp group (p < 0.0048, Student t test). Significantly more adenocarcinomas were found in the OPZ+Hp (60%) than in the Hp (7%) group animals.. Long-term PPI administration promotes development of adenocarcinoma, which is associated with the progression of atrophic corpus gastritis in MGs infected with H pylori.

Topics: Adenocarcinoma; Animals; Body Weight; Cocarcinogenesis; Disease Models, Animal; Disease Progression; Drug Administration Schedule; Gastrins; Gastritis, Atrophic; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Male; Metaplasia; Proton Pump Inhibitors; Stomach; Stomach Neoplasms

The effect of Helicobacter pylori treatment on the potential reversal of atrophic body gastritis (ABG) is controversial. Body atrophy reversal was evaluated in a cohort of H. pylori-negative and treated H. pylori-positive ABG patients.. Observational long-term follow-up cohort study including 300 ABG patients with at least one follow-up gastroscopy with three biopsies from the antrum and three from the body performed no earlier than 1 year after diagnosis was included. H. pylori was diagnosed by Giemsa-stain and serology. H. pylori-positive patients (n = 192) were treated with bismuth-based triple regimen.. After a mean follow-up of 5.2 years, body atrophy reversal was observed in 42/300 patients (14%). Body atrophy reversal occurred more frequently in patients treated for H. pylori than in H. pylori-negative ones (21.3% vs 0.9%, p < 0.00001) and was observed between 2 and 8 years after treatment in 52% of cases. Predictive factors for body atrophy reversal at Cox-regression analysis were mild atrophy (HR 2.14; 95% CI 1.12-4.1), moderate-severe inflammation (HR 5.3; 95% CI 1.64-17.3), and absence of intestinal metaplasia (HR 2.4; 95% CI 1.2-4.8).. Body atrophy reversal was observed in about 20% of ABG patients treated for H. pylori infection, and about 50% of reversals occurred during long-term follow-up.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Anemia, Pernicious; Antibodies; Female; Follow-Up Studies; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Intestines; Male; Metaplasia; Middle Aged; Parietal Cells, Gastric; Pepsinogen A; Proportional Hazards Models; Pyloric Antrum; Regression Analysis; Retrospective Studies; Young Adult

Gastric carcinoids type 1 (GC1) are neuroendocrine tumors (NETs) arising from the enterochromaffin-like (ECL) cells in patients with chronic atrophic gastritis (CAG). The treatment of GC1 has been endoscopic polypectomy or surgical tumor excision and antrectomy. One year treatment with somatostatin analogs (SSAs) diminished tumor load and ECL cell density. The effect persisted 1 year after treatment was discontinued. However, the optimal SSA dose and treatment duration are unknown.. The aim of the present work was to study macroscopic and histopathological changes in the stomach and serum markers gastrin and chromogranin A (CgA) in GC1 patients 5 years after 1 year of octreotide long-acting release (LAR) treatment.. Five patients with GC1 were included 5 years after the initial year of octreotide LAR treatment. All patients underwent upper gastrointestinal endoscopy including tumor and mucosal biopsies from oxyntic mucosa, chest and abdominal computer tomography and octreotide scintigraphy. Fasting serum gastrin and CgA were also measured.. At 5 years, one patient had a highly malignant gastric tumor, one patient had an increased number of GCs, regional and distant metastases and three patients had an increased number of GCs. Serum gastrin and CgA increased to pre-treatment levels after 1 year of follow-up and were unchanged at the 5-year follow-up.. The disease had progressed in all five GCs patients treated with octreotide for 12 months at 5 years of follow-up. This suggests that, if started, octreotide treatment should not be discontinued in these patients.

Topics: Aged; Antineoplastic Agents, Hormonal; Biopsy; Carcinoid Tumor; Chromogranin A; Disease Progression; Enterochromaffin-like Cells; Female; Follow-Up Studies; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Male; Middle Aged; Octreotide; Stomach Neoplasms; Tomography, X-Ray Computed; Tumor Burden

An algorithm (GastroPanel) for the non-invasive diagnosis of atrophic gastritis has been previously proposed, based on serum pepsinogen-I, gastrin-17, and Helicobacter pylori (H. pylori) antibodies. The aim of the present study was to evaluate whether serum markers correlate with and predict gastric atrophy in gastroesophageal reflux disease (GERD) patients.. The baseline data of the prospective ProGERD study, a study on the long-term course of GERD (n=6215 patients), served to select patients with atrophic gastritis diagnosed in biopsies from gastric antrum and corpus, and control cases without atrophy. A total of 208 pairs were matched for age, sex, GERD status (erosive vs non-erosive), presence of Barrett's esophagus, and histological H. pylori status were retrieved. Serum pepsinogen-I, gastrin-17, and H. pylori antibodies were determined using specific enzyme immunoassays.. A significant negative correlation was found between the degree of corpus atrophy and the level of serum pepsinogen-I. A previously-reported negative correlation between the degree of antral atrophy and serum gastrin-17 could not be confirmed. The low sensitivity (0.32) and specificity (0.70) of the GastroPanel algorithm were mainly due to over diagnosis and under diagnosis of advanced atrophy in the antrum.. The diagnostic validity of the GastroPanel algorithm to diagnose gastric atrophy non-invasively is not sufficient for general use in GERD patients.

Topics: Adult; Aged; Aged, 80 and over; Algorithms; Barrett Esophagus; Biomarkers; Biopsy; Case-Control Studies; Endoscopy, Gastrointestinal; Europe; Female; Gastrins; Gastritis, Atrophic; Gastroesophageal Reflux; Helicobacter pylori; Humans; Immunoenzyme Techniques; Male; Matched-Pair Analysis; Middle Aged; Pepsinogen A; Predictive Value of Tests; Prospective Studies; Reproducibility of Results; Sensitivity and Specificity; Severity of Illness Index; Young Adult

The Operative Link for Gastritis Assessment (OLGA) staging system has been proposed as a histopathological reporting system of gastric atrophy. Noninvasive methods for indirect evaluation of gastric mucosal atrophy by biomarkers are also being introduced.. To analyze gastric mucosal atrophy by biomarkers, pepsinogen I (PgI), pepsinogen II (PgII), PgI/PgII ratio, fasting gastrin-17 (G-17), stimulated gastrin-17 (sG-17), in relation to OLGA gastritis stage.. Gastric biopsies were taken from 269 prospective patients referred for upper endoscopy because of dyspeptic problems and evaluated by two expert pathologists (D.J. and P.S.). Atrophy was assessed according to the OLGA staging system. Pg I, PgII, Pg I/II, G-17, sG-17 were determined in a plasma sample.. The mean levels of PgI and PgI/PgII decreased significantly from 90.8 μg/l and 7.6 in stage 0 gastritis to 64.3 μg/l and 4.3 in high-stage gastritis. The mean values of G-17 and sG-17 were significantly higher among patients with stage II gastritis compared with stage 0 and high-stage gastritis.The proportion of patients with normal mucosa and nonatrophic gastritis according to biomarkers decreased from 78% in stage 0 to 22% in high-stage (III-IV) gastritis. Among the latter no case with normal mucosa, according to biomarkers, was observed.. A significant inverse correlation between the mean levels of PgI, PgI/II ratio and the OLGA stage was observed. Percentage of dyspeptic patients with normal mucosa, by blood biomarkers, decreased with increasing OLGA gastritis stages. OLGA staging system provides a good frame for scientific analysis of gastric mucosal atrophy.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Prospective Studies

Gastric type I carcinoid is a rare neoplasm, deriving from enterochromaffin-like cells (ECL), mainly affecting women with autoimmune gastritis. The approach to treatment, either endoscopic, medical or surgical, is not well defined, particularly in multifocal tumours or carcinoids with rapid growth/frequent recurrence.. To determine whether an anti-G17 vaccination might interfere on the natural history of gastric type I carcinoid.. Padua teaching Hospital, outpatient clinic.. Three patients with type I gastric carcinoid in autoimmune gastritis were administered, after informed consent and ethic committee approval, with a vaccine against gastrin 17 (G17), a synthetic peptide that stimulates specific and high-affinity anti-G17 antibodies, and followed up endoscopically and clinically for a mean of 36 months.. Gastric histology and specifically carcinoid growth/recurrence and trend in time in gastrin, G17, pepsinogens, chromogranin A and clinical parameters.. Following vaccination, carcinoid regression was observed in 2/3 patients and, in one of the patients, even the disappearance of ECL hyperplasia, with a reduced ECL cells stimulation, confirmed by a significant reduction in chromogranin A levels. Regression was observed in the two patients that showed a more clear local response to the vaccine. Increased autoantibody titre was observed, but no appearance of new autoimmune diseases.. Anti-G17 vaccination induced regression of type I gastric carcinoid and could be considered for the treatment of this tumour, when endoscopic removal is not indicated.

Topics: Aged; Cancer Vaccines; Carcinoid Tumor; Female; Gastrins; Gastritis, Atrophic; Humans; Immunoenzyme Techniques; Male; Pilot Projects; Prognosis; Stomach Neoplasms; Survival Rate; Tumor Microenvironment; Vaccination

Decreased plasma gastrin-17 (G-17), particularly after protein stimulation, is indicative of atrophy in the antral stomach mucosa. Available data on the value of this biomarker is inconclusive. Our study was aimed to evaluate the performance of the G-17 test in Caucasian and Asian patients for antral atrophy evaluation either in fasting state or after protein stimulation.. 241 dyspeptic patients aged 55 and above from Latvia (125), Lithuania (76) and Taiwan (40) were enrolled. G-17 levels were detected in plasma samples obtained either during fasting or after a protein-rich test meal. Levels <1 pmol/L at fast and <5 pmol/L after stimulation were considered indicative of atrophy.. The sensitivity of the test was 15.8%, its specificity 88.7%, and the overall accuracy 83% in the fasting state, and 36.8, 86.5, and 82.6%, respectively, after stimulation. In the Caucasian subgroup, the corresponding figures were 15.4, 91.5, and 86.6% in the fasting state and 30.8, 92.6, 88.6% after stimulation; but for the Asian subgroup the corresponding figures were 16.7, 73.5, and 65% (fasting) and 50, 52.9, and 52.5% (stimulated).. The performance of G-17 was better after protein stimulation. G-17 was highly specific in the Caucasian, but not in the Asian subgroups. Still the low test sensitivity either at fast or following protein stimulation does not allow us to recommend it for wide screening purpose to diagnose antral atrophy.

Topics: Aged; Aged, 80 and over; Atrophy; Biomarkers, Tumor; Dietary Proteins; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Predictive Value of Tests; Reproducibility of Results; Sensitivity and Specificity

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

To study the association between Helicobacter pylori (H. pylori) infection and autoimmune type atrophic gastritis.. Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology, immunoblot-based serology, and histology to reveal a past or a present H. pylori infection. In addition, serum markers for gastric atrophy (pepsinogen I, pepsinogen I/II and gastrin) and autoimmunity [parietal cell antibodies (PCA), and intrinsic factor (IF), antibodies] were determined.. Of the 14 patients with severe gastric atrophy, as demonstrated by histology and serum markers, and no evidence for an ongoing H. pylori infection, eight showed H. pylori antibodies by immunoblotting. All eight had elevated PCA and 4/8 also had IF antibodies. Of the six immunoblot-negative patients with severe corpus atrophy, PCA and IF antibodies were detected in four. Among the patients with low to moderate grade atrophic gastritis (all except one with an ongoing H. pylori infection), serum markers for gastric atrophy and autoimmunity were seldom detected. However, one H. pylori negative patient with mild atrophic gastritis had PCA and IF antibodies suggestive of a pre-atrophic autoimmune gastritis.. Signs of H. pylori infection in autoimmune gastritis, and positive autoimmune serum markers in H. pylori gastritis suggest an etiological role for H. pylori in autoimmune gastritis.

Topics: Aged; Autoantibodies; Autoimmune Diseases; Biomarkers; Female; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Immunoblotting; Immunoenzyme Techniques; Intrinsic Factor; Malabsorption Syndromes; Male; Middle Aged; Parietal Cells, Gastric; Pepsinogen A; Pepsinogen C; Risk Factors; Severity of Illness Index; Vitamin B 12 Deficiency

Atrophic gastritis is defined as a chronic inflammatory process in gastric mucosa leading to loss of glandular cells. It is considered a precancerous condition, thus its early diagnosis is of importance. Although histo-pathologic studies remain as the gold standard of diagnosis, non-invasive methods suitable for screening purposes are being developed. This includes measurement of serum gastric profile.. Two hundred and fifty 250 patients who were planned to undergo upper gastrointestinal endoscopy were randomly selected to be included in this study. Serum levels of pepsinogen I and II, gastrin-17 and anti-Helicobacter pylori (Hp) antibody were measured and the results were compared with that of histopathologic assessment of biopsy specimens obtained during endoscopy.. IgG anti-Hp, PGII and PGI/PGII ratio showed correlation with age. PGI/PGII ratio showed best sensitivity (96.1%) and negative predictive value (97.7%). PGI has the highest specificity (94.6%), and PGII also had a high negative predictive value (90.7%). IgG anti-Hp showed poor sensitivity and specificity (58.8% and 26.5%, respectively).. Pepsinogen I/II ratio appears to be the most suitable single measurement for screening purposes in atrophic gastritis.

Topics: Adult; Antibodies, Bacterial; Biopsy; Female; Gastrins; Gastritis, Atrophic; Helicobacter pylori; Humans; Male; Pepsinogen A; Pepsinogen C; Predictive Value of Tests; Sensitivity and Specificity

Topics: Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Zollinger-Ellison Syndrome

Autoimmune metaplastic atrophic gastritis (AMAG) is an early manifestation of pernicious anemia that precedes the hematologic changes by years to decades. It is associated with metaplastic changes and neoplasms, including pyloric gland adenomas (PGAs). We investigated the frequency of PGAs and other lesions in all nonconsultation gastric biopsies and resections (1988 to 2008) diagnosed as AMAG. We further selected cases confirmed as AMAG by immunohistochemical identification of the gastric body (negative gastrin) and linear and nodular enterochromaffin-like cell hyperplasia (chromogranin). From this subset, all polyps and neoplasms were reviewed. We identified a total of 41,245 patients with gastric biopsies or resections from 46.7% males and 53.3% females comprising patients self-identified as 67.0% white, 23.6% African-American, 1.4% Asian, 0.8% non-White Hispanic, and 7.2% other or unknown. AMAG was diagnosed in 461 patients (1.1%), and had the following percentages based on race: 1.1% White, 1.3% African-American, 1.4% Asian, and 2.7% non-White Hispanic. The female:male ratio was 2:1 with an overall median age at presentation of 67.0 years. Of the 461 patients with AMAG, 143 had endoscopically identifiable lesions. These lesions (n=240) consisted of 179 polyps (138 hyperplastic polyps, 20 oxyntic mucosa pseudopolyps, 18 intestinal-type gastric adenomas, and 3 PGAs), 46 well-differentiated neuroendocrine neoplasms (carcinoid), 1 gastrointestinal stromal tumor, 3 lymphomas, and 11 adenocarcinomas. In summary, AMAG occurred with similar frequency across all racial groups. Although PGAs are associated with AMAG, they remain rare in the setting of AMAG.

Topics: Adenoma; Aged; Autoimmune Diseases; Baltimore; Biopsy; Chromogranins; Female; Gastrectomy; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Immunohistochemistry; Male; Metaplasia; Middle Aged; Polyps; Precancerous Conditions; Stomach; Stomach Neoplasms

To investigate the effect of a high-protein diet on corpus atrophic gastritis in Helicobacter pylori-infected Mongolian gerbils, H. pylori was administered orally to 5-wk-old Mongolian gerbils; and the animals were then fed a control diet (Group C); a high-fat diet (Group F: 40% fat); a high-protein diet (Group P: 32% protein); or a high-fat, high-protein diet (Group FP: 40% fat, 32% protein) for 50 wk beginning at 7 wk of age. In uninfected animals, the mucosal thickness of the corpus was significantly greater in Group P and Group FP than in Group C (P < 0.05). In infected animals, the serum gastrin level was significantly decreased in Group FP and marginally significantly decreased in Group P (P = 0.057) in comparison to Group C. The mucosal thickness of the corpus was significantly greater in Group P and Group FP than in Group C (P < 0.05). Mean inflammation and atrophy scores in the corpus were significantly lower in the high-protein groups (Groups P and FP) than in the control groups (Groups C and F; both inflammation and atrophy: P < 0.05). In conclusion, long-term administration of a high-protein diet suppresses corpus atrophic gastritis in H. pylori-infected Mongolian gerbils.

Topics: Animals; Antibodies, Bacterial; Body Weight; Caseins; Dietary Fats; Dietary Proteins; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Male; Metaplasia; Organ Size; Severity of Illness Index; Specific Pathogen-Free Organisms; Stomach; Stomach Neoplasms

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

To detect whether muscovite exerts its protective role in the progression of atrophic gastritis (AG) and evaluate the possible mechanism.. AG rats were established and then randomly divided into groups administrated with different doses of muscovite for 8 weeks. Histological changes in gastric antrum and the number of parietal cells, chief cells, and G/D cells were observed. Serum gastrin and prostaglandin E2 (PGE2) were evaluated by enzyme-linked immunosorbent assay (ELISA). The expression of proliferating cell nuclear antigen (PCNA), epidermal growth factor receptor (EGFR), C-erbB-2, p21, p53, p16 and bcl-2 in gastric tissue were detected by immunohistochemistry. The concentrations of TNF-alpha and IL-1beta secreted by THP-1 cells were detected when incubated with different doses of muscovite.. The grade of inflammation in muscovite groups was lower (p < 0.05), while the thickness and number of gastric glands were significantly elevated in muscovite groups (p < 0.01). The expression height of PCNA in the muscovite group was higher than in the AG group (p < 0.01). Immunohistochemistry results showed a positive expression rate of EGFR; p16 in muscovite-treated AG rats was increased (p < 0.05), while C-erbB-2 and p21 were decreased (p < 0.05). Serum gastrin and PGE2 were significantly elevated in the high-dose muscovite-treated rats (p < 0.05). In vitro studies showed that muscovite had a dose-dependent adsorption of TNF-alpha and IL-1beta.. Muscovite could reverse gastric gland atrophy and intestinal metaplasia by promoting cell proliferation and revitalization in gastric mucosa in AG rats.

Topics: Adsorption; Aluminum Silicates; Animals; Cell Line, Tumor; Cell Proliferation; Dinoprostone; ErbB Receptors; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Interleukin-1beta; Male; Metaplasia; Proliferating Cell Nuclear Antigen; Rats; Rats, Sprague-Dawley; Receptor, ErbB-2; Regeneration; Tumor Necrosis Factor-alpha

Atrophy of the stomach mucosa is considered to be premalignant lesion for gastric cancer development; easy identification of this condition from a blood-sample would allow identifying the group of individuals at increased risk for cancer development.. The objective of the current study was to validate a biomarker method (pepsinogen I/II ratio and gastrin-17) for indirect detection of atrophy of the stomach mucosa versus standard histopathology in Caucasian and Asian populations.. Altogether, 241 patients aged 55 and above referred for upper endoscopy due to dyspeptic symptoms (125 from Latvia, 76 from Lithuania, and 40 from Taiwan) were enrolled. Pepsinogen I, pepsinogen II, gastrin-17 (the latter after stimulation with protein-rich meal) and IgG/IgA antibodies to Helicobacter pylori infection were determined by ELISA method; standard histopathology according to the updated Sydney classification read by two independent expert pathologists was used for the comparison.. Pepsinogen I/II ratio below 3 was well related to atrophy (moderate to severe) in the corpus part of the stomach (P < 0.0001) with 83.3% sensitivity and 87.1% specificity. Gastrin-17 below 5 pmol/L was related to atrophy in the antral part (P = 0.007) with 36.8% sensitivity and 86.5% specificity.. Decreased pepsinogen I/II ratio is a reliable marker for atrophy in the corpus, and may be recommended for identification of individuals with this type of atrophy. The utility of gastrin-17 for the detection of atrophy in the antral part of the stomach still requires further evaluation due to the low sensitivity.

Topics: Aged; Biomarkers; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Latvia; Lithuania; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Sensitivity and Specificity; Taiwan

We describe a 30-year-old man in whom upper endoscopy revealed multiple gastric carcinoids. The peripheral blood gastrin level was 2400 ng/ml (normal range, <200 ng/ml). Mucosal biopsy of the gastric body and fundus showed no atrophy; typical type A chronic atrophic gastritis was thus unlikely. Neither abdominal computed tomography nor selective angiography showed any evidence of tumor in the pancreas or at its periphery. However, the possibility of microgastrinoma could not be ruled out. We performed radioguided surgery with a somatostatin analog, diethylenetriamine pentaacetic acid-D-Phe1-octreotide labeled with (111)In (Octreo Scan). The location of the carcinoids was confirmed. Gastrinoma was ruled out. Total gastrectomy was performed, and the gastrin level decreased to the normal range. Macroscopically, 20 carcinoid tumors, measuring 30 mm in maximum diameter, were confirmed. Microscopic examination showed large numbers of endocrine cell micronests. Hyperplasia of parietal cells was observed, suggesting early-stage type A chronic atrophic gastritis. The antrum contained increased numbers of gastrin-positive cells, which probably caused the preoperative hypergastrinemia.

Topics: Adult; Carcinoid Tumor; Gastrectomy; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Male; Parietal Cells, Gastric; Radiopharmaceuticals; Somatostatin; Stomach Neoplasms; Surgery, Computer-Assisted

Prevalence of atrophic gastritis in various population of Siberia with serological tests was studied. Representative samples of Novosibirsk adult population and also urban and rural population of Yakutia were examined. 348 persons at the age more than 45 years (180 males and 168 females) were studied. Concentration of pepsinogen I, gastrin 17 and antibodies to Helicobacter pilori in blood serum was estimated with immune-enzyme analysis ("Biohit GastroPanel", "Biohit", Finland). In addition, domestic test-systems were used for detection cytotoxic (expressing CagA-protein) strains H. pylori. Level of markers (pepsinogen, gastrin, antibodies to Helicobacter pilori and antibodies to CagA H. pilori) in observing populations had no difference between males and females, and also did not depend on age. Occurrence of atrophy in body of stomach in Novosibirsk population, urban and rural population of Yakutia was 10.1, 16.7 and 25.6% respectively, and in antral part--10.7, 25.6 and 8.9% respectively. Total atrophy was registered in 1% in all groups. Helicobacter infection was detected in 78-88% of population. Domestic immune-enzyme test-systems were comparable with data of histological examination and demonstrated greater sensitivity at H. pylori detection vs. foreign. High prevalence of atrophic gastritis in various groups of Siberia population was noticed, which must be was bounded with great level of H. pylori infection in population.

Topics: Aged; Antibodies, Bacterial; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter pylori; Humans; Immunoenzyme Techniques; Male; Middle Aged; Pepsinogen A; Population Surveillance; Prevalence; Rural Population; Siberia; Urban Population

Topics: Adult; Biopsy; Carcinoid Tumor; Chronic Disease; Female; Follow-Up Studies; Gastrectomy; Gastrins; Gastritis, Atrophic; Humans; Lymph Node Excision; Neoplasms, Multiple Primary; Radiography, Abdominal; Stomach; Stomach Neoplasms; Time Factors; Tomography, X-Ray Computed; Treatment Outcome

Cancer of stomach is currently regarded as the final result of a staged multifactor process during which the microenvironment affects cells and causes their changes. One of the main triggering factors is Hp infection. Adenocarcinoma of stomach develops via stages of gastritis, precancerous changes, and cancer. The possibility to prevent cancer ensues from the potential irreversibility of premalignant processes in gastric mucosa, in the first place its atrophy; hence, the importance of its early diagnosis. The state of the endoscopic service in this country is inadequate for mass screening of patients with symptoms of dyspepsia. "GastroPanel", a new serological test for the diagnosis of gastric pathology provides information about histological and functional characteristics of gastric mucosa in the antral and fundal regions of the stomach. The method determines serum gastrin-17, pepsinogen-1, and IgG expressed in response to Hp infection. Our results demonstrate high diagnostic efficiency of "GastroPanel" as a screening technique for atrophic gastritis and assessment of stomach cancer risk.

Topics: Adolescent; Adult; Aged; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Mass Screening; Middle Aged; Neoplasm Staging; Pepsinogen A; Peptide Fragments; Stomach Neoplasms; Young Adult

Topics: Carcinoid Tumor; Female; Gastrins; Gastritis, Atrophic; Humans; Kidney Failure, Chronic; Kidney Transplantation; Middle Aged; Remission Induction; Stomach; Stomach Neoplasms

To assess serologically diagnosed gastric body atrophy (GBA) by histology in a sample of the general population.. GBA is a precursor lesion in gastric cancer. Data on GBA in a primary health care community in the Netherlands have not been reported.. Thirty-four subjects of 997 consecutive adults from a Dutch family practice had serologic GBA, according to hypergastrinemia (>100 ng/L), hypopepsinogenemia A (<17 microg/L), and a low pepsinogen A/C ratio (<1.6). Two years later, 25 subjects of this group, agreed in serologic retesting and gastroscopy with biopsies for histologic assessment according to the Sydney system.. At serologic retesting, 20 of 25 subjects again fulfilled the serologic criteria of GBA. Histologic examination of the corpus biopsies showed advanced GBA in 18 subjects (75%) of 24 (1 subject had no corpus biopsies) and 17 of 19 (89%) subjects with repeated positive serology. After disclosure of serology results, reexamination of the biopsies revealed GBA also in the 2 patients with initially insufficient evidence of GBA, giving a concordance of 100% (19/19). One subject with normal serum gastrin at retesting had both antral and body atrophy giving a concordance between serologic and histologic GBA of 95% (19/20). No adenomatous polyps, tumors, or dysplastic alterations were found.. Identification by serology of asymptomatic patients with advanced GBA in primary care is adequately possible and useful in selecting for endoscopy.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Atrophy; Autoantibodies; Autoimmune Diseases; Biopsy; Chronic Disease; Cohort Studies; Diagnosis, Differential; Endoscopy; Female; Gastric Fundus; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Netherlands; Pepsinogens; Prevalence; Pyloric Antrum; Serologic Tests

Gastric endocrine tumors associated with autoimmune chronic atrophic gastritis (gastric carcinoid type I) are almost exclusively benign lesions with little risk of deep invasion of the gastric parietal wall. For this reason, the role of octreotide in the treatment of these neoplastic lesions is controversial. Nine patients with more than five type I gastric endocrine tumors each <1 cm in size, without invasion of the muscularis propria and with Ki-67 index lower than 3%, were treated with long-acting somatostatin analogs for 12 months. After 6 months and again after 12 months, all the patients underwent upper gastrointestinal (GI) endoscopy with multiple biopsies. The plasma chromogranin A (CgA) levels and the gastrin levels in the serum were also determined. In all patients, the gastric neoplastic lesions disappeared after 12 months of somatostatin analog therapy. We also observed a significant reduction of CgA and gastrin levels at 6 and at 12 months of therapy as compared with the baseline values. We demonstrate that somatostatin analog treatment provokes the pathological regression of type I gastric carcinoids. This therapeutic approach should be considered as a valid option in selected patients with multiple type I gastric endocrine tumors.

Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents, Hormonal; Carcinoid Tumor; Chromogranin A; Chronic Disease; Endosonography; Female; Gastrins; Gastritis, Atrophic; Humans; Immunoenzyme Techniques; Male; Middle Aged; Octreotide; Parietal Cells, Gastric; Stomach Neoplasms; Treatment Outcome

To analyse diagnostic potential of "serological gastrobiopsy" in patients with various gastroduodenal diseases.. A total of 244 patients with gastroduodenal pathology have been examined. The diagnoses made morphologically were compared with those made by the serological method. The diagnosis of duodenal ulcer, gastric ulcer, atrophic gastritis, nonatrophic gastritis was made in 155, 31, 43 and 15 patients, respectively. The type of chronic gastritis was diagnosed by the levels of gastrin-17, pepsinogen I, pepsinogen II and antibodies to Helicobacter pylori in blood serum. The diagnoses made serologically were compared with those made morphologically.. The highest accuracy of a serological diagnosis of mucosal atrophy of the antral stomach was observed in gastric ulcer (80.6%) and duodenal ulcer (71.6%) in high sensitivity and low specificity. The accuracy of the diagnosis of gastric body mucosa atrophy in atrophic gastritis was 60.5%, in gastric ulcer--51.6%, in duodenal ulcer 58.7% in high specificity and low sensitivity. Serological diagnosis of gastric atrophy was accurate in 71.7%. In weak morphological picture of gastric body atrophy false negative serological diagnosis is possible. No false positive results occurred in diagnosis of gastric body mucosal atrophy (specificity 100%). A negative correlation was found between the severity of gastric body atrophy and pepsinogen I serum level (r = -0.380), pepsinogen I to pepsinogen II in blood serum (r = -0.392). No differences were revealed in gastrin-17 levels in the serum in different atrophy severity in the antral mucosa.. "Serological gastrobiopsy"provides satisfactory accuracy of atrophic gastritis diagnosis in gastroduodenal diseases.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Biopsy; Diagnosis, Differential; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter pylori; Humans; Immunoenzyme Techniques; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Sensitivity and Specificity; Serologic Tests

GastroPanel (Biohit, Helsinki, Finland) is a serum test kit that measures Helicobacter pylori antibodies (HPABs) and pepsinogens I and II and gastrin 17, which reflect the degree of atrophic gastritis. We assessed whether GastroPanel can replace endoscopic biopsies in the diagnostics of H. pylori in children and whether the H. pylori-infected children show markers for atrophic gastritis. Eighty children (median age, 6.8 years; range, 0.6-18.7 years) underwent gastroscopy for H. pylori-related abdominal complaints (n = 40), surveillance after surgery for gastrointestinal tract malformations (n = 20), gastroesophageal reflux (GER) (n = 10), and miscellaneous diseases (n = 10). Gastric biopsies and a serum sample were obtained from all 80 children. HPAB levels of 38 and 15 IU were tested as cutoff values for H. pylori gastritis. The biopsies showed H. pylori-positive gastritis in 30 children, 9 had gastritis not associated with H. pylori, and 41 had normal biopsies. Atrophic gastritis was not found. The sensitivity and specificity of HPAB for H. pylori were 47% and 98% (cutoff, 38 IU), and 73% and 85% (cutoff, 15 IU), respectively. The assays of pepsinogens and gastrin did not improve sensitivity. None of the markers of pepsinogen (PG) I, PGII, and gastrin 17 (G17) indicated atrophic gastritis. GastroPanel is too insensitive for H. pylori screening and does not replace endoscopy. Markers indicative of atrophic gastritis were negative in all children with H. pylori gastritis.

Topics: Adolescent; Antibodies, Bacterial; Child; Child, Preschool; Endoscopy; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Infant; Pepsinogen A; Reagent Kits, Diagnostic

Helicobacter pylori infection induces chronic gastritis and lowers gastric juice ascorbic acid concentrations. We investigated how H. pylori eradication affected multiple variables that could prevent or delay development of new or occult gastric cancer in patients with early gastric cancer treated by endoscopic mucosal resection. Gastric juice pH, nitrite concentrations, and total vitamin C concentrations, serum concentrations of vitamin C and specific H. pylori antibody, and intensity of neutrophil infiltration in gastric mucosa were determined before and after successful H. pylori eradication. Successful eradication increased acid output and ascorbic acid secretion into gastric juice, accompanied by disappearance of polymorphonuclear infiltration from the surface epithelium and decreased gastric juice nitrite concentrations. Our data suggest that H. pylori eradication decreases the nitrosation rate as the ratio of vitamin C to nitrite increases. This decreases reactive oxygen species and nitric oxide, eliminating their damaging effect on DNA and reducing cell turnover.

Topics: Aged; Aged, 80 and over; Ascorbic Acid; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Nitrites; Stomach Neoplasms

Currently the screening and diagnosis of gastric cancer and atrophic gastritis are mainly made by endoscopy and biopsy. The aim of this study was to evaluate the use of serum tests: serum pepsinogen I (PGI pepsinogen I/II ratio (PGR), gastrin-17 (G-17) and H. pylori-immunoglobulin G (IgG) antibodies to screen atrophic gastritis and gastric cancer.. A total of 458 patients were recruited, and each underwent endoscopy with biopsies before the serum tests were performed. These patients were divided into five groups based on the endoscopic and histological findings: 92 patients in the atrophic gastritis group, 58 in the gastric ulcer group, 90 in the duodenal ulcer group, 141 in the gastric cancer group (40 early gastric cancer and 101 advanced gastric cancer) and 77 (including mild non-atrophic gastritis) served as a control group. Serum samples for PGI and II, G-17, and H. pylori-IgG antibodies estimation were analyzed by ELISA.. PGI and PGR values decreased significantly both in atrophic gastritis and gastric cancer groups (P<0.01). For the best discrimination of atrophic gastritis, the cut-off values of PGI and PGR were 82.3 microg/L and 6.05, respectively. The PGI, PGR and G-17 values were related significantly with the grades and/or sites of atrophic gastritis (P<0.01). Patients with atrophic corpus gastritis had low PGI and PGR values and high G-17 level, and patients with atrophic antral gastritis had low G-17 level. G-17 increased significantly in the gastric cancer group (P<0.01). PGI and PGR values were significantly lower in patients with advanced gastric cancer than in patients with early gastric cancer, while there was no difference in G-17 level between them. The positivity rate of H. pylori-IgG antibodies was 54.55% in the control group. The PGI level was higher in H. pylori positive patients than in H. pylori negative ones (P<0.001), while there was no difference in G-17 level between them. The positivity rates of H. pylori-IgG antibodies were over 85% in all other four groups.. Low serum PGI, PGR and G-17 values are biomarkers of atrophic antral gastritis. Atrophic be screened by serum PGI and PGR values. Gastric cancer can be screened on the basis of increased serum G-17 and remarkedly low serum PGI and PGR values. The H. pylori infection is related to the change of PG level.

Topics: Antibodies, Bacterial; Biomarkers; Biomarkers, Tumor; Endoscopy, Gastrointestinal; Female; Gastrins; Gastritis, Atrophic; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Pepsinogens; Stomach Neoplasms

Non-cardia gastric adenocarcinoma is positively associated with Helicobacter pylori infection and atrophic gastritis. The role of H pylori infection and atrophic gastritis in cardia cancer is unclear.. To compare cardia versus non-cardia cancer with respect to the premorbid state of the stomach.. Nested case-control study. To each of 129 non-cardia and 44 cardia cancers, three controls were matched. Serum collected a median of 11.9 years before the diagnosis of cancer was tested for anti-H pylori antibodies, pepsinogen I:II and gastrin.. Non-cardia cancer was positively associated with H pylori (OR 4.75, 95% CI 2.56 to 8.81) and gastric atrophy (pepsinogen I:II <2.5; OR 4.47, 95% CI 2.71 to 7.37). The diffuse and intestinal histological subtypes of non-cardia cancer were of similar proportions and both showed a positive association with H pylori and atrophy. Cardia cancer was negatively associated with H pylori (OR 0.27, 95% CI 0.12 to 0.59), but H pylori-positive cardia cancer showed an association with gastric atrophy (OR 3.33, 95% CI 1.06 to 10.5). The predominant histological subtype of cardia cancer was intestinal and was not associated with gastric atrophy compared with the diffuse subtype ((OR 0.72, 95% CI 0.19 to 2.79) vs (OR 3.46, 95% CI 0.32 to 37.5)). Cardia cancer in patients with atrophy had an intestinal: diffuse ratio (1:1) similar to non-cardia cancer (1.9:1), whereas cardia cancers in patients without atrophy were predominantly intestinal (7:1).. These findings indicate two aetiologies of cardia cancer, one associated with H pylori atrophic gastritis, resembling non-cardia cancer, and the other associated with non-atrophic gastric mucosa, resembling oesophageal adenocarcinoma. Serological markers of gastric atrophy may provide the key to determining gastric versus oesophageal origin of cardia cancer.

Topics: Adenocarcinoma; Adult; Biomarkers; Cardia; Case-Control Studies; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Precancerous Conditions; Risk Factors; Stomach Neoplasms

Ghrelin is mainly produced by the endocrine cells of the gastric oxyntic mucosa. For this reason we decided to investigate the modification of the circulating levels not only of total but also of acylated ghrelin in a series of patients with chronic atrophic gastritis.. Twenty-five patients with chronic atrophic gastritis and 25 healthy subjects were studied. In all 50 subjects gastrin and total and acylated ghrelin levels were evaluated. All patients underwent endoscopy with multiple biopsies, and the possibility of Helicobacter pylori infection was investigated.. Significantly higher acylated ghrelin levels (82.8 +/- 61.3 vs. 35.1 +/- 17.1 pmol/l), acylated/total ghrelin ratio (0.422 +/- 0.202 vs. 0.152 +/- 0.085) and gastrin levels (1071 +/- 816 vs. 66 +/- 22 ng/l) were observed in the 25 patients with chronic atrophy than in the healthy subjects. Otherwise, no significant relationships were found when total ghrelin was correlated with the presence of atrophy, or with gastrin levels. In the healthy subjects, but not in the patients, acylated and total ghrelin levels were significantly higher in female than in male patients.. The increase in acylated ghrelin levels and in the acylated/total ghrelin ratio in patients with atrophy of the body and fundus can be explained by hypothesizing an increase in the acylating process in the presence of gastric atrophy. It suggests that there may be a compensatory increase in plasma active ghrelin concentration in response to gastric atrophy, a condition which causes a loss of ghrelin-producing cells and an increase in gastric pH.

Topics: Acylation; Adult; Aged; Aged, 80 and over; Analysis of Variance; Biomarkers; Case-Control Studies; Chronic Disease; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Ghrelin; Humans; Linear Models; Male; Middle Aged; Sex Factors

Helicobacter pylori is a major risk factor for atrophic gastritis and gastric cancer. Various extragastric manifestations of H. pylori infection have also recently been suggested. However, the correlation between H. pylori and colorectal cancer (CRC) is controversial. The aim of this study was to examine the correlation between H. pylori, serum gastrin level, and atrophic gastritis with CRC.. Subjects were patients with CRC; controls were participants of a health check-up program that was conducted between October 1998 and March 2002 at four hospitals in Nagano Prefecture. For 121 newly diagnosed CRC cases, two controls matched by age (within 3 years), gender, and residence were randomly selected from the program participants. We conducted questionnaires and obtained blood samples from the cases and their controls. Consequently, the CRC cancer pairs consisted of 113 cases and 226 controls.. Neither H. pylori infection nor gastrin level nor atrophic gastritis showed any association with a risk for CRC. However, serologically determined atrophic gastritis demonstrated significant elevation in odds ratios (ORs) for rectal cancer (OR = 3.15, 95% confidence interval; 1.19-8.35).. Gastric conditions such as chronic H. pylori infection and atrophic gastritis are unlikely to increase the risk for CRC, although atrophic gastritis may increase the risk of rectal cancer.

Topics: Adult; Aged; Case-Control Studies; Colorectal Neoplasms; Confidence Intervals; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Humans; Japan; Middle Aged; Odds Ratio; Risk Factors; Surveys and Questionnaires

Autoimmune gastritis is frequently associated with autoimmune thyroiditis and other organ-specific autoimmune diseases, and may lead to atrophic body gastritis (ABG). We studied the diagnostic use of the measurement of serum ghrelin compared with other markers of gastric damage in predicting the presence of ABG in patients with autoimmune gastritis.. We studied 233 patients with autoimmune gastritis and 211 control subjects. All patients and control subjects were screened for circulating parietal cell antibodies (PCAs) and were tested for serum ghrelin, gastrin, pepsinogen I and II, and anti-Helicobacter pylori antibody levels. A total of 52 patients and 28 control subjects underwent a gastric endoscopy.. In PCA/positive patients, mean (+/-sd) serum ghrelin levels were significantly lower (238 +/- 107 pmol/liter), and mean (+/-sd) serum gastrin levels were significantly higher (81.2 +/- 128.3 ng/ml), with respect to PCA/negative patients (282 +/- 104 pmol/liter and 20.7 +/- 13.3 ng/ml, respectively; P < 0.0001). Serum ghrelin and gastrin levels were inversely correlated (P = 0.004). A total of 40 patients had ABG documented by the gastric biopsy (90% in PCA/positive patients and 10% in PCA/negative patients). The receiver operating characteristic curve analysis revealed that a cutoff value for serum ghrelin of 188 pmol/liter was associated with the highest sensitivity and specificity (97.3 and 100%, respectively) in detecting gastric atrophy and was superior to gastrin (P = 0.012), PCA (P = 0.002), and the pepsinogen I/II ratio (P = 0.016) measurements.. Our study demonstrates that ghrelin secretion is negatively affected by autoimmune gastritis, and its serum level represents the most sensitive and specific noninvasive marker for selecting patients at high risk for ABG.

Topics: Adult; Aged; Aged, 80 and over; Autoantibodies; Biomarkers; Biopsy; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Ghrelin; Humans; Male; Middle Aged; Parietal Cells, Gastric; Pepsinogen A; Predictive Value of Tests; ROC Curve; Thyroid Function Tests

Topics: Autoimmune Diseases; Diagnosis, Differential; Duodenal Neoplasms; Early Diagnosis; Gastrinoma; Gastrins; Gastritis, Atrophic; Humans; Multiple Endocrine Neoplasia Type 1; Neuroendocrine Tumors; Pancreatic Neoplasms; Zollinger-Ellison Syndrome

The authors describe a current approach to the laboratory diagnosis of chronic gastritis, by using the plates of serological tests: pepsinogen I (PG-I), gastrin 17, and antibodies to Helicobacter pylori (HP). These tests and a questionnaire were used to examine 168 persons aged 45-70 years, who were a random population sample. Almost a fourth of the adult population was observed to have pronounced gastric mucosal atrophic changes, which might be associated with the high prevalence of HP infection. The concentration of PG-I is high in the persons infected with HP, its cytotoxic strains in particular, its elevated level servers as a valid marker of peptic ulcer disease and gastroesophageal reflux.

Topics: Aged; Aged, 80 and over; Antibodies, Bacterial; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Sensitivity and Specificity; Serologic Tests

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

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

Atrophic corpus gastritis predisposes to vitamin B12 deficiency and gastric cancer. Little is known about the seroprevalence of atrophic corpus gastritis in the general population of Western Europe.. To investigate the seroprevalence of atrophic corpus gastritis in a West-European primary care community in relation to Helicobacter pylori infection and autoimmunity.. Nine hundred and ninety-seven consecutive persons attending one general practice were asked to participate in the study by completing a questionnaire and donating fasting blood. Gastrin, pepsinogen A and C, and antibodies to H. pylori and parietal cells were measured by well-validated immunological methods. Criteria for serological atrophic corpus gastritis were pepsinogen A < 17 microg/l, pepsinogen A/C ratio <1.6, and gastrin >100 ng/l.. Thirty-four participants (3.4%) fulfilled the serological criteria of atrophic corpus gastritis. Twenty-one of them (62%) and 17 of 34 (50%) age-matched and sex-matched nested controls were H. pylori positive [NS; odds ratio, 1.62 (0.62-4.24)], while 15 of them (44%) and one of 34 controls had antibodies to parietal cells [P < 0.005; odds ratio, 24.0 (3.00-201)].. The seroprevalence of atrophic corpus gastritis in this primary care community is 3.4%. When compared with controls, the approximate relative risk of having atrophic corpus gastritis was significantly higher (P < 0.025) for antibodies to parietal cells (24.0) than to H. pylori (1.62). In view of the decreasing risk of H. pylori infection in the western world, it is likely that the impact of H. pylori on the development of atrophic corpus gastritis will further diminish.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Autoimmunity; Case-Control Studies; Female; Gastrins; Gastritis, Atrophic; Helicobacter pylori; Humans; Male; Middle Aged; Netherlands; Parietal Cells, Gastric; Pepsinogens; Primary Health Care; Seroepidemiologic Studies

To study the pathologic change and molecular regulation in cell proliferation and apoptosis of gastric mucosa in rats with chronic atrophic gastritis (CAG), and evaluate the possible mechanisms.. Rats were administered with 60% alcohol or 2% salicylate sodium, 20 mmol/L deoxycholate sodium and 0.1% ammonia water to establish chronic atrophic gastritis (CAG) models. The gastric specimens were prepared for microscopic view with hematoxylin and eosin (H-E) and alcian blue (A-B) stain. The number of infiltrated inflammatory cells, the thickness of the mucosa gland layer (microm) and the number of gastric glands were calculated. The damage of barrier in mucosa with erosion or ulceration, and the thickness of mucin were examined by scanned electron microscope (SEM). The levels of PGE(2), EGF (epiderminal growth factor) and gastrin in the serum were measured with radioimmunoassay or ELISA method. The immunohistochemistry method was used to observe the number of G cells, the expression of protein of EGFR (EGF receptor), C-erbB-2, p53, p16 and bcl-2 in gastric tissue.. Under SEM observation, the gastric mucosa was diffused erosion or ulceration and the thickness of mucin was decreased. Compared with normal rats, the grade of inflammatory cell infiltration in CAG rats was elevated, whereas the thickness and number of gastric gland were significantly lower (P<0.05). Compared with normal level of (0.61+/-0.28) microg/L, EGF in CAG (2.24+/-0.83) microg/L was significantly higher (P<0.05). The levels of PGE(2) and gastrin in serum were significantly lower in CAG rats than that in normal rats (P<0.05). Immunohistochemistry detection showed that the number of G cell in antrum was lower in CAG group (P<0.05). Immuno-stain showed EGFR protein expression in the basal and bilateral membrane, and the cytoplasma in atrophic gastric gland, while negative expression was observed in normal gastric epithelial cells. Positive staining of p53 and p16 protein was localized in the nucleus of epithelial cells. The former was higher positively expressed in atrophic gland, while the later was higher positively stained in normal gastric tissue. bcl-2 protein was positively stained in the cytoplasma in atrophic gastric gland, while very weakly stained in normal gastric tissue.. The pathological findings in gastric gland accorded with the Houston diagnostic criteria of antrum-predominant CAG. CAG in rats was related with the damage of barrier in gastric mucosa and the misbalance of cell proliferation and apoptosis. There was high protein expression of oncogene, while inhibitor of suppressor gene in CAG rats indicated high trend of carcinogenesis.

Topics: Animals; Chronic Disease; Epidermal Growth Factor; ErbB Receptors; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Immunohistochemistry; Male; Proto-Oncogene Proteins c-bcl-2; Rats; Rats, Sprague-Dawley; Tumor Suppressor Protein p53

Atrophic gastritis has been shown to involve either the oxyntic gland area, resulting in hypergastrinemia and hypopepsinogenemia I, the antral gland area, causing hypogastrinemia without change in serum pepsinogen I (diffuse antral gastritis; DAG), or the entire gastric mucosa (multifocal atrophic gastritis; MAG), resulting in both hypogastrinemia and hypopepsinogenemia I; and rare atrophic gastritis limited to the oxyntic gland area, with antibodies against oxyntic cells and/or intrinsic factor (autoimmune metaplastic atrophic gastritis; AMAG). This study was performed on 126 patients with various forms of gastritis and on 126 age- and gender-matched controls, who were subjected to endoscopy with biopsy, H. pylori testing (13C-UBT, serology), assays for serum gastrin and pepsinogen I, and testing for basal and pentagastrin-induced gastric acid secretion. The following groups of patients were examined: group I (N = 22), with AMAG; group II (N = 53), with DAG; group III (N = 51), with MAG; and group IV (N = 126), age- and gender-matched controls without gastritis. The following changes were found. In group I very high serum gastrin and very low pepsinogen I were observed, and all patients were achlorhydric and H. pylori negative. In group II, with low serum gastrin and normal pepsinogenemia and gastric chlorhydria, all patients were H. pylori positive. In group III, with lower serum gastrin and lower pepsinogen I levels and reduced chlorhydria, all patients were also H. pylori positive. And all group IV controls, with normal serum gastrin and pepsinogen I and normal gastric acid secretion without antral or fundic gastritis, were H. pylori negative. We conclude that measurements of serum gastrin and pepsinogen I and gastric acid secretion as well as testing for H. pylori infection may be useful in noninvasive diagnosis of various types of atrophic gastritis and in identification of patients with premalignant gastritis and a high risk of gastric cancerogenesis.

Topics: Adult; Aged; Aged, 80 and over; Biomarkers; Biopsy, Needle; Cohort Studies; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter pylori; Humans; Immunohistochemistry; Inflammation Mediators; Male; Middle Aged; Pepsinogen A; Probability; Prognosis; Retrospective Studies; Risk Assessment; Sensitivity and Specificity; Severity of Illness Index; Statistics, Nonparametric

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

Helicobacter pylori-associated atrophic gastritis is known to be a significant risk factor for gastric cancer. Among the well-known parameters of atrophic gastritis are the levels of serum gastrin-17 (G-17) and pepsinogen I (PG1), which are biomarkers of gastric antral and corpus mucosal activity, respectively. The aim of study was to compare the production of G-17 and PG1 in patients with or without stomach mucosal atrophy and to investigate the utility of serum PG1 and/or G-17 concentrations for the objective evaluation of atrophic gastritis.. A total of 178 dyspeptic Helicobacter pylori-positive patients underwent diagnostic upper gastrointestinal endoscopy with biopsy. The degree of histologic gastric mucosal atrophy was compared with the fasting levels of PG1, and to the postprandial levels of G-17 detected by enzyme immunoassay.. A decrease in serum G-17 levels along with worsening of the antral atrophy was observed; the serum levels of PG1 were reduced during progression of the corpus atrophy. In the multifocal atrophic gastritis, values for PG1 and G-17 serum concentrations were significantly lower than the respective cut-off values. Statistical analysis revealed statistically significant differences between the serum levels of PG1 and G-17 measured at different stages of stomach mucosal atrophy.. A strong reverse correlation was found between histologic/ endoscopic antral atrophy and serum G-17 levels, and between corpus atrophy and serum PG1 levels.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Biomarkers; Biopsy; Endoscopy, Digestive System; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Middle Aged; Pepsinogen A; Pyloric Antrum; Sensitivity and Specificity; Severity of Illness Index

This study, carried out on 51 patients with multifocal atrophic gastritis (MAG) and 92 age and sex-matched dyspeptic controls, was designed to examine both exocrine (gastric acid) and endocrine (gastrin) gastric secretion before and after therapeutic intervention including Helicobacter pylori eradication and vitamin C treatment.. Fasting and gastrin-releasing peptide-induced gastric acid secretion, serum levels of gastrin and proinflammatory (IL-1beta, IL-8, TNF-alpha) as well as gastric mucosal gene expression of ornithine decarboxylase (ODC), cyclooxygenase 2 (COX-2) and growth factors (epidermal growth factor and transforming growth factor alpha) were determined before and after the eradication of Helicobacter pylori and therapy with large doses (1 g/d) of vitamin C for 3 months.. The H. pylori eradication, assessed by C-urea breath test, and vitamin C therapy failed to reverse the histological atrophy of the gastric mucosa but improved significantly the functional status of the atrophied mucosa, especially its exocrine and endocrine secretory activities, attenuated the expression of premalignant markers such as ODC and COX-2, raised the production of growth factors and diminished the release of proinflammatory cytokines.. These results indicate that MAG may be considered as an environmental disease of the gastric mucosa, whose functional status can be improved by the eradication of H. pylori combined with antioxidant therapy with large doses of vitamin C.

Topics: Adult; Aged; Anti-Bacterial Agents; Antioxidants; Ascorbic Acid; Case-Control Studies; Cyclooxygenase 2; Cytokines; Epidermal Growth Factor; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Ornithine Decarboxylase; RNA, Messenger; Transforming Growth Factor alpha

To compare the prevalence of chronic atrophic gastritis (CAG) in Japan, China, Tanzania, and the Dominican Republic and to assess the usefulness of Helicobacter pylori infection and serum gastrin level as markers of CAG.. The subjects were volunteers from local communities in Japan (n=859), China (n=1741), Tanzania (n=573), and the Dominican Republic (n=1215). Each individual underwent a health checkup and blood sampling for measurement of serum pepsinogen I and II, pepsinogen I /II ratio, serum gastrin, and H. pylori antibodies, and responded to a questionnaire on upper digestive tract diseases.. The prevalences of H. pylori infection (23.5-96.1%), CAG (5.6-60.4%), and serum gastrin (62.0-136.5 pg/ml) varied by age, sex, and country. Serum gastrin level for men differed in each country according to age. In Tanzanian men, the median gastrin level (101.0 pg/ml) was the highest in the 40 to 49 years age group (p < 0.01) while there was no significant difference among different age groups in Tanzanian women. Serum gastrin level in subjects > or = 70 years was higher than in other age groups in both sexes in the Dominican Republic (males, 92.5, females, 136.5 pg/ml). The prevalence of H. pylori infection increased (p < 0.01) with advancing age in Japan (only for women) and the Dominican Republic but was high in all age groups of both sexes in China and Tanzania. The prevalence of CAG increased (p < 0.01) with age in both sexes in Japan, China (women only), and the Dominican Republic, but not in Tanzania. The odds ratio of CAG in H. pylori infected subjects was 5.3 times that in H. pylori-negative subjects. The odds ratio of CAG increased by 0.6%/1 pg/ml increase in serum gastrin.. Our results indicated that H. pylori infection, serum gastrin, and advancing age are good markers of CAG and that the prevalence of CAG is the highest in Japan.

Topics: Adult; Age Distribution; Aged; Aged, 80 and over; Asia, Eastern; Dominican Republic; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Prevalence

Histology is the gold standard for diagnosis of atrophy but is hampered by observer variation. A reliable method to overcome this issue is morphometric analysis of gastric mucosa. Serum pepsinogens and gastrin have been proposed in the diagnostic work-up of gastric atrophy although diagnostic accuracy of these tests is considered unsatisfactory.. To evaluate the diagnostic accuracy of gastric serum profile in relation both to morphological and morphometric diagnosis of gastric atrophy.. Ninety-four dyspeptic out-patients underwent upper endoscopy and evaluation of serum levels of PGI, PGII and 17-gastrin. Diagnostic accuracy of gastric serum profile was tested by receiver operating characteristic curves and by evaluation of sensitivity and specificity in relation to both histology and morphometric analyses.. As far as concern to histological evaluation, only PGI/PGII ratio showed an acceptable diagnostic accuracy in discrimination of gastric atrophy, while, when morphometric analysis was considered as reference, both serum PGI level and PGI/PGII ratio showed an excellent performance. However, both PGI and PGI/PGII ratio showed low sensitivity and high specificity.. Serological gastric profile corresponds better with the morphometric diagnosis of atrophy, even if, because of the low sensitivity, today this could only be used as screening test of chronic atrophic gastritis.

Topics: Adult; Aged; Chronic Disease; Dyspepsia; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Pepsinogens; ROC Curve; Sensitivity and Specificity

To evaluate serum pepsinogen I (PG I) and gastrin-17 (G-17) levels in patients with Helicobacter pylori (H. pylori)-associated chronic atrophic gastritis, with reference to endoscopical Kimura-Takemoto's staging, chromoendoscopical and histological features.. 267 dyspeptic H. pylori-infected patients were examined by chromoendoscopy with biopsy sampling according to the Sydney System and according to Kimura-Takemoto's scale. Simultaneous assessment of serum pepsinogen I (PG I) and gastrin-17 (G-17) levels by enzyme immunoassay was performed. The serologic and morphologic results were compared with correlation analysis.. There was strong reverse correlation between the stomach mucosal atrophy (antral part or corpus) and the proper serologic markers (respectively, G-17 or PG I) in H. pylori-associated chronic gastritis when gastric biopsies taken according to the Sydney System were assessed. The use of Kimura-Takemoto's scale has revealed the decrease of serum PG I levels only at 0-2 and 0-3 grades of the corpus mucosa atrophy. Probably, these results reflects the development of functional failure of the stomach corpus mucosa at late stages of atrophy when its compensatory capacity becomes insufficient. There were not any advantages in sampling biopsies for the detecting of intestinal metaplasia (IM) by the Sydney System, or by Kimura-Takemoto's scheme. The obvious concordance between histologically proven extent of IM and the number of IM foci detected by chromoendoscopy has been revealed.. The biopsy sampling for the diagnosis of precancerous changes of the stomach mucosa after non-invasive screening of atrophic gastritis (e.g., by means of EIA) should be based preferably on the visual signs acquired via chromoendoscopy than through routine endoscopy, independently of the scheme of examination of stomach mucosa, either according to the Sydney System, or to the Kimura-Takemoto's scale.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Atrophy; Endoscopy; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Male; Middle Aged; Pepsinogen A

Topics: Aged; Diagnosis, Differential; Female; Gastrins; Gastritis, Atrophic; Gene Expression Regulation, Enzymologic; Helicobacter Infections; Helicobacter pylori; Humans; Middle Aged; Ornithine Decarboxylase; Prostaglandin-Endoperoxide Synthases; Stomach Neoplasms

The mechanism of progression from gastric endocrine cell hyperplasias (ECHs) to carcinoid tumor (GCT) is still unknown. In these lesions, the distribution of metaplastic Paneth, gastrin and pancreatic acinar cells developing due to consequences of corporal mucosal atrophy has not been investigated in detail. In this study, 33 gastric endoscopic biopsies with endocrine cell lesions were examined. In all cases except 6 with solitary GCT, complete-type (small intestine) intestinal metaplasia (IM) with Paneth cells was observed. The density of lysozyme-positive Paneth cells in IMs in cases with GCTs was less than those in ECH alone. The density of gastrin-positive cells in IMs and average number of micronodules of ECHs were similar. Pancreatic acinar metaplasia (PAM) was observed in 6 cases of GCTs with ECH. The size of GCTs with ECH was smaller than those without ECH. By image analysis, the percentage of Ki67 (MIB-1, proliferation marker) expressing cells of GCTs with ECH was 5.1+/-0.6%, and GCT without ECH 7.8+/-1%. Our results indicate that few Paneth cells and many PAMs in atrophic corporal mucosa are seen more frequently in cases of GCTs with ECH, compared to those in ECH alone. Gastrin-positive cells in the corporal IM may stimulate enterochromaffin-like (ECL) cells, which may induce hyperplasia, dysplasia or neoplasia by augmenting the effects of hypergastrinemia through a paracrine mechanism on local gastrin-sensitive cells.

Topics: Enteroendocrine Cells; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Ki-67 Antigen; Paneth Cells; Tumor Suppressor Protein p53

A decrease in pepsinogen and gastrin levels 1-3 months after Helicobacter pylori eradication is well known. However, few data are available on the long-term progression of these decreases beyond 1 year after eradication, and there has been no investigation into whether pepsinogen and gastrin levels return to normal levels as defined by data from H. pylori-negative patients with dyspepsia.. We studied the effect of H. pylori eradication on pepsinogen and gastrin levels for more than 1 year, and compared levels to those in H. pylori-negative patients with dyspepsia. We also investigated the effect of H. pylori eradication on the course of atrophic corpus gastritis as reflected by histology, and on PGI levels and PG I/II ratio.. We enrolled 172 H. pylori-positive patients with dyspepsia who had undergone successful eradication therapy of more than 1 year's duration and 101 non-treated H. pylori-negative patients with dyspepsia. H. pylori status was assessed at entry and at each endoscopy after eradication by culture, histological results, the rapid urease test and the urea breath test. In both groups, patients were evaluated for fasting serum pepsinogen I and II and gastrin using a radioimmunoassay technique, and underwent detailed histological assessment according to the updated Sydney System.. In the H. pylori-negative patients, mean serum pepsinogen I and II, I/II ratio and gastrin levels were 52.6 +/- 20.8 ng/mL, 9.2 +/- 4.2 ng/mL, 6.0 +/- 1.7 and 53.5 +/- 29.2 pg/mL, respectively. In H. pylori-positive patients with long-term eradication, pepsinogen I and II, I/II ratio and gastrin levels were 81.3 +/- 46.6 ng/mL, 25.9 +/- 17.1 ng/mL, 3.4 +/- 1.3 and 131.9 +/- 130.8 pg/mL, respectively, before treatment. At 1-3 months after eradication, serum pepsinogen I and II levels in the H. pylori-positive patients decreased to levels similar to those in the negative patients, whereas pepsinogen I/II ratio and gastrin levels remained lower and higher, respectively, than in the negative patients. Serum pepsinogen I/II ratio and gastrin levels then became similar between the groups at 12-15 months after eradication. In histological findings, inflammation and neutrophil activity decreased by 1-3 months, and atrophy in the corpus and metaplasia in the antrum decreased by 12-15 months.. The results suggest that atrophic corpus gastritis and superficial gastritis are reversible, as indicated by both histological and serological findings in a long-term follow-up study.

Topics: Dyspepsia; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogens

To study regulative action of mica monomer granule preparation on gastrin (GAS), somatostatin (SS) and G cells as well as D cells of gastric mucosa in experimental chronic atrophic gastritis (CAG) rat.. CAG rats were treated with mica monomer granule preparation with three different dosages--high, moderate and low level respectively. Changes of blood serum GAS, blood plasma SS and G cells as well as D cells of gastric mucosa in CAG rats were observed and detected with ELISA method, RIA method and immunocytochemistry method.. Mica monomer granule of three different dosages could increase the quantity of G cells as well as D cells of gastric mucosa and the concentration of blood serum GAS and decrease the content of blood plasma SS in CAG rat at different level respectively. It was more effective in high and moderate dosage groups.. Mica has the pharmacological action of protecting gastric mucosa, promoting the palingenesis of gastric gland and enhancing blood stream of gastric mucosa consequently to abate the inflammation reaction of gastric mucosa. Its effective mechanism is associated with the neuroendocrine regulative mechanism of promoting the secretion of gastric acid and gastric pepsin by increasing the amount of G cells as well as D cells and the concentration of blood serum GAS, and reducing inhibiting action on GAS secretion and enhancing the secretion of GAS by decreasing the content of SS.

Topics: Aluminum Silicates; Animals; Dose-Response Relationship, Drug; Gastric Mucosa; Gastrin-Secreting Cells; Gastrins; Gastritis, Atrophic; Materia Medica; Rats; Rats, Sprague-Dawley; Somatostatin; Somatostatin-Secreting Cells

Elevated serum gastrin and a low pepsinogen A/C ratio are well-recognized markers for atrophic body gastritis (ABG). We have shown that the presence of body atrophy is also associated with elevated serum pro-inflammatory cytokines. This study tested the hypothesis that serum cytokines provide additional information to gastrin and pepsinogens in screening for ABG.. Two hundred and twenty-six consecutive patients were investigated on referral for upper gastrointestinal endoscopy: 150 were patients with gastro-oesophageal reflux disease, receiving acid inhibitory medication either with proton pump inhibitors (n = 113) or with histamine2-receptor antagonists (n = 37), and 76 were nontreated controls, who had normal endoscopic findings. Gastric mucosal biopsies were sampled for histological examination (Sydney classification). Serum samples were analyzed for gastrin, chromogranin A (CgA), and pepsinogens A and C by RIA, and for the interleukins (IL)-1beta, IL-6, and IL-8 by ELISA.. Subjects with ABG had significantly higher serum gastrin (P < 0.01) and serum CgA (P < 0.01) levels and significantly lower pepsinogen A/C ratios (P < 0.001) than those without ABG. Additionally, serum IL-1beta, IL-6 and, especially, IL-8 levels were significantly higher in the subjects with than in those without ABG (P < 0.0001, for all cytokines). To optimize the detection of body atrophy we defined the ABG index: the ratio between the simultaneously measured IL-8 and pepsinogen A/C. The area under the ROC curve for the ABG index was significantly greater than that for serum gastrin and for serum pepsinogen A/C alone (0.91 +/- 0.029 vs. 0.72 +/- 0.042, and vs. 0.83 +/- 0.031, P = 0.018 and P = 0.049). Using the ABG index at a cut-off value of 1.8 pg mL-1, 91% of the cases were classified correctly.. The ratio between serum IL-8 and pepsinogen A/C accurately predicts the presence of ABG. We therefore propose the ABG index as a noninvasive screening test for ABG in population-based studies.

Topics: Adult; Aged; Biomarkers; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-1; Interleukin-6; Interleukin-8; Male; Mass Screening; Middle Aged; Pepsinogen A; Pepsinogen C; Pepsinogens; ROC Curve; Sensitivity and Specificity

H. pylori (Hp) -induced atrophic gastritis is a well-known risk factor for the development of gastric cancer. Whether Hp eradication can prevent or retard the progress of atrophy and metaplasia has been the topic of numerous studies but the subject remains controversial. Recently, the increased expression of ornithine decarboxylase (ODC), gastrin and cyclooxygenase (COX)-2 has been shown to be increased in premalignant lesions in gastric mucosa and to play an essential role in the malignant transformation. The aim of the study is to assess the effect of eradication therapy on atrophic gastritis and analyze the gene expression for ODC, COX-2 and gastrin in gastric mucosa after succesful eradication in patients with atrophic gastritis. Twenty patients with chronic atrophic gastritis including both corpus and antrum of the stomach were included in this study. Four antral mucosal biopsy specimens were obtained from antrum and four from corpus. The histopathologic evaluation of gastritis was based on Sydney classification of gastritis. All patients were Hp positive based on the [13C] urea breath test (UBT) and the presence of anti-Hp IgG and anti-CagA-antibodies detected by ELISA. The patients were then eradicated with triple therapy consiting of omeprazol (2 x 20 mg), amoxycillin (2 x 1 g) and clarithromycin (2 x 500 mg) for seven days and vitamin C 1 g/day for three months. In gastric mucosal samples obtained from the antrum and corpus before and after eradication, the mRNA expression for ODC, COX-2, and gastrin was assessed by reverse-transcription polymerase chain reaction (RT-PCR). In all patients the gastric secretory analysis was performed by measuring gastric acid output and serum gastrin levels. After triple therapy the successful eradication assessed by UBT was observed in 95% of patients. In 45% of patients the infection with CagA-positive Hp strain was observed. Three months after eradication a significant reduction in the gastric activity (neutrophilic infiltrate) and severity (mononuclear infiltrate) of gastritis was observed. The atrophy score improved in both antrum and corpus after eradication. The expression of COX-2 and ODC was significantly up-regulated in the gastric mucosa of patients with atrophic gastritis and significantly reduced after eradication therapy. In all successfully eradicated patients with atrophic gastritis a significant increase in gastric acid secretion and decrease in serum gastrin were observed. We conclude that: (1) H

Topics: Amoxicillin; Anti-Ulcer Agents; Clarithromycin; Cyclooxygenase 2; Drug Therapy, Combination; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gene Expression; Helicobacter Infections; Helicobacter pylori; Humans; Isoenzymes; Male; Membrane Proteins; Middle Aged; Omeprazole; Ornithine Decarboxylase; Peroxidases; Prostaglandin-Endoperoxide Synthases; RNA, Messenger

Gastric carcinoid is a rare tumour that is associated with chronic atrophic gastritis in the majority of cases. It usually occurs in the 6th or 7th decade of life and is rarely diagnosed in patients under 30 years of age.. We describe a case of multiple gastric carcinoids in a 23-year-old woman with systemic lupus erythematosus and atrophic autoimmune gastritis--an association that has not been reported previously.. The combination of atrophic autoimmune gastritis and gastric carcinoid with other autoimmune disorders has rarely been reported in the English medical literature.. The fact that it mostly concerns (relatively) young patients may suggest a potential causative relation between those autoimmune disorders and the early development of atrophic gastritis with hypergastrinaemia, which subsequently leads to the occurrence of gastric carcinoid tumours at a young age.

Topics: Adult; Antiphospholipid Syndrome; Carcinoid Tumor; Female; Gastrectomy; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Lupus Erythematosus, Systemic; Stomach; Stomach Neoplasms

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

Long term Helicobacter pylori infection leads to atrophic gastritis but the relation between H pylori infection and autoimmune related atrophic gastritis (AIG) remains unclear. We studied the effects of H pylori infection on the pathophysiology of AIG in mice.. BALB/c nu/nu mice (n=40) with or without H pylori infection received splenocytes from neonatally thymectomised mice to induce AIG. Half of the mice were orally infected with H pylori prior to AIG induction. Histological findings, and local and systemic immune responses were serially evaluated.. Two and six months after transfer, parietal cells in uninfected mice were depleted while those in infected mice were well preserved. The degree of gland atrophy (p<0.01), hyperplasia (p<0.01), gastric pH (p<0.05), and serum gastrin levels of infected mice were significantly lower than those of uninfected mice. Serum antiparietal cell antibody levels gradually decreased in infected mice, and were significantly lower than those of uninfected mice at six months (p<0.05). Real time polymerase chain reaction studies revealed significantly higher interleukin 4 (p<0.05) and transforming growth factor beta (p<0.05) gene expression in the gastric mucosa in infected mice than in uninfected mice at both two and six months after AIG induction.. H pylori infection inhibited the development of AIG in mice. Th2-type immune responses and transforming growth factor beta in the gastric microenvironment might be involved in the inhibitory effects of H pylori infection on the development of AIG, in which Th1-type responses have an important role.

Topics: Animals; Antibodies; Autoimmune Diseases; Cytokines; Enzyme-Linked Immunosorbent Assay; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Hydrogen-Ion Concentration; Immunohistochemistry; Mice; Mice, Inbred BALB C; Mice, Nude; Parietal Cells, Gastric; Polymerase Chain Reaction; RNA, Messenger; Up-Regulation

The most common types of benign gastric polyps are fundic gland polyps, hyperplastic polyps, and adenomas. The aim of this study was to determine on which morphological and functional background benign gastric polyps develop. The study includes 85 consecutive patients with gastric polyps and sex- and age-matched controls without polyps selected at random from a general population sample. The type of polyp was hyperplastic in 52 (61%), fundic gland in 18 (21%), adenoma in 10 (12%), carcinoid in 2 (2%), hamartoma in 2 (2%), and inflammatory fibroid in 1 (1%) of the cases. Routine biopsies from the gastric corpus and antrum were examined for presence of gastritis and H. pylori. Blood samples were analyzed for H. pylori antibodies, H+,K+-ATPase antibodies, gastrin, and pepsinogen I. Patients with hyperplastic polyps had increased P-gastrin concentrations and S-H+,K+-ATPase antibody titers and decreased S-pepsinogen I concentrations with a high prevalence of atrophic corpus gastritis or pangastritis. A similar pattern was observed among patients with adenomas, whereas patients with fundic gland polyps had normal serology and a lower prevalence of gastritis and H. pylori infection than controls. In conclusion, hyperplastic polyps and adenomas are generally associated with atrophic gastritis. Patients with fundic gland polyps seem to have a sounder mucosa than controls. Whereas the risk of malignant gastric neoplasia is increased in patients with hyperplastic polyps or adenomas, this does not seem to be the case in patients with fundic gland polyps.

Topics: Adenomatous Polyps; Adult; Aged; Aged, 80 and over; Antibodies; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Humans; Male; Middle Aged; Pepsinogen A; Polyps; Prospective Studies; Sodium-Potassium-Exchanging ATPase; Stomach Neoplasms

Topics: Cell Division; Chronic Disease; Enterochromaffin Cells; Gastric Mucosa; Gastrinoma; Gastrins; Gastritis, Atrophic; Histamine; Humans; Hyperplasia; Pancreatic Neoplasms; Zollinger-Ellison Syndrome

Until recently, the association of primary hyperparathyroidism and gastric carcinoid, with or without hypergastrinaemia, had been considered an incomplete form of multiple endocrine neoplasia type 1. This is because it seemed unlikely that the rare joint appearance of these diseases could occur only by chance. It is now possible to evaluate the pathogenetic involvement of the multiple endocrine neoplasia type 1 gene in many, apparently sporadic, clinical conditions. This is a case report of a female mimicking multiple endocrine neoplasia type 1 due to the presence of hyperparathyroidism, gastric carcinoid, and hypergastrinaemia. However, involvement of the MEN-1 gene (exons 2-10) was not detected, whereas hypergastrinaemia was attributed to a chronic atrophic gastritis.

Topics: Aged; Carcinoid Tumor; Diagnosis, Differential; Female; Gastrins; Gastritis, Atrophic; Gene Expression; Humans; Hyperparathyroidism; Multiple Endocrine Neoplasia Type 1; Stomach Neoplasms

Relatives of patients with gastric cancer are at increased risk of developing this disease, especially if they are infected by Helicobacter pylori. Moreover, H. pylori-related atrophic gastritis and hypochlorhydria are well-documented risk factors for noncardia gastric cancer. Serum pepsinogen I (sPGI) and II (sPGII) levels are low in this condition. The aim of our study was to assess by means of a 'Gastropanel' blood test, including sPGI, sPGII, gastrin-17 (G-17) and antibodies anti-H. pylori (IgG-Hp). both functional and morphological features of gastric mucosa in Hp + ve subjects with a family history of gastric cancer.. Twenty-five Hp + ve subjects consecutively referred to our department for gastrointestinal complaints, selected as first-degree relatives of patients suffering from gastric cancer, were enrolled in the study and then matched for sex and age with 25 dyspeptic and Hp + ve subjects with no family history of gastric neoplasia. Blood samples were taken for determination of gastropanel in all patients; in addition, antibodies against CagA were analysed.. No statistically significant differences were detected between the two groups as regards alcohol consumption, coffee intake and smoking habits. Mean sPGI levels in Group A (83.4 +/- 58.4 microg/L) were significantly lower than those in Group B (sPGI 159.5 +/- 80.6 microg/L; P < 0.0001) as well as sPGII (12.5 microg/L = 6.24 versus 20.6 +/- 58 microg/L; P < 0.006). No statistical difference was found between the two groups in relation to G-17 levels, IgG-Hp titres and antibodies against CagA.. First-degree relatives of patients with noncardia gastric cancer affected by H. pylori infection present lower sPGI and sPGII levels, possibly due to the increased frequency of atrophic lesions in these patients.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Antigens, Bacterial; Bacterial Proteins; Biomarkers; Dyspepsia; Family Health; Female; Gastrins; Gastritis, Atrophic; Genetic Predisposition to Disease; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Stomach Neoplasms

Helicobacter pylori infection is often diagnosed with non-endoscopic methods, such as serology or breath or antigen stool tests. These tests provide information on the presence or absence of the H. pylori gastritis only. We investigated whether atrophic gastritis can be diagnosed and typed non-endoscopically if the serum levels of pepsinogen I (S-PGI) and gastrin-17 (S-G-17) are assayed in connection with H. pylori testing.. The present investigation is an observational case-control study comprising 100 selected dyspeptic outpatients with (cases) or without (controls) advanced (moderate or severe) atrophic gastritis. Before the blood tests, all patients underwent a diagnostic gastroscopy with multiple biopsies. The series of cases includes 56 patients. Eight had an advanced antrum limited atrophic gastritis, 13 had resected antrum (in two of whom the corpus mucosa in the stump was atrophic), and 30 had corpus-limited atrophic gastritis. Four patients had an advanced atrophic gastritis in both the antrum and corpus (multifocal atrophic gastritis), and the whole stomach was removed in one patient. Twenty of the 44 controls had a non-atrophic H. pylori gastritis. Both the antrum and corpus were normal and healthy in 24 patients. The S-PGI and S-G-17 were determined with EIA methods using monoclonal antibodies to PGI and amidated G-17. Postprandial S-G-17 (S-G-17prand) was measured 20 min after a protein-rich drink. The H. pylori antibodies were assayed with a polyclonal EIA method.. A low S-PGI (<25 microg/l; an empirical cut-off with best discrimination) was found in 31 of 37 patients (84%) with and in 3 of 63 patients (5%) without corpus atrophy in the biopsy specimens. A low S-G-17prand (<5 pmol/l) was found in all 8 patients with H. pylori-associated antral atrophy and in 11 of 14 patients (79%) with resected antrum but in 3 of 20 control patients (15%) with H. pylori-related non-atrophic gastritis. Median and mean values of both S-G-17prand and S-PGI decreased with increasing grade of antral and corpus atrophy, respectively. Among all patients with atrophic gastritis (multifocal atrophic gastritis, or atrophic gastritis limited to antrum or corpus) or resected stomach, 50 of 56 patients (89%; Cl 95%: 81%-97%) had a low S-PGI and/or a low S-G-17prand with positive H. pylori serology. Such low values werc found in 3 of the 44 control patients (7%; CI 95%: 0%-14%).. Low serum levels of G-17prand and PGI are conceivable biomarkers of atrophic antral and corpus gastritis, respectively. A low S-G-17prand is a sign of the multifocal or antrum-limited atrophic gastritis in patients infected with H. pylori.

Topics: Antibodies, Bacterial; Antibodies, Monoclonal; Biomarkers; Case-Control Studies; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Sensitivity and Specificity

Our aim was to study the serum pepsinogen levels in gastric cancer patients in our population in relation to histology and the presence of Helicobacter pylori.. Forty-six patients with gastric cancer and 70 controls were studied prospectively in a 1-year period. Serum levels of pepsinogen I (PG I), pepsinogen II (PG II), and gastrin were measured by radioimmunoassay.. The mean PG I levels for cancer patients and controls were 83.5 microg/l and 60.9 microg/l, respectively (P = 0.03), the mean PG II levels were 27.2 microg/l and 12.1 microg/l respectively (P < 0.0001). The PG I/II ratio was significantly lower in cancer patients (P = 0.04) and in those with Helicobacter infection. Serum pepsinogen levels were not affected by any pathological characteristics. Histology showed that the prevalence of chronic gastritis, intestinal metaplasia, and gastric atrophy was 97%, 56%, and 15%, respectively.. The prevalence of gastric atrophy is low in our population, and serum pepsinogen measurement is not useful as a screening tool for gastric cancer in this population.

Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Case-Control Studies; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Prospective Studies; Stomach Neoplasms

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

Enterochromaffin-like cell hyperplasia of the gastric body mucosa occurs in hypergastrinaemic conditions such as atrophic body gastritis and Zollinger-Ellison syndrome. However, the time course of change or factors involved are not known.. To compare the rate of change of enterochromaffin-like cell proliferation in patients with atrophic body gastritis and Zollinger-Ellison syndrome.. From a consecutive series of atrophic body gastritis and Zollinger-Ellison syndrome patients, studied at the time of first diagnosis, 10 atrophic body gastritis (4 with pernicious anaemia) and 14 Zollinger-Ellison syndrome (4 with multiple endocrine neoplasia type 1) patients were followed-up for a median time of 48 months.. At entry and during follow-up patients underwent: plasma gastrin determination, endoscopic sampling of body mucosa for qualitative assessment of enterochromaffin-like cell hyperplasia pattern and degree of glandular atrophy, qualitative and morphometric analyses of body mucosa endocrine cells.. At time of diagnosis, enterochromaffin-like cell lesions were more severe in atrophic body gastritis than in Zollinger-Ellison syndrome. During follow-up, no significant variations were observed in gastrin values, enterochromaffin-like cell patterns and grade of body mucosa atrophy in atrophic body gastritis. In contrast, gastrin levels were significantly increased [median 1200 (235-2625) vs 1947 (225-5200) pg/ml; p<0.001)] as was total volume density of enterochromaffin-like cells [median 1.60 (0.53-4.06) vs 3.18 (1.35-21.13)% of mucosal epithelial component; (p<0.005)] in Zollinger-Ellison syndrome. Micronodular hyperplasia of enterochromaffin-like cells, present in only one patient at diagnosis, was observed in 8 Zollinger-Ellison syndrome patients at follow-up.. These data suggest that the progression of enterochromaffin-like cell growth in human gastric mucosa requires an increase of and/or a prolonged exposure to severe hypergastrinaemia.

Topics: Adult; Aged; Disease Progression; Enterochromaffin-like Cells; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Immunohistochemistry; Male; Middle Aged; Prospective Studies; Zollinger-Ellison Syndrome

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

Recently, it has been recognized that Helicobacter pylori (H. pylori) infection is associated with an exaggeration of basal and meal gastrin secretion. We investigate whether there is a relationship between H. pylori-related chronic gastritis and G-cell and D-cell number and granule density index of G and D cells. - The number of antral G cells and D cells and granule density index of D and G cells are compared between thirty two patients with H. pylori-related chronic gastritis and twelve patients without H. pylori and inflammation. Antral mucosal biopsy specimens are examined using light and electron immunohistochemical techniques. - The number of G cells is the same in either infected or uninfected patients (98.40 +/- 11.39, 109.25 +/- 12.76 vs 101.17 +/- 7.72 for infected patients with non atrophic and with mild atrophic chronic gastritis and uninfected controls, respectively) except for the cases with moderate gastric mucosal atrophy, where G cells (58.22 +/- 5.63) decrease in number. The number of D cells is decreased in all patients with H. pylori-related gastritis. G cell granule density index is significantly (p < 0.05) increased in patients with H. pylori-related chronic gastritis than in controls (3.15 +/- 0.43 vs 2.528 +/- 0.01). D cell granule density index is similar between patients with H. pylori chronic gastritis and controls (3.18 +/- 0.05 vs 3.166 +/- 0.12). It is concluded that decreased D cells number in patients with H. pylori-related chronic gastritis might be one of the reasons for the existing hypergastrinaemia.

Topics: Adolescent; Adult; Cytoplasmic Granules; Female; Gastrin-Secreting Cells; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Male; Microscopy, Immunoelectron; Middle Aged; Pyloric Antrum; Somatostatin; Somatostatin-Secreting Cells

There is interest in the development of GERD after Helicobacter pylori eradication. In contrast, the development of duodenal erosions after therapy has received scant attention. Patients were examined after eradication of H pylori infection to determine the frequency of post-therapy duodenal erosions (primary outcome) and whether there was a relation between development of duodenal and esophageal erosions. Additionally, factors were searched for that would identify patients at increased risk for duodenal erosions.. A single-center, endoscopist-blinded, observational study was conducted of 196 patients in whom H pylori was eradicated. The presence of esophageal or duodenal erosions was evaluated 4 weeks and 6 months after eradication. Serum gastrin and pepsinogen I (PG I) and II (PG II) levels were also determined for 83 patients entering the study during its final year.. Multiple small duodenal erosions developed in 8.6% of patients after H pylori eradication and were more common in patients with pre-eradication duodenal ulcer (27.8%) compared with those with gastric ulcer (6.7%) or atrophic gastritis (1.4%) (p < 0.05). Duodenal erosions were associated with high levels of PG I before and after eradication. The frequency of duodenal erosions decreased over time (3.1% by 6 months).. Duodenal erosions occur after H pylori eradication and appear to be related to duodenal ulcer and increased PG I levels, both of which are associated with increased acid secretion. Measurement of PG I may help to identify patients who have duodenal erosions develop after H pylori therapy for studies of the pathogenesis of these lesions.

Topics: Duodenal Ulcer; Duodenum; Endoscopy, Digestive System; Esophagus; Female; Follow-Up Studies; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Prospective Studies; Stomach Ulcer; Time Factors

Helicobacter pylori is involved in the induction of atrophic body gastritis (ABG). During the progression of atrophic gastritis the disappearance of H. pylori has been documented and in time serology is the only sign that indicates a previous infection. It has been shown that a positive serology, in ABG patients without histological evidence of infection, indicates an active H. pylori infection.. To investigate in a population of patients with ABG the prevalence of H. pylori infection on the basis of histology and serology.. A total of 150 consecutive outpatients with atrophic body gastritis were diagnosed on the basis of a screening system.. All patients had a detailed assessment including measurement of specific anti-H. pylori antibodies, parietal cell antibodies, and fasting gastrin, gastroscopy with biopsies from gastric antrum and body.. 24.6% of patients were histologically and serologically negative (Group A). 52.7% H. pylori was not detected on histology but IgG to H. pylori were in all these patients elevated (Group B). 22.6% of patients were found to be positive at histology in the corpus mucosa; all but one of these patients had elevated circulating IgG to H. pylori (Group C). Mean corporal atrophy score in Group B patients was statistically lower than in Group A patients (2.43 +/- 0.08 vs. 2.75 +/- 0.09; p <.05), but was statistically higher than in Group C patients (1.79 +/- 0.11; p <.001). Thus, in corporal mucosa a gradient of atrophy was shown: Group C < Group B < Group A. A similar gradient was observed for the presence of pernicious anemia being lowest in Group C 11.8% increasing to 45.6% in Group B and being highest in Group C 75.6%. A statistical correlation was obtained (r =.04791, p <.05) between the histological score of corporal atrophy and the titer of antibodies to parietal cells and an inverse correlation was obtained (r = -.2322, p <.0001) between the histological score of corporal atrophy and IgG to H. pylori.. This study shows that two-thirds of ABG patients have evidence of H. pylori infection. This suggests that atrophic gastritis of the corpus is a spectrum of damage where H. pylori is a key agent able to induce gastric atrophic damage and also gastric autoimmunity.

Topics: Adult; Aged; Aged, 80 and over; Antigens, Bacterial; Autoantibodies; Bacterial Proteins; Female; Gastric Acid; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Male; Middle Aged; Parietal Cells, Gastric; Prevalence

Chromogranin A (CgA) is a sensitive marker for neuroendocrine neoplasia. Enterochromaffin-like cell hyperplasia secondary to hypergastrinemia also leads to CgA increase in blood. Treatment with inhibitors of acid secretion, atrophic gastritis and infection with Helicobacter pylori are prevalent conditions leading to hypergastrinemia. We therefore wanted to study whether concomitant determination of gastrin could increase the utility of CgA as a marker of neuroendocrine neoplasia.. CgA and gastrin concentrations were determined by radioimmunoassay methods, while pepsinogen I (used to diagnose severe atrophic gastritis) was determined by a commercial immunoenzymatic assay.. Among 100 patients with elevated CgA, we found that 29% had hypergastrinemia. Vice versa, CgA was elevated in 23 out of 26 (88.5%) in a population of patients with hypergastrinemia. By determining pepsinogen I in blood in patients with hypergastrinemia, a proportion of them was diagnosed as having severe atrophic gastritis.. We conclude that determination of gastrin in blood in patients with CgA elevation will increase the utility of CgA in the diagnosis of neuroendocrine tumors.

Topics: Biomarkers, Tumor; Chromogranin A; Chromogranins; Enterochromaffin-like Cells; Gastric Mucosa; Gastrinoma; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Immunoenzyme Techniques; Neuroendocrine Tumors; Pepsinogen A; Radioimmunoassay; Stomach; Stomach Neoplasms

In the presence of atrophic body gastritis, gastric carcinoid develops from gastric-body mucosa enterochromaffin-like cells. Few data exist on the prevalence of enterochromaffin-like dysplastic lesions in atrophic body gastritis patients and their presumed risk of evolution to carcinoid has never been assessed prospectively in humans. The aim of the present study was to investigate the prevalence and incidence of dysplastic and neoplastic enterochromaffin-like cell lesions in a consecutive series of patients with atrophic body gastritis.. A total of 130 atrophic body gastritis patients at diagnosis and 96 atrophic body gastritis patients at follow-up (median 30 months) underwent gastroscopy with multiple biopsies and fasting gastrinaemia evaluation. In patients with enterochromaffin-like cell dysplasia, a more detailed bioptic sampling at follow-up was performed.. Of the 130 atrophic body gastritis patients, only one (0.7%) had a gastric carcinoid polyp, whereas enterochromaffin-like cell dysplasia was found in five patients (3.8%). At follow-up only one out of the 96 atrophic body gastritis patients (1%) was diagnosed as having a carcinoid polyp at 41 months. Enterochromaffin-like cell dysplasia was present in four additional patients (4.2%). Two atrophic body gastritis pernicious anaemia patients with enterochromaffin-like cell dysplasia developed a gastric carcinoid in the follow-up. Among nine atrophic body gastritis patients with enterochromaffin-like cell dysplasia, the incidence of carcinoid tumour was 22% compared to 1.1% of atrophic body gastritis patients without dysplasia (odds ratio: 26.00; 95% confidence interval: 2.089-323.52). During the follow-up, fasting gastrin levels increased significantly only in atrophic body gastritis patients with enterochromaffin-like cell dysplasia (mean 677.4 +/- 66.1 vs 1112.2 +/- 185.6; P = 0.0287).. This study provides the first clinical evidence that, in hypergastrinaemic atrophic body gastritis patients, enterochromaffin-like cell dysplasia carries a markedly increased risk for development of type I gastric carcinoid. This suggests that a more detailed endoscopic/bioptic procedure in this subgroup of atrophic body gastritis patients is able to detect gastric carcinoid at an early stage.

Topics: Adult; Aged; Aged, 80 and over; Carcinoid Tumor; Enterochromaffin-like Cells; Female; Follow-Up Studies; Gastrins; Gastritis, Atrophic; Humans; Immunohistochemistry; Male; Middle Aged; Odds Ratio; Precancerous Conditions; Prevalence; Prospective Studies; Risk; Stomach Neoplasms

Hypergastrinemia occurs frequently in association with acid suppression and Helicobacter infection, but its role in the progression to gastric atrophy and gastric cancer has not been well defined.. The effects of hypergastrinemia, and possible synergy with Helicobacter felis infection, were investigated in insulin-gastrin (INS-GAS) transgenic mice.. INS-GAS mice initially showed mild hypergastrinemia, increased maximal gastric acid secretion, and increased parietal cell number but later progressed to decreased parietal cell number and hypochlorhydria. Development of gastric atrophy was associated with increased expression of growth factors, heparin-binding epidermal growth factor and transforming growth factor alpha. At 20 months of age, INS-GAS mice showed no evidence of increased enterochromaffin-like cell number, but instead exhibited gastric metaplasia, dysplasia, carcinoma in situ, and gastric cancer with vascular invasion. Invasive gastric carcinoma was observed in 6 of 8 INS-GAS mice that were >20 months old. Helicobacter felis infection of INS-GAS mice led to accelerated (< or = 8 mo) development of intramucosal carcinoma (85%), with submucosal invasion (54%) and intravascular invasion (46%; P < or = 0.05).. These findings support the unexpected conclusion that chronic hypergastrinemia in mice can synergize with Helicobacter infection and contribute to eventual parietal cell loss and progression to gastric cancer.

Topics: Animals; Cell Count; Epidermal Growth Factor; Epithelial Cells; Gastric Acid; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Heparin; Heparin-binding EGF-like Growth Factor; Hyperplasia; Hypertrophy; Intercellular Signaling Peptides and Proteins; Metaplasia; Mice; Mice, Transgenic; Stomach Neoplasms; Transforming Growth Factor alpha

Our aim was to evaluate the relationship between gastric emptying and demographic, clinical, histological, and secretory features in patients with nonautoimmune fundic atrophic gastritis. Only 31% of 45 patients with fundic atrophic gastritis presented with achlorhydria. Scintigraphic gastric emptying of solids was delayed compared to healthy controls. Patients with achlorhydria showed gastric emptying rates lower than those with preserved acid secretion. Significant, but weak, correlations were observed between emptying rates and both peak acid output (Rs = 0.33) and serum gastrin levels (Rs = -0.36), but not with grading of mucosal atrophy. No symptom differences were observed between patients with or without achlorhydria, but a weak correlation was detected between peak acid output and the severity of epigastric pain (Rs = 0.40). In conclusion, patients with fundic atrophic gastritis present delayed gastric emptying that is weakly related to the reduction of the acid secretion and the raising of serum gastrin levels rather than to the severity of the atrophy.

Topics: Achlorhydria; Adult; Aged; Dyspepsia; Female; Gastric Acid; Gastric Emptying; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged

Atrophic gastritis has been shown to be one of the long term sequelae of Helicobacter pylori infection.. To determine the prevalence of atrophic gastritis in outpatients, to study the accuracy of serological methods for revealing atrophy, and to define the association of H pylori infection with atrophic gastritis in these patients.. A total of 207 consecutive outpatients referred for gastroscopy were included. Biopsy specimens from the antrum and corpus were assessed histologically according to the Sydney system. Serum samples were studied for H pylori IgG and IgA antibodies by enzyme immunoassay, CagA antibodies by immunoblot, pepsinogen I by an immunoenzymometric assay, gastrin by radioimmunoassay, and parietal cell antibodies by indirect immunofluorescence.. Histological examination revealed atrophic gastritis in 52 (25%) of 207 patients. H pylori and CagA antibodies were strongly associated with atrophic antral gastritis but poorly associated with atrophic corpus gastritis. Low serum pepsinogen I was the most sensitive and specific indicator of moderate and severe atrophic corpus gastritis. All six patients with moderate atrophic corpus gastritis had H pylori infection but eight of 10 patients with severe atrophic corpus had increased parietal cell antibodies and nine had no signs of H pylori infection.. Atrophic antral gastritis was strongly associated with CagA positive H pylori infection. Severe atrophic corpus gastritis was not determined by H pylori tests but low serum pepsinogen I, high gastrin, and parietal cell antibodies may be valuable in detecting these changes.

Topics: Adult; Aged; Aged, 80 and over; Antigens, Bacterial; Autoantibodies; Bacterial Proteins; Female; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin A; Immunoglobulin G; Male; Middle Aged; Parietal Cells, Gastric; Pepsinogen A; Prevalence; Sensitivity and Specificity; Serologic Tests; Stomach

Whether gastric acid secretion decreases with age is still controversial. With the discovery of Helicobacter pylori, the association of this bacterium with gastric acid secretion has also been discussed. The aim of this study was to investigate the relationship between gastric acid secretion, age and H. pylori infection.. The presence of H. pylori infection, the grade of fundic atrophic gastritis (FAG), and gastric acid secretion were investigated in 280 subjects without localized lesions in the upper gastrointestinal tract. Helicobacter pylori infection was confirmed by Giemsa and immunohistochemical staining, and FAG of biopsy specimens was graded on a scale of 0-4.. Both basal and maximal acid output decreased with age in H. pylori-positive subjects, while they did not change with age in H. pylori-negative subjects. Gastric acid secretion decreased with the progression of FAG. An age-correlated decrease in gastric acid secretion in H. pylori-positive subjects depended on an increasing prevalence of FAG with age.. In the population studied, advancing age had no influence on gastric acid secretion in H. pylori-negative subjects. Gastric acid secretion decreases with age in H. pylori-positive subjects because of the increasing prevalence of FAG with age.

Topics: Adolescent; Adult; Aged; Aging; Antibodies, Bacterial; Biopsy; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Prevalence; Retrospective Studies; Risk Factors

The common but incompletely understood entity of malabsorption of food bound cobalamin is generally presumed to arise from gastritis and/or achlorhydria.. To conduct a systematic comparative examination of gastric histology and function.. Nineteen volunteers, either healthy or with low cobalamin levels, were prospectively studied without prior knowledge of their absorption or gastric status.. All subjects underwent prospective assessment of food cobalamin absorption by the egg yolk cobalamin absorption test, endoscopy, histological grading of biopsies from six gastric sites, measurement of gastric secretory function, assay for serum gastrin and antiparietal cell antibodies, and direct tests for Helicobacter pylori infection.. The six subjects with severe malabsorption (group I) had worse histological scores overall and lower acid and pepsin secretion than the eight subjects with normal absorption (group III) or the five subjects with mild malabsorption (group II). However, histological findings, and acid and pepsin secretion overlapped considerably between individual subjects in group I and group III. Two distinct subgroups of three subjects each emerged within group I. One subgroup (IA) had severe gastric atrophy and achlorhydria. The other subgroup (IB) had little atrophy and only mild hypochlorhydria; the gastric findings were indistinguishable from those in many subjects with normal absorption. Absorption improved in the two subjects in subgroup IB and in one subject in group II who received antibiotics, along with evidence of clearing of H pylori. None of the subjects in group IA responded to antibiotics.. Food cobalamin malabsorption arises in at least two different gastric settings, one of which involves neither gastric atrophy nor achlorhydria. Malabsorption can respond to antibiotics, but only in some patients. Food cobalamin malabsorption is not always synonymous with atrophic gastritis and achlorhydria, and hypochlorhydria does not always guarantee food cobalamin malabsorption.

Topics: Achlorhydria; Adult; Aged; Aged, 80 and over; Biopsy; Case-Control Studies; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Helicobacter pylori; Humans; Intrinsic Factor; Malabsorption Syndromes; Male; Middle Aged; Parietal Cells, Gastric; Prospective Studies; Schilling Test; Vitamin B 12 Deficiency

Adrenomedullin (AM) is a novel hypotensive and vasorelaxing peptide recently isolated from human phaeochromocytoma tissue, and is widely distributed in various organs. In this study we examined the localization of AM-immunoreactive (IR) cells in the gastric mucosa and AM-IR cell density in antral atrophic gastritis.. Gastric mucosal tissues were taken from the gastric body and antral mucosa of 52 patients (27 men, 25 women; mean age 56.0 (range 20-86) years). Immunohistochemical analysis revealed that AM-IR cells were present in the pyloric glands, but not in the fundic glands, and that AM-IR cells were stained positively for chromogranin A and gastrin. The percentage of AM-IR cells vs chromogranin A- and gastrin-IR cells was 42 and 56%, respectively. The number of AM-IR cells decreased with the progression of severity of atrophic changes in the pyloric gland, and also of mononuclear cell infiltration. There was no correlation between the number of AM-IR cells and the degree of neutrophilic infiltration. Similar findings were also obtained for gastrin-IR cells.. AM-IR cells are present in the endocrine cells including gastrin-IR cells in the pyloric glands. These results suggest that AM may contribute to gastrin secretion in the pyloric glands.

Topics: Adrenomedullin; Adult; Aged; Aged, 80 and over; Antihypertensive Agents; Cell Count; Chromogranin A; Chromogranins; Enteroendocrine Cells; Female; Gastrins; Gastritis, Atrophic; Humans; Immunohistochemistry; Leukocyte Count; Male; Middle Aged; Peptides; Vasodilator Agents

Intravenously administered secretin stimulates pancreatic polypeptide (PP) release in patients with endocrine enteropancreatic tumors, but data in patients with nontumorous disorders are controversial. Therefore, we aimed to evaluate the plasma PP pattern after secretin administration in healthy subjects and in patients with gastroduodenal diseases investigated for recurrent ulcer disease and/or hypergastrinemia.. Synthetic secretin was given as an intravenous bolus (2U/kg) in ten patients with Zollinger Ellison syndrome, ten with duodenal ulcer, ten with atropic gastritis and ten healthy volunteers. Blood samples were taken before and at regular intervals for 30min after secretin injection. Plasma PP and gastrin levels were measured by radioimmunoassay.. Secretin promptly and significantly (P<0.01) increased PP plasma levels in all groups of subjects without any differences in peak values. There were no significant correlations between PP and gastrin plasma levels.. Secretin at pharmacological doses is a powerful stimulus for PP release.

Topics: Adult; Aged; Duodenal Ulcer; Female; Gastrins; Gastritis, Atrophic; Humans; Kinetics; Male; Middle Aged; Pancreatic Polypeptide; Secretin; Zollinger-Ellison Syndrome

Previous studies have shown a high prevalence of gastric parietal cell antibodies (PCA) in type 1 diabetes, which can be accompanied by (sub)clinical autoimmune gastric disease. This study aimed to determine the grade of associated autoimmunity and to assess the pattern of prevalence of PCA by gender, age, duration of disease, age at onset of diabetes, and human leukocyte antigen (HLA) type in an adult type 1 diabetic population. Furthermore, to examine the clinical significance of being PCA positive, manifestations of gastric autoimmune disease were studied in PCA-positive and PCA-negative patients. The population studied consisted of 497 type 1 diabetics (men/women, 252/245; mean age, 40.8 +/- 12.1 yr; mean duration of disease, 16.4 +/- 10.4 yr; mean age at onset, 26.9 +/- 13.5 yr; mean hemoglobin A1c, 8.1 +/- 1.6%). Associated autoantibodies were present in 39% and PCA were present in 20.9% of the subjects, particularly in older patients. Gender, duration, and age at onset of diabetes did not influence the appearance of PCA. Antithyroid peroxidase antibodies (aTPO) were more frequent in PCA-positive patients than in those without PCA (33.6% vs. 22.4%; P = 0.025), suggesting an association between gastric and thyroid autoimmunity. We could demonstrate an association between PCA and the HLA DR5 haplotype (P = 0.001) as well, but not with HLA DR3 and/or DR4. In the PCA-positive group, iron deficiency anemia was detected in 15.4%, and pernicious anemia was found in 10.5% of subjects. These autoimmune gastric manifestations were significantly more prevalent in PCA-positive diabetics than in PCA-negative subjects, in whom the percentages were 6.9% and 0.5%, respectively (P = 0.01 and P < 0.0001). PCA were prevalent in 84.6% of patients with pernicious anemia. A gastroscopic and anatomopathological examination performed in a subgroup of 30 patients with gastric symptoms revealed atrophic gastritis in 13 of 14 PCA-positive patients and in 9 of 16 PCA-negative subjects (P = 0.04). PCA were present in 59.1% of patients with atrophic gastritis. In conclusion, a high prevalence of parietal cell antibodies and associated autoimmune gastric disease is present in PCA-positive type 1 diabetics, recommending its screening. Early detection of PCA and iron deficiency anemia, pernicious anemia, and atrophic gastritis and the subsequent care could reduce the morbidity of type 1 diabetes.

Topics: Adult; Aging; Anemia, Pernicious; Autoantibodies; Autoimmune Diseases; Diabetes Mellitus, Type 1; Female; Gastrins; Gastritis, Atrophic; Glycated Hemoglobin; HLA-DR1 Antigen; Humans; Iron; Male; Middle Aged; Parietal Cells, Gastric; Risk Factors; Sex Characteristics

Mucolipidosis type IV (ML-IV) is an autosomal recessive lysosomal storage disease that causes severe neurologic abnormalities. The brain disease is characterized by pigmented cytoplasmic granules in neurons and accumulation of lamellated membrane structures in lysosomes. The gastrointestinal disease in ML-IV was not previously recognized. Clinical examination of 20 patients with ML-IV (age range, 2-23 years) at the National Institutes of Health showed hypergastrinemia and constitutive achlorhydria. Endoscopic biopsy specimens from the gastric fundus, body, and antrum and from the duodenum of four such patients (ages 4, 6, 7, and 22 years) were evaluated histologically and by electron microscopy. Histologically, all gastric fundus and body biopsy specimens showed parietal cells in normal numbers. However, a striking cytoplasmic vacuolization of parietal cells was seen on hematoxylin and eosin stain. Electron microscopy showed the parietal cells to be markedly distended by large lysosomes containing lamellar, concentric, and cystic membranous inclusions. Additionally, chronic atrophic gastritis and enterochromaffin-like (ECL) cell hyperplasia were observed. Foveolar and chief cells in stomach and duodenum biopsy specimens were normal. We conclude that the cytoplasmic lysosomal inclusions in gastric parietal cells is a unique histologic feature of gastric biopsy in ML-IV.

Topics: Achlorhydria; Adult; Biopsy; Child; Child, Preschool; Enterochromaffin-like Cells; Female; Gastric Fundus; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Hyperplasia; Inclusion Bodies; Lysosomes; Male; Mucolipidoses; Parietal Cells, Gastric

The aims of this study were to illustrate the malignant potential of gastric enterochromaffin-like (ECL) cell carcinoids (ECLomas) associated with hypergastrinemia, and the gradual neoplastic progression of such tumours. In addition, we examined whether the tyramide signal amplification (TSA) technique could visualize immunohistochemical (IHC) neuroendocrine (NE) features in the dedifferentiated neoplastic ECL cells which were not detected by conventional methods.. Conventional histopathological and IHC methods for visualizing ECL cells and cell proliferation were used in addition to the TSA technique.. Our patient was followed for 5 years. During that period, her ECLoma displayed all the signs of classical tumour progression, ultimately with the appearance of metastases in the regional lymph nodes, the liver and the skin. The neoplastic ECL cells became progressively dedifferentiated with an increasing number of Ki-67 immunoreactive (IR) cell nuclei. In addition, there was a substantial decrease in argyrophil and IR NE cells that could be visualized by conventional methods. By applying the TSA technique, however, the number of IR tumour cells increased considerably.. ECLomas secondary to hypergastrinemia should be closely followed for signs of clinical and histopathological tumour progression. Such ECLomas deserve early, active, radical surgical treatment. The TSA technique is a valuable tool for visualizing the characteristic IHC features in dedifferentiated NE cells.

Topics: Aged; Carcinoid Tumor; Cell Differentiation; Chromogranin A; Chromogranins; Enterochromaffin Cells; Female; Gastrins; Gastritis, Atrophic; Histidine Decarboxylase; Humans; Immunohistochemistry; Ki-67 Antigen; Serotonin; Stomach Neoplasms

We present here familial occurrence of two patients with gastric carcinoid. Both patients, a sister and older sister, had type A chronic atrophic gastritis with hypergastrinemia. This is the first case report of familial occurrence of gastric carcinoid associated with type A chronic atrophic gastritis in the world literature. The possible mechanism of familial occurrence in the patients is discussed.

Topics: Adult; Carcinoid Tumor; Chronic Disease; Female; Gastrins; Gastritis, Atrophic; Humans; Pedigree; Stomach Neoplasms

Topics: Anemia, Iron-Deficiency; Duodenum; Gastrins; Gastritis, Atrophic; Humans; Stomach

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

Beta-microseminoprotein is a 94-kDa protein present on most mucosal surfaces in the body. It is produced in mucin cells but is also found in a particular type of cells (E-cells) in the gastric antral mucosa. Most of these cells also contain gastrin. In atrophic corpus gastritis the gastrin-producing cells become hyperplastic, and the patients have hypergastrinemia. We wanted to ascertain whether there is a similar effect on the E-cells and on the concentration of beta-microseminoprotein in serum.. Antral biopsy specimens from 10 patients with atrophic corpus gastritis and 10 controls were stained immunohistochemically for beta-microseminoprotein and gastrin. beta-Microseminoprotein and gastrin were measured by radioimmunoassay in serum from 15 women with atrophic corpus gastritis and 31 healthy female blood donors.. There was a 3.5-fold increase of the number of E-cells (which also were hypertrophic) and a 2.1 times higher serum concentration of beta-microseminoprotein in the patients with atrophic corpus gastritis than in the control subjects. Gastrin was seen in 28% of the E-cells in patients with atrophic corpus gastritis, compared with 87% in normal antral mucosa. There was no correlation between the serum concentrations of beta-microseminoprotein and gastrin.. In atrophic corpus gastritis antrum E-cells undergo hyperplasia and hypertrophy, and the proportion of E-cells containing gastrin decreases. Increased amounts of beta-microseminoprotein are secreted to the blood but uncorrelated with gastrin.

Topics: Adult; Aged; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Immunohistochemistry; Male; Middle Aged; Peptides; Prostatic Secretory Proteins; Pyloric Antrum; Radioimmunoassay

Since there is a significant overlap in serum cobalamin concentrations between healthy and cobalamin-deficient individuals, we wanted to compare two different principles for use as supplementary tests to serum cobalamin concentration in patients with suspected cobalamin malabsorption and deficiency.. Clinical study of consecutive patients.. The catchment area of Sahlgrenska University Hospital, Göteborg.. A total of 112 patients with suspected cobalamin deficiency who had not previously undergone gastrointestinal surgery.. Gastroduodenoscopy with biopsies taken from the gastric body and the duodenum, Schilling test, and measurement of serum methylmalonic acid (MMA), total homocysteine (Hcy), pepsinogens A and C, and gastrin.. Number of patients with gastric body atrophy identified with the combination of MMA and Hcy, and pepsinogen A combined with pepsinogen C or gastrin.. About 95% of the patients with severe gastric body atrophy had abnormal concentrations of serum pepsinogen A and/or gastrin or pepsinogen A/C ratio, whereas 65% had abnormal metabolite concentrations. Serum pepsinogen A combined with pepsinogen C identified 100%, and combined with gastrin 88%, of the patients with gastric body atrophy and elevated metabolite tests, and 67 and 75%, respectively, of those who had not yet developed elevated metabolite tests.. Pepsinogen A, combined with pepsinogen C or gastrin, should be the first option in evaluating patients with suspected cobalamin deficiency who have not previously undergone gastrointestinal surgery.

Topics: Adult; Aged; Algorithms; Diagnosis, Differential; Female; Gastrins; Gastritis, Atrophic; Homocysteine; Humans; Male; Methylmalonic Acid; Middle Aged; Pepsinogen A; Pepsinogen C; Predictive Value of Tests; Vitamin B 12 Deficiency

Topics: Abdominal Pain; Adult; Anemia, Pernicious; Carcinoid Tumor; Diagnosis, Differential; Female; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Hyperplasia; Precancerous Conditions; Pyloric Antrum; Stomach Neoplasms

It is not known whether plasma chromogranin analysis could be a complement to histology for detection and grading of gastric fundic mucosal endocrine cell proliferation in hypergastrinemic (type-A) atrophic gastritis.. Gastric biopsy sections (body and antrum) from 43 patients with type-A gastritis (9 with gastric carcinoid) were examined for density and micronodules of argyrophil endocrine cells. Fasting blood samples were analyzed for chromogranin A and B, gastrin, and somatostatin.. All patients with carcinoid and 17 of the 34 without carcinoid had micronodules in the gastric fundic mucosa. The median plasma chromogranin A concentration was 5.7 (3.5-40.0) nmol/l in patients with carcinoid, 4.5 (3.0-9.5) nmol/l in patients with micronodules, and 3.7 (0.8-6.0) nmol/l in patients without micronodules. Overall, chromogranin A concentrations correlated to endocrine cell densities in the fundic mucosa (r = 0.64, P < 0.001) and to gastrin concentrations (r = 0.71, P < 0.001). Plasma somatostatin and chromogranin B concentrations did not differ significantly between the groups.. In type-A gastritis, analysis of plasma chromogranin A may be a useful complement to histology in estimating the endocrine cell mass. Moreover, subclinical type-A gastritis may be a source of error when chromogranin A analysis is used in the search for neuroendocrine neoplasia.

Topics: Aged; Anemia, Pernicious; Biopsy; Carcinoid Tumor; Chromogranin A; Chromogranins; Enterochromaffin Cells; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Male; Stomach Neoplasms

Iron absorption is known to be impaired in the setting of gastric achlorhydria, yet gastric atrophy is not usually considered an aetiological factor for iron deficiency anaemia. We aimed to determine the prevalence of achlorhydric gastric atrophy in patients with iron deficiency and no identifiable source of gastrointestinal blood loss, and to assess whether gastric, as well as duodenal, biopsies should be routinely performed in these patients.. Forty-one consecutive patients with iron deficiency anaemia and no specific gastrointestinal symptoms or evidence of a bleeding lesion on faecal occult blood testing or upper gastrointestinal or colonic endoscopy.. As well as routine duodenal biopsies, samples were taken from gastric corpus and antrum for evidence of gastric atrophy. Achlorhydria was considered to be present if plasma gastrin measured on a sample obtained with the patient fasting was over 200 ng/l. Serum was tested for intrinsic factor and gastric parietal cell antibodies.. Haemoglobin concentrations ranged from 4.1 to 10.9 g/dl. Eight (20%) of the 41 patients had corpus-predominant or generalized atrophy and high plasma gastrin levels, of whom six had serum intrinsic factor and/or gastric parietal cell antibodies: two also had Giardia lamblia organisms in duodenal biopsies. Four other patients (10%) had villous atrophy of the duodenum.. As well as confirming the importance of seeking coeliac disease in patients with iron deficiency anaemia, our results suggest that achlorhydric gastric atrophy is also a common association. Gastric biopsies should be taken in patients with no other explanation for anaemia. The finding of Giardia organisms in two achlorhydric patients, with a possible contributory role, suggests that duodenal biopsies should be obtained even if serum coeliac-related antibodies are absent.

Topics: Adolescent; Aged; Aged, 80 and over; Anemia, Iron-Deficiency; Biopsy; Duodenum; Endoscopy, Gastrointestinal; Female; Folic Acid; Follow-Up Studies; Gastrins; Gastritis, Atrophic; Hemoglobins; Humans; Male; Middle Aged; Prevalence; Prospective Studies; Stomach; Vitamin B 12

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

Previous study showed that duodenal ulcer (DU) patients infected with Helicobacter pylori (H. pylori) have increased basal and pentagastrin- or GRP-induced gastric acid secretion and that these disturbances reversed fully after eradication of H. pylori. This study was designed to compare the gastric acid secretory profile, plasma gastrin levels and growth factors (EGF and TGF alpha) expression in gastric mucosa in DU patients with those in atrophic gastritis patients before and six months after verified eradication of H. pylori. In DU patients, basal and stimulated (GRP and pentagastrin) gastric acid secretion was significantly higher than in healthy controls. Six months following the eradication of H. pylori with triple therapy (omeprazole+clarithromycin+amoxicillin), this secretion returned to normal value. In contrast, in patients with atrophic gastritis, such eradication of H. pylori resulted in a significant increase in basal and pentagastrin- and GRP-stimulated acid secretion. Mucosal expression of immunoreactive EGF and TGF alpha was significantly enhanced in H. pylori positive DU and atrophic gastritis patients but this elevation disappeared or was markedly decreased 6 months upon the eradication of H. pylori. We conclude that 1) H. pylori infection is accompanied both in DU and atrophic gastritis patients by an enhanced plasma gastrin and increased mucosal expression of EGF and TGF alpha, 2) basal and GRP-induced acid secretion is significantly elevated in DU, whereas that in atrophic gastritis patients is greatly reduced, and 3) the H. pylori eradication restores gastric acid and plasma gastrin release as well as the mucosal expression of growth factors in DU and atrophic gastritis.

Topics: Adult; Duodenal Ulcer; Epidermal Growth Factor; Gastric Acid; Gastric Mucosa; Gastrin-Releasing Peptide; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Male; Transforming Growth Factor alpha

A 48-year-old male with type A atrophic gastritis developed multiple gastric carcinoids and a pituitary adenoma. Laboratory tests revealed high levels of serum gastrin and growth hormone (GH). He underwent subtotal gastrectomy, resulting in a return of the previously elevated gastrin level to normal. Serum GH concentration remained high. Three months after the surgery, the pituitary tumor, composed greatly of GH-immunoreactive cells, was partially removed. Since hypergastrinemia plays a pivotal role in gastric carcinoid formation and induces GH-releasing factor (GHRH) release resulting in GH-producing pituitary tumor formation, GH-producing pituitary adenoma might be a clinical manifestation in type A gastritis.

Topics: Adenoma; Carcinoid Tumor; Follow-Up Studies; Gastrectomy; Gastrins; Gastritis, Atrophic; Gastroscopy; Growth Hormone; Growth Hormone-Releasing Hormone; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Neoplasms, Multiple Primary; Pituitary Neoplasms; Stomach Neoplasms; Tomography, X-Ray Computed

This study aimed to estimate the prevalence and type of chronic gastritis in an asymptomatic working population and to determine whether a combination of serum pepsinogen levels and Helicobacter pylori serology could be used to identify a subgroup with atrophic gastritis at elevated risk of gastric carcinoma. A 10% subsample of 544 male volunteer factory workers aged 18-63 years and participating in a larger study underwent endoscopy and biopsy. Of these men, 29 were seropositive for Helicobacter pylori; all but three (89.7%) had chronic gastritis. Serum pepsinogen A levels increased with progression from a corpus predominant pattern of gastritis through pangastritis to an antral predominant pattern. Nine subjects had corpus atrophy, which was in most cases accompanied by fasting hypochlorhydria and hypergastrinaemia. A combination of pepsinogen A below 80 ng ml-1 and Helicobaceter pylori seropositivity detected corpus atrophy with sensitivity 88.9% and specificity 92.3%. A second screening stage, using a pepsinogen A/C ratio of below 2.5 as a cut-off, resulted in a reduction in numbers requiring further investigation but with some loss of sensitivity (77.8%). Application of this two-stage screening programme to the original sample of 544 workers would have resulted in 11 (2.2%) men being selected for follow-up, excluding 25 (5.1%) false negatives. Our results suggest that a combination of serum pepsinogen levels and Helicobacter pylori serology could be useful as a biomarker strategy for detection of individuals at increased risk of gastric carcinoma and for non-invasive investigation of the natural history of Helicobacter pylori gastritis.

Topics: Adolescent; Adult; Biomarkers; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Occupational Diseases; Pepsinogens; Prevalence; Risk Factors; Stomach Neoplasms

To evaluate the association of both Helicobacter pylori (Hp) infection and advancing age with increased prevalence of atrophic gastritis.. Two hundred and thirty-eight subjects who had no esophagitis, peptic ulcers, or malignancies in the upper gastrointestinal tract were divided into three groups according to age: group A, < 30 yr; group B, 30-49 yr; group C, > or = 50 yr. Two biopsy specimens were obtained from the lesser curvature of the antrum and two from the anterior and posterior walls of the fundus to assess the degree of gastritis and histological evidence of Hp infection. Hp infection was evaluated by Giemsa staining and serum IgG antibodies. Serum gastrin (SG) and pepsinogen (PG) were determined by radioimmunoassay.. In all age groups, the prevalence of atrophic gastritis was significantly more common in subjects with evidence of Hp infection. In Hp-positive subjects, the prevalence of atrophic gastritis increased with advancing age. Atrophic gastritis was extremely rare, regardless of age, in Hp-uninfected patients. SG increased, and PG I and the PG I:II ratio decreased with age in Hp-positive subjects. This trend was not apparent in Hp-negative subjects.. Our results suggest that Hp infection is a stronger predictor than advancing age for atrophic gastritis.

Topics: Adult; Aging; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogens; Prevalence; Radioimmunoassay; Risk Factors

The effects of long term (6-month), high (500-micrograms), once a day administration of octreotide on enterochromaffin-like (ECL) cell proliferation were evaluated in eight patients with hypergastrinemic atrophic gastritis at risk for the development of gastric carcinoids. Fasting gastrin levels were determined during treatment and up to 6 months after the end of treatment. Chromogranin A, hCG alpha, and somatostatin-immunostained cells were morphometrically evaluated in biopsy specimens of corpus mucosa taken before and after treatment. The results showed that gastrin levels significantly decreased from 950 to 238 ng/L (-74.9%; P < 0.01) at the end of treatment, a decrease that persisted 6 months after the end of treatment (450 ng/L; P < 0.05). The volume density of CgA cells (mostly ECL cells) decreased from 3.7% to 2.1% of the epithelial component (-43%; P < 0.014), that of hCG alpha-storing ECL cells decreased by 85% (P < 0.0007), and that of somatostatin-stained cells decreased by 74% (P < 0.04). No clinically significant side-effects were found. It is concluded that octreotide treatment as used in the present study is safe and effective in reducing hypergastrinemia and associated ECL cell changes in patients with atrophic gastritis. The decrease in D cells is consistent with the occurrence of somatostatin receptors and related autocrine regulation in these cells.

Topics: Adult; Biopsy; Chromogranin A; Chromogranins; Enterochromaffin Cells; Fasting; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastrointestinal Agents; Glycoprotein Hormones, alpha Subunit; Humans; Male; Middle Aged; Octreotide; Somatostatin

Helicobacter pylori causes chronic gastritis in all infected individuals and thus may be a risk factor for the ultimate development of trophic gastritis and gastric cancer. The serum levels of pepsinogen A, pepsinogen C and gastrin can be used as markers for both non-atrophic and atrophic gastritis.. We determined the serum levels of gastrin, pepsinogen A and pepsinogen C and the pepsinogen A/C ratio in 150 H. pylori-negative and 186 H. pylori-positive individuals.. The H. pylori infected patients had significantly higher serum levels of pepsinogen A, pepsinogen C and gastrin and a significantly lower pepsinogen A/C ratio. In the non-infected patients, none of the respective serum values changed with increasing age. In contrast, in the infected patients, the pepsinogen A level and pepsinogen A/C ratio decreased significantly with increasing age.. H. pylori infection increases serum levels of pepsinogen A, pepsinogen C and gastrin and decreases the pepsinogen A/C ratio. In infected subjects, levels of pepsinogen A and the pepsinogen A/C ratio decrease with ageing. These findings support the concept of H. pylori as a risk factor for the development of atrophic gastritis.

Topics: Adolescent; Adult; Age Factors; Aged; Biomarkers; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Middle Aged; Pepsinogens; Risk Factors

A now 54-year-old woman was 32 years ago found to have immune thrombocytopenia and 3 years ago ANA-positive and HBsAg-negative hepatitis with cirrhotic metaplasia. Numerous small asymptomatic carcinoids with marked hypergastrinaemia (1626 ng/l) were also first found 3 years ago. No gastrinoma could be found. Severe arthralgia was the main symptom on admission.. Gastroscopy revealed a polypoid carcinoid, 1 cm in diameter. There was total achlorhydria. No pernicious anaemia or carcinoid syndrome was found.. Total gastrectomy with construction of a jejunal substitute stomach was performed. Histology showed typical chronic-atrophic gastritis type A, all stages of an argyrophilic endocrine cell hyperplasia, as well as microcarcinoidosis and multicentric carcinoid, in part with submucosal infiltration and lymph node metastases. Immunohistology revealed immune reaction for the global endocrine marker. No specific hormones were demonstrable in the carcinoid cells. The postoperative course was without complications. Serum gastrin levels have since been normal.. The case confirms the possibility of an achlorhydria-hypergastrinaemia-carcinoid sequence. Now new stage-related therapeutic guidelines for this disease are needed.

Topics: Achlorhydria; Autoimmune Diseases; Carcinoid Tumor; Female; Follow-Up Studies; Gastrectomy; Gastrins; Gastritis, Atrophic; Gastroenterostomy; Humans; Jejunum; Lymphatic Metastasis; Middle Aged; Stomach; Stomach Neoplasms; Time Factors

To explore the state of the gastric mucosa in individuals with and without peptic ulcer disease from populations with contrasting peptic ulcer risks.. Pepsinogen A, pepsinogen C, gastrin and Helicobacter pylori antibodies are serological markers of gastritis. A decreasing pepsinogen A-C ratio and pepsinogen A level are known to reflect an increasing severity of corpus atrophy, whereas gastrin levels decrease with an increasing severity of antral atrophy when corpus atrophy is present. Helicobacter pylori-positive men, with and without a peptic ulcer history, were the focus of the study.. In 190 Japanese and 425 Dutch male employees, of similar age (mean age 49 years) and level of occupation, fasting serum samples were analysed in the same laboratory for IgG antibodies to H. pylori, pepsinogen A, pepsinogen C and gastrin. Any history of ulcer disease was verified through case notes.. The H. pylori seropositivity rate was higher in the Japanese men (72%) than in the Dutch (33%). There were 23 (12%) Japanese and 18 (4%) Dutch men with a verified duodenal ulcer history, and 14 (7%) Japanese and two (0.5%) Dutch men with a verified gastric ulcer history. H. pylori-positive men with a duodenal ulcer history differed from the H. pylori-positive men without an ulcer history in that they had a significantly higher mean pepsinogen A level (64 and 51 micrograms/l in Japanese men and 71 and 57 micrograms/l in Dutch men) and also a higher mean pepsinogen A-C ratio, whereas pepsinogen C and gastrin levels did not differ. In H. pylori-positive gastric ulcer patients the mean gastrin level was significantly lower than in H. pylori-positive men without ulcer disease (17 and 37 pmol/l in Japanese men), whereas pepsinogen levels were similar.. This study suggests that in H. pylori-positive duodenal ulcer patients there is less mucosal atrophy of the corpus and in H. pylori-positive gastric ulcer patients more atrophy of the antrum than in H. pylori-positive individuals without peptic ulcer disease.

Topics: Adrenergic beta-Antagonists; Adult; Aged; Case-Control Studies; Chi-Square Distribution; Duodenal Ulcer; Employment; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Japan; Male; Middle Aged; Netherlands; Pepsinogens; Prevalence; Stomach Ulcer

Serological markers of gastritis, like pepsinogen A, pepsinogen C, gastrin, and Helicobacter pylori antibodies, can be used to explore the state of the gastric mucosa in populations with contrasting cancer risks. A decreasing pepsinogen A:C ratio and an increasing serum gastrin are known to reflect an increasing severity of atrophic corpus gastritis, which is a precursor of gastric cancer. In 723 subjects (without gastroduodenal surgery) from Japanese (n = 225) and Dutch (n = 498) working populations, which had a similar composition of age (mean 48 years), sex (male to female ratio 6:1), and type of occupation, fasting serum samples were analysed for IgG antibodies to H pylori, pepsinogen A, pepsinogen C, and gastrin in the same laboratory. H pylori infection was significantly more prevalent in the Japanese than in the Dutch (74.7% and 31.3%); as was a very low pepsinogen A, indicative of severe mucosal atrophy (4.4% and 1.6%). Among subjects with and without severe mucosal atrophy the H pylori seropositivity rate was similar. Between the Japanese and the Dutch there were significant differences in mean gastrin (31.8 and 13.4 pmol/l) and pepsinogen A:C ratio (1.7 and 2.9). These intercountry differences were as great for H pylori negative subjects (gastrin: 23.7 and 10.3 pmol/l, pepsinogen A:C ratio: 2.4 and 3.2) as for H pylori positive subjects (gastrin: 34.6 and 20.1 pmol/l, pepsinogen A:C ratio: 1.5 and 2.5). The intercountry difference in gastrin nearly disappeared after stratification into categories of pepsinogen A:C ratio. In conclusion, the intercountry differences in pepsinogen A:C ratio and gastrin reflect a higher prevalence of mild and severe mucosal atrophy of the corpus in the Japanese than in the Dutch, both among H pylori positive and negative subjects. Thus, these findings suggest that in the Japanese the development of atrophic gastritis is in part unrelated to H pylori.

Topics: Adult; Age Distribution; Aged; Antibodies, Bacterial; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Japan; Male; Middle Aged; Netherlands; Pepsinogens; Prevalence; Seroepidemiologic Studies

A 41-year-old woman with a chronic atrophic gastritis after endoscopic investigation diagnosed a carcinoid at the corpus of the stomach. There were more lesions in the mucosa of the stomach in the form of dysplasias. The labor investigation indicated an hypergastrinaemia. We performed a resection of the basis of the carcinoid. It has shown to be histologically tumor-free as the rest of the stomach. A gastrectomy was not necessary. After resection the patient was under therapy with vitamin B-12. The level of gastrin in blood was normal under this treatment. Two years later the patient remained symptom-free. Regular endoscopic investigations show a stagnation of the growth of the dysplastic lesions of the mucosa of the stomach.

Topics: Adult; Biomarkers, Tumor; Carcinoid Tumor; Chromogranins; Diagnosis, Differential; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Stomach Neoplasms; Synaptophysin

To document our experience with gastric carcinoids over the past decade and to identify lesion frequency and the existence of a relationship to low acid states.. Retrospective case series.. Tertiary care referral center.. A consecutive sample of 16 patients with gastric carcinoids was evaluated over the last decade. Only two cases were recorded in the prior decade. Ages ranged from 30 to 93 years (mean, 65.9 years). There were eight men and eight women. Three patients were unavailable for follow-up.. Therapy included total gastrectomy (n = 4), subtotal gastrectomy (n = 3), endoscopic polypectomy (n = 3), and endoscopic surveillance (n = 6).. Pathobiological tumor characteristics and survival.. All carcinoids were of gastric fundic origin. None of the patients exhibited the carcinoid syndrome. Chronic atrophic gastritis was the most frequently observed comorbid pathologic condition (63%). Half of the patients had multiple polypi. Mean follow-up was 4.7 years (n = 13). There were 10 survivors. The only related death occurred in a patient with a solitary tumor.. Diagnosis of the complex and ill-defined entity of gastric carcinoid is increasing. This may be due to an increased awareness and increased upper gastrointestinal endoscopy rate rather than an increase in real incidence. Criteria for prediction of malignant progression are not available. Multiple gastric carcinoids associated with hypergastrinemia predominantly display nonaggressive behavior. Conservative gastric surgery may be appropriate therapy for such patients.

Topics: Adult; Aged; Aged, 80 and over; Carcinoid Tumor; Comorbidity; Connecticut; Female; Follow-Up Studies; Gastrectomy; Gastric Acid; Gastric Fundus; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Incidence; Male; Middle Aged; Polyps; Retrospective Studies; Stomach Neoplasms; Survival Rate

To evaluate the possible relationship between Helicobacter pylori infection and gastric carcinoma, and its precursor lesion, intestinal metaplasia, in a Japanese population.. H. pylori infection was identified by the presence of anti-H. pylori immunoglobulin (Ig)G. The frequency of H. pylori infection was compared in 109 patients with gastric carcinoma, the same number of patients with atrophic gastritis and asymptomatic controls matched for age, sex and place of birth. To study the relation between H. pylori and intestinal metaplasia, sera and gastric antral and corpus mucosal biopsies were obtained from 58 asymptomatic controls, 92 patients with chronic gastritis and 80 patients with peptic ulcer.. The presence of IgG antibody to H. pylori was significantly more frequent in those with gastric carcinoma than in asymptomatic controls (87.2 versus 74.3%; odds ratio 2.4; 95% confidence interval 1.2-4.8). The positive rates of H. pylori IgG antibody were 80.7% in patients with atrophic gastritis. Mean serum gastrin and pepsinogen II levels in H. pylori-positive patients were higher than those in H. pylori-negative patients. Serum gastrin and pepsinogen I levels were significantly higher in controls than gastric carcinoma patients (P < 0.01 and P < 0.05, respectively). Serum pepsinogen I:II ratios were significantly lower in controls than in gastric carcinoma patients (P < 0.01). Intestinal metaplasia was strongly associated with H. pylori infection, and was only found in patients with IgG antibodies to H. pylori.. These results suggest that H. pylori infection is associated with the development of gastric cancer by providing a suitable environment for carcinogenesis of the gastric mucosa, such as gastric atrophy and intestinal metaplasia.

Topics: Enzyme-Linked Immunosorbent Assay; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Intestines; Japan; Male; Metaplasia; Pepsinogens; Stomach Neoplasms

We conducted this study to identify the endocrine and neurocrine mechanisms of gastric mucosal protection in rats with experimental atrophic gastritis (erosive atrophic antritis) induced by prolonged exposure to taurocholate. This resulting gastritis was characterized by a significant reduction of parietal cell mass, a decrease in mucosal thickness, decreased numbers of pyloric glands, infiltration by inflammatory cells, and fibrotic proliferation in the gastric mucosa. Mucosal erosions were also prominent. These morphologic and morphometric findings indicate the presence of erosive atrophic gastritis, as previously described. Fasting levels of serum gastrin increased significantly in the rats with gastritis versus controls, whereas the mucosal gastrin levels did not differ significantly from those of controls. Mucosal levels of somatostatin decreased significantly, and vasoactive intestinal peptide (VIP) increased significantly in the pyloric sphincter region. These findings suggest that these peptides and neuropeptides are involved in the induction of this form of gastritis. The peptides may play an important role in the mechanisms of gastric mucosal protection (i.e., gastrin is an aggressive and somatostatin is a defensive factor, and VIP promotes the reflux of bile into the stomach by relaxing the pyloric sphincter).

Topics: Animals; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Male; Parietal Cells, Gastric; Radioimmunoassay; Rats; Rats, Wistar; Somatostatin; Taurocholic Acid; Vasoactive Intestinal Peptide

In order to ascertain possible abnormalities in somatostatin and gastrin secretion in patients with duodenal ulcer, the author compared bombesin-stimulated somatostatin and gastrin secretion by antral mucosal explants in patients with duodenal ulcer, those with atrophic gastritis and normal controls. An organ culture technique was employed. This excluded neurogenic, hormonal and circulatory influences. Bombesin in concentrations of 10(-7) M to 10(-5) M stimulated gastrin and somatostatin secretion at a dose-dependent manner. In all subjects, bombesin (10(-7) M) stimulated antral gastrin release and increased explant gastrin content significantly (p < 0.05). Bombesin significantly increased somatostatin release and explant somatostatin content in normal subjects (p < 0.05) but not in patients with duodenal ulcer (p > 0.05). In the presence of bombesin, the total net increase of gastrin in medium and explants was greater in duodenal ulcer patients (31.57 +/- 5.20 ng/mg wet w.) compared with normal subjects (19.63 +/- 4.50 ng/mg wet w.) (p < 0.01). The total net increase of somatostatin in the presence of bombesin was significantly less in duodenal ulcer patients (0.10 +/- 0.02 ng/mg wet w.) than in normal subjects (1.45 +/- 0.24 ng/mg wet w.) (p < 0.01). The results suggest that abnormalities in somatostatin and gastrin secretion of the antrum contribute to the pathogenesis of increased gastric acid secretion in duodenal ulcer.

Topics: Adult; Bombesin; Culture Techniques; Dose-Response Relationship, Drug; Duodenal Ulcer; Female; Gastrins; Gastritis, Atrophic; Humans; Intestinal Mucosa; Male; Middle Aged; Somatostatin

Gastric acid secretion has been considered to decline with increasing age but this view is being re-evaluated as the importance of Helicobacter pylori infection emerges. This study aimed to determine the effect of age, H pylori, and gastritis with atrophy on the serum gastrin concentration, gastric secretory volumes, and acid output in healthy, asymptomatic men. Young men (mean (SD) age 22.9 (0.6) years; n = 22) were compared with old men (72.9 (1.2) years; n = 28) in respect of basal serum gastrin and basal, sham fed, pentagastrin stimulated maximal and peak acid secretion. Antral, corpus, and fundal biopsy specimens were taken for histology and H pylori status (histology, culture, and rapid urease test). H pylori associated gastritis was present in three of 22 young (13.6%) and 16 of 28 old (57.1%) men. Gastritis with atrophy was present in 11 old subjects, 10 of whom were H pylori positive. These subjects had higher mean (SD) serum gastrin concentrations than old subjects without atrophy and young subjects (61.8 (9.2); 40.0 (2.9); 36.8 (2.3) pmol/l respectively; p < 0.001). H pylori infected subjects had higher gastrin values than uninfected subjects, overall (55.3 (5.9); 36.0 (1.8) pmol/l; p < 0.001) and in subjects without atrophy (45.3 (4.2); 36.0 (1.8) pmol/l; p < 0.03). In subjects without H pylori infection, gastrin values did not differ with age (old 37.1 (1.7); young 35.4 (2.1) pmol/l). The maximal gastric secretory volume was lower in old subjects with atrophy. Acid output (mmol/h) in subjects with atrophy was lower than in subjects with no atrophy (basal: 3.0(1.1); 5.1(0.7); p=NS; sham led: 5.4 (1.4); 9.3 (0.8); p<0.02; maximal: 18.9 (4.0); 31.4(1.8); p<0.002; peak: 25.1(5.3); 43.4(2.7); p<0.003). However, acid secretion in old subjects without atrophy was not different to that in young subjects, irrespective of H pylori status. These results did not differ when acid output was expressed as mmol/h/kg lean body mass or mmol/h/kg fat free body weight. Using multiple linear regression analysis, gastritis with atrophy was the only factor that had an independent negative effect on acid secretion. In healthy men without atrophy, gastric acid secretion is preserved with ageing and is independent of H pylori status. Atrophy, which is closely related to H pylori infection, is associated with a decline in acid secretion. Increased basal serum gastrin is related to both atrophy and H pylori infection but not to ageing per se.

Topics: Adolescent; Adult; Age Factors; Aged; Basal Metabolism; Biopsy; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Severity of Illness Index; Stomach

The aim of the study was to evaluate whether treatment with 200 micrograms/d of the somatostatin analogue octreotide (SMS 201-995) for three months can influence the trophic action exerted by hypergastrinemia on endocrine cells of the oxyntic mucosa, a condition potentially leading to hyperplasia and carcinoid tumors. Endocrine cells were morphometrically investigated in Grimelius silver stained sections of endoscopic biopsies of oxyntic mucosa collected from 13 hypergastrinemic patients with Zollinger-Ellison syndrome (ZES) (n = 5), antral G cell hyperfunction (AGCH) (n = 4) and atrophic gastritis type A (AG-A) (n = 4) before and after 3 months treatment and 3 months after drug discontinuance. The treatment induced a reduction of the volume density (P < 0.015), profile cross sectional area (P < 0.05) and number of cell profiles per unit area (P < 0.015) of argyrophil cells. A rebound of all these parameters was observed 3 months after drug withdrawal with values usually exceeding those at the entry, except in cases of AG-A. The patients' plasma gastrin concentrations presented similar variations showing a significant relation with all morphometric parameters of argyrophil cells. Also, the cell content in alpha subunit of human chorionic gonadotropin was related to the plasma gastrin levels, a finding confirming the close gastrin dependence of the expression of this protein by oxyntic endocrine cells. No significant changes were observed in mucosal somatostatin D cells. These results indicate that variations in circulating gastrin levels are the most likely factor responsible for the hypotrophic effect of octreotide on oxyntic argyrophil cells (mostly corresponding to the ECL cells) of hypergastrinemic patients.

Topics: Adult; Aged; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Octreotide; Parietal Cells, Gastric; Pyloric Antrum; Stomach Diseases; Zollinger-Ellison Syndrome

The development of gastric enterochromaffin-like (ECL)-cell hyperplasia in humans may be associated with extreme hypergastrinaemia, as occurs in Zollinger-Ellison syndrome (ZES) and pernicious anaemia (type A gastritis). More recently, endocrine cell hyperplasia has been found in all forms of chronic atrophic gastritis and even in cases of focal atrophy. Serum gastrin levels, non-antral gastric endocrine (argyrophil) cell growth, and the severity and type of concomitant gastritis were monitored in 66 unoperated and 8 antrectomized patients with poorly responsive peptic ulcer or reflux oesophagitis during up to 5 years' treatment with high-dose omeprazole, 40 mg daily. A small subgroup of patients (23%) had serum gastrin concentrations of more than four times the normal upper limit. These patients also had hyperplasia of the gastric argyrophil cells. More importantly, the same subgroup of patients had high-grade (atrophic) gastritis. Micronodular hyperplasia of argyrophil cells was significantly more frequent in biopsies showing atrophic gastritis (48%) than in biopsies showing only superficial gastritis (3.6%). It is concluded that, as previously demonstrated in untreated patients with gastric ulcer, the argyrophil cell hyperplasia observed during high-dose omeprazole therapy is related to the progression of chronic atrophic gastritis rather than to serum gastrin levels.

Topics: Biopsy; Esophagitis, Peptic; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Longitudinal Studies; Omeprazole; Peptic Ulcer; Severity of Illness Index

Sixty-four consecutive patients which on upper gastrointestinal endoscopy had endoscopic signs of atrophic body gastritis were investigated with standard histology examinations of gastric biopsies, serology and/or culture for Helicobacter pylori and with standard blood chemistry profile. A histologic diagnosis of atrophy could be made in only 27 of the 64 patients (42%). Of these 27 patients, 5 had the pernicious anaemia (PA) type (19%), 22 had not (81%). Past and/or present H. pylori infection was found in 16/22 non-PA patients (73%) but in none of the PA patients (p = 0.00572). The present study thus confirms earlier findings that non-PA type atrophic body gastritis is more common than the PA type and suggests that, as opposed to PA-type atrophy, it is related to H. pylori infection.

Topics: Adult; Aged; Aged, 80 and over; Anemia, Pernicious; Antibodies, Bacterial; Endoscopy, Gastrointestinal; Enzyme-Linked Immunosorbent Assay; Female; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Prevalence; Radioimmunoassay

Serum concentrations of group I pepsinogens (pepsinogen-I) and gastrin were determined in patients with dementia disorders in order to assess the relationship, if any, between these indices of gastric mucosal function and serum cobalamin (vitamin B12) levels. A significant positive correlation between pepsinogen-I and B12 and, as expected, an inverse relationship between gastrin and pepsinogen-I concentrations was found, indicating that vitamin B12 deficiency was mainly determined by gastric mucosal atrophy (atrophic gastritis) in this West-Swedish sample of patients with dementia disorders. Patients with low B12 but normal gastrin and pepsinogen-I concentrations should, therefore, be further evaluated for possible nutritional deficiency, as well as nongastric causes of poor B12 assimilation from the diet.

Topics: Aged; Aged, 80 and over; Dementia; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Intestinal Absorption; Male; Pepsinogens; Vitamin B 12; Vitamin B 12 Deficiency

To evaluate the characteristics of the gastric mucosa in women with fundic glandular polyps, we examined gastric acid secretion, fasting serum levels of pepsinogen I and gastrin, and gastric histology in 11 female patients with fundic polyps, and compared the results with 30 female controls without endoscopic abnormalities and 50 female patients with gastric foveolar hyperplastic polyps. No significant difference was found in gastric and secretion and fasting serum levels of pepsinogen I and gastrin between the patients with fundic glandular polyps and the control subjects. Histological examination showed that atrophic gastritis was generally not found in the patients with fundic glandular polyps. In contrast, gastric acid secretion and fasting serum levels of pepsinogen I were significantly lower and serum gastrin levels were significantly higher in the patients with foveolar hyperplastic polyps than in the other two groups. Also, patients with foveolar hyperplastic polyps had a higher prevalence and further advanced atrophic gastritis in the fundus than did the other two groups. Our investigations demonstrated that fundic glandular polyps arise from gastric mucosa without atrophic gastritis, whereas foveolar hyperplastic polyps develop from mucosa affected by atrophic gastritis, especially type A gastritis.

Topics: Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Middle Aged; Pepsinogens; Polyps; Stomach Neoplasms

Being pepsinogen A (PGA) levels generally reduced and pepsinogen C (PGC) increased in gastric cancer patients, PGA/PGC ratio has been proposed as a useful marker of the tumour. We tested PGA, PGC and Gastrin (G) levels in patients with gastric cancer (39) and, as a control, in patients with epithelial dysplasia (21), chronic atrophic gastritis (57), gastric ulcer (11) or subjects lacking major or minor endoscopic and microscopic changes at gastroscopy (48). PGA and PGA/PGC levels were significantly reduced in gastric cancer patients (p less than 0.005 and p less than 0.0001 respectively with analysis of variance). Gastrin levels were also reduced in the same patients (p less than 0.005). We therefore adopted an index number (PGA x Gastrin) which was also dramatically reduced in gastric cancer (p less than 0.005); using an arbitrarily chosen cut-off, the "marker" showed very high sensitivity (76%), specificity (96%) and overall accuracy (74%, by Youden J test). We therefore suggest the use of the index number PGA x G in the diagnosis of gastric cancer, as the most useful gastrin presently available, to our knowledge.

Topics: Biomarkers, Tumor; Chronic Disease; Gastrins; Gastritis, Atrophic; Humans; Mathematics; Pepsinogens; Sensitivity and Specificity; Stomach Neoplasms; Stomach Ulcer

The possibilities to screen atrophic corpus gastritis with serum pepsinogen I (S-PGI) and serum gastrin (S-gastrin) concentrations have been studied in 774 subjects: 71 index subjects selected from a general population at random, 353 of their first-degree relatives, 276 first-degree relatives of patients with gastric cancer, 53 patients with pernicious anaemia, and 21 of their relatives. Discrimination function analysis was calculated from members of random and gastric carcinoma families. S-PGI less than 30 ng/ml had a high sensitivity for severe diffuse atrophic corpus gastritis (SDAG) alone (89.5%) and SDAG + severe patchy atrophic corpus gastritis (SPAG) (89.1%). Respective figures for specificity were 91.5% and 94.8%. The discriminatory power of S-PGI less than 30 ng/ml and S-PGI less than 25 ng/ml was of the same order. The sensitivity of low S-PGI decreased sharply in detection of slighter forms of atrophic corpus gastritis. The sensitivity of S-gastrin greater than 100 pmol/l to discriminate SDAG was 57.9% and SDAG+SPAG 58.7%. Respective figures for specificity were 90.2% and 92.2%. Diffuse and patchy atrophic changes behaved similarly regarding S-PGI and S-gastrin mean concentrations. Accordingly, the biopsy specimen with the severest atrophic changes indicates the degree of atrophy, which associates closely with the changes in S-PGI and S-gastrin. In conclusion, severe atrophic (diffuse or patchy) corpus gastritis may be screened from a general population with high sensitivity and specificity by low S-PGI less than 30 ng/ml, whereas an increased level of S-gastrin is too insensitive for this.

Topics: Aged; Anemia, Pernicious; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Pepsinogens; Predictive Value of Tests; Sensitivity and Specificity; Stomach Neoplasms

Serum pepsinogen I (S-PGI) and serum gastrin (S-gastrin) were examined in the screening of three types of atrophic gastritis with inherent high risk of gastric cancer: in 102 cases with severe atrophic corpus gastritis (SACG), in 5 cases with severe atrophic antrum gastritis (SAAG), and in 15 cases with severe atrophic pangastritis (SAPG) (atrophy both in corpus and in antrum) found among 916 subjects from three family series (265 from gastric cancer families, 425 from randomly selected control families and 226 from pernicious anaemia families). There is no way to screen directly atrophic gastritis restricted to the antral mucosa. In pangastritis atrophy of antral glands causes a failure of the hypergastrinemic reaction of achlorhydria. The combination of S-PGI less than 25 micrograms/l + S-gastrin less than 200 pmol/l detected 80.0% of our cases with SAPG, and only 17 subjects of 794 (2.1%) were false positives i.e. who had not advanced atrophic gastritis. The risk of gastric cancer may be significantly higher in SAPG than in SACG. The estimated prevalence of SAPG was 3% in random-family members over 60 years. The combination of S-PGI and S-gastrin is recommended when the cost/benefit ratio in the screening program of gastric cancer is considered and people from a general population are selected for endoscopic studies.

Topics: Anemia, Pernicious; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Middle Aged; Pepsinogens; Risk Factors; Stomach Neoplasms

In patients suffering from chronic pancreatitis with concomitant atrophic antral gastritis, gastrinemia is less whereas the response of pancreatic enzymic secretion to pentagastrin is more potent than in patients suffering from chronic pancreatitis without atrophic alterations in the gastroduodenal mucosa. The pancreas-stimulating effect of pentagastrin administered in a dose of 6 micrograms/kg is approximately equal to the action of 0.5 U/kg pancreozymine and noticeably yields to the effect of 1.5 U/kg pancreozymine (according to the criteria for output of intraduodenally secreted lipase and trypsin). The same diagnostic dose of pentagastrin used commonly for gastric secretion studies not only stimulates pancreatic enzyme secretion but also enhances the activity of beta-cells of Langerhans' islets of the pancreas in accordance with insulinemia and blood C-peptide determined by RIA.

Topics: C-Peptide; Cholecystokinin; Chronic Disease; Dose-Response Relationship, Drug; Gastrins; Gastritis, Atrophic; Humans; Insulin; Islets of Langerhans; Pancreas; Pancreatitis; Pentagastrin; Recurrence

Histological examination of the gastric mucosa was performed in 44 patients with primary Sjögren's syndrome with extraglandular symptoms (mean age 51.9, range 22-76). Biopsy specimens were taken from each of three separate regions: the antrum, the corpus, and the transitional zone between the antrum and the corpus. The incidence of chronic atrophic gastritis was considerably higher in patients with Sjögren's syndrome than in the controls. In the young patients with Sjögren's syndrome atrophic lesions were more common both in the antrum and in the corpus than in the control group. In middle aged patients, however, only the antrum, and in the elderly only the corpus, was much more commonly affected than in the controls. All three types of chronic atrophic gastritis occurred in patients with Sjögren's syndrome. Decreased gastric acid secretion was associated mainly with atrophic gastritis of types A and AB, whereas hypergastrinaemia occurred almost exclusively in gastritis of type A.

Topics: Adult; Aged; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Immunoglobulin G; Middle Aged; Sjogren's Syndrome

A 51 year-old woman with vomitus, intermittent epigastric pain and heartburn had chronic sideropenic anemia. Gastroscopy revealed a subcardial, submucosal tumor. The tumor was removed totally by endoscopic polypectomy. Histologically it was identified as a carcinoid. The endocrinologic examination showed hypergastrinemia caused by chronic atrophic gastritis. The association of this gastric carcinoid with chronic atrophic gastritis type A, hypergastrinemia, hyperplasia of the gastrin-producing antral cells and micronodular hyperplasia of endocrine cells in the gastric fundus, confirms the hypothesis about the pathogenesis of these extremely rare gastric tumors.

Topics: Carcinoid Tumor; Chronic Disease; Female; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Middle Aged; Stomach; Stomach Neoplasms

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

Fundic argyrophil cells were studied for a mean period of 68.7 months (range, 11-170) in 18 patients with fundic atrophic gastritis and achlorhydria. Initially, 12 patients had hyperplasia of the argyrophil cells, the severity of which was assessed using a semiquantitative classification based on the number of argyrophil clusters per square millimeter. At the end of the study, the degree of hyperplasia was unchanged in 9 patients, had decreased in 2, and had increased in 1; no significant increase in the number of argyrophil clusters, precarcinoid changes, or carcinoid tumors were observed and the high level of gastrinemia [mean, 4.8 (range, 1.9-8.1) times the upper limit for normal) did not change significantly. Of the 6 patients with no hyperplasia at the outset of the study, 4 continued without hyperplasia and 2 presented a low-grade hyperplasia at the 20th and 130th month. Gastrinemia increased significantly in the last patient and stayed normal in the other 5. This study argues in favor of the stable appearance of fundic argyrophil cells in patients with atrophic gastritis and stable gastrinemia.

Topics: Achlorhydria; Aged; Aged, 80 and over; Anemia, Pernicious; Biopsy; Female; Gastric Fundus; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Hyperplasia; Male; Middle Aged; Schilling Test

A patient with pernicious anemia, atrophic non-antral gastritis, hypergastrinemia, and widespread hyperplasia of enterochromaffin-like cells and manifest enterochromaffin-like cell carcinoma was followed up during 39 months, including 15 months after gastric resection. In this case normalization of gastrin levels did not prevent the development of multiple gastric carcinoids in the fundic mucosa, suggesting that factors other than gastrin are of importance in the pathogenesis.

Topics: Anemia, Pernicious; Carcinoid Tumor; Follow-Up Studies; Gastrectomy; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Male; Middle Aged; Stomach Neoplasms

Pretrophic and moderately atrophic gastritis is found in the antrum in patients with noncomplicated duodenal ulcer. Normal mucosa or superficial gastritis were observed in the gastric body. Statistically significant worsening of the gastritis of both stomach areas without pronounced atrophic forms, stable decrease of the acid production and the number of parietal cells with a mild increase of the gastrin-producing cells of the antrum are found 1 to 8 years after the selective proximal vagotomy.

Topics: Adult; Chronic Disease; Duodenal Ulcer; Female; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Histocytochemistry; Humans; Male; Postoperative Period; Pyloric Antrum; Time Factors; Vagotomy, Proximal Gastric

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

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

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

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

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

Previous studies have shown that hyperplastic endocrine cells of the oxyntic mucosa in patients with atrophic gastritis may express immunoreactivity for the alpha-subunit of human chorionic gonadotropin (alpha-HCG, common to all glycoprotein hormones). Since this endocrine proliferation is regarded as dependent on the trophic effect of the concomitant hypergastrinemia, the relation between immunohistochemical expression of alpha-HCG by oxyntic endocrine cells and serum levels of gastrin were investigated. The study was performed on endoscopic gastric biopsies of the oxyntic mucosa from 49 patients subdivided into the following groups: A) with histologically normal mucosa and normogastrinemia (22 cases), B) with atrophic gastritis and normogastrinemia (12 cases), C) with normal mucosa and hypergastrinemia (Zollinger-Ellison syndrome, retained antrum) (7 cases) and D) with atrophic gastritis and hypergastrinemia (with or without pernicious anemia) (8 cases). The alpha-HCG immunoreactive cells were found in all hypergastrinemic patients (groups C and D), regardless of the concomitant pathological condition of the mucosa. These cells accounted for 7.8% to 44.7% of the number of Grimelius argyrophil cells in consecutive serial sections. In contrast, alpha-HCG-containing cells were exceptional or absent in most normogastrinemic patients. Their number was sizable in only two cases of group A and three cases of group B, where it ranged from 2.5% to 14.8% of the number of argyrophil cells. It was concluded that expression of alpha-HCG is another feature of oxyntic endocrine cells associated with hypergastrinemia in addition to those previously recognized such as development of hyperplasia and/or carcinoid tumors.

Topics: Adolescent; Adult; Aged; Chorionic Gonadotropin; Chronic Disease; Endocrine Glands; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Immunologic Techniques; Middle Aged; Parietal Cells, Gastric; Staining and Labeling

Topics: Achlorhydria; Antacids; Carcinoid Tumor; Enterochromaffin Cells; Gastrins; Gastritis, Atrophic; Histamine H2 Antagonists; Humans; Hyperplasia; Peptic Ulcer; Risk; Somatostatin; Stomach Neoplasms; Vagotomy, Proximal Gastric

Topics: Calcitonin; Female; Gastrins; Gastritis, Atrophic; Humans; Hyperparathyroidism; Male; Middle Aged; Multiple Endocrine Neoplasia; Prolactin

Topics: Adult; Duodenal Ulcer; Female; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Pyloric Antrum; Somatostatin; Stomach Ulcer

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

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

Gastric mucosal pepsinogen A phenotype, serum pepsinogen A level, serum pepsinogen C level, serum pepsinogen A/pepsinogen C ratio, and serum gastrin level were evaluated as potential markers for gastric cancer or its precursors in 19 healthy volunteers and 341 patients from the gastroscopy program. Gastric cancer, atrophic gastritis, and intestinal metaplasia of the stomach were associated with pepsinogen A phenotypes, characterized by an intense fraction 5, and with a low serum pepsinogen A level (less than 25 micrograms/l), a low serum pepsinogen A/pepsinogen C ratio (less than 1.5), and a high serum gastrin level (greater than 79 ng/l). The specificity of pepsinogen A phenotypes with an intense fraction 5 for gastric cancer or its precursors was 95.1% with a sensitivity of 20.4%. The sensitivity and specificity of the noninvasive tests were evaluated with the receiver operating characteristic. For clinical purposes, a serum pepsinogen A/pepsinogen C ratio less than 1.8 is the most suitable test, with a sensitivity of 74% and a specificity of 76% for gastric cancer or its precursors, with a reference population of patients with benign gastric disorders. However, the sensitivity and specificity of the single or combined tests are too low for population screening purposes.

Topics: Adult; Aged; Gastrins; Gastritis, Atrophic; Humans; Intestines; Isoenzymes; Metaplasia; Middle Aged; Pepsinogens; Phenotype; Stomach Neoplasms

Grimelius reaction and immunohistochemical PAP method were used to study endocrine cells producing gastrin (G-cells), somatostatin (D-cells) and gamma-endorphin (GER-cells) in gastric and duodenal mucosa of 95 males with atrophic gastritis with intestinal and pyloric metaplasia. The number of cells was counted per 1 mm2 of the mucosa. In the cases of marked intestinal metaplasia the number of G-, GER- and especially D-cells in the pyloric region non-metaplastic epithelium decreases and is approaching to its number in the duodenum of the control group. In the foci of marked pyloric metaplasia of gastric corpus the number of G- and GER-cells is almost the same as in the zones of gastric metaplasia of duodenum, and is approximating their number in the pyloric region of controls, thus allowing the designation of pyloric metaplasia as a complete one.

Topics: Adolescent; Adult; Aged; APUD Cells; Biopsy; Duodenal Ulcer; Duodenum; Endorphins; gamma-Endorphin; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Histocytochemistry; Humans; Immunoenzyme Techniques; Metaplasia; Middle Aged; Pylorus; Somatostatin; Stomach Ulcer

Fifty-eight subjects including controls, patients with duodenal ulcer, non-operated or treated with a superselective vagotomy underwent endoscopic fundic and antral biopsies. Histologic classification of the two mucosae was performed. We examined the relationship between the histologic grade of gastritis in the two mucosae, then between the histologic aspect of the antral mucosa and antral gastrin-and somatostatin-cell densities, the basal intraluminal secretion of gastrin and somatostatin. There was a significant correlation between the histologic aspect of fundic or antral mucosa and the age of patients, except in the case of vagotomized patients. Fundic and antral histologic patterns were also correlated in each patient, except for vagotomized. Gastrin and somatostatin cell densities showed no variation in function of the degree of inflammation of non atrophic gastritis. These cell densities showed a tendency to decrease in atrophic gastritis, especially when intestinal metaplasia was present. Intraluminal gastrin secretion was increased in patients with mild atrophic gastritis (p less than 0.05 to p less than 0.02) in comparison with those whose histology was roughly normal. It was also increased in severe atrophic gastritis. The highest intraluminal secretion of somatostatin was observed in patients with mild atrophic gastritis while this secretion fell noticeably in those showing severe atrophic gastritis, as compared to the other groups. This work seems to suggest a relationship between intraluminal peptides and the evolution of gastritis. While results are still preliminary, they do not indicate that these peptides, thus released, play any pathophysiologic role.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Duodenal Ulcer; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Prospective Studies; Somatostatin; Vagotomy, Proximal Gastric

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

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

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

Duodenal gastrin concentration was measured in endoscopic forceps biopsy specimens of the juxta-pyloric duodenal mucosa in patients with various gastrointestinal disorders. Duodenal gastrin concentration was 5.9 +/- 1.2 ng/mg (mean +/- 1 SEM) in control patients. Duodenal gastrin concentration was similar to control values in patients with duodenal ulcer, pyloric channel ulcer, vagotomy and pyloroplasty, and gastric atrophy and hypergastrinemia. In gastric ulcer patients, duodenal gastrin concentration, 2.8 +/- 0.6 ng/mg, was significantly less than the control value (P less than 0.05). Duodenal gastrin concentration was approximately one third of antral gastrin concentration in control, duodenal ulcer, and gastric ulcer patients and was approximately one fifth of antral gastrin concentration in vagotomy and pyloroplasty patients and gastric atrophy patients. Duodenal and antral gastrin concentrations were significantly correlated in normal controls and in gastric ulcer patients. The finding of normal duodenal gastrin concentration in patients with vagotomy and pyloroplasty and patients with gastric atrophy suggests that, unlike antral gastrin concentration, duodenal gastrin concentration is unaffected by a decrease in acid secretion rate. The low duodenal gastrin concentration in gastric ulcer patients indicates that the duodenum may be involved in the pathophysiology of gastric ulcer disease.

Topics: Biopsy; Duodenal Ulcer; Duodenum; Gastrins; Gastritis, Atrophic; Gastrointestinal Diseases; Humans; Intestinal Mucosa; Pyloric Antrum; Stomach Ulcer

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

Five patients with megaloblastic anemia due to deficiency of vitamin B12 and achlorhydria and six normal controls participated in the study. The patients with pernicious anemia (PA) had elevated plasma gastrin levels, as expected, and lower plasma somatostatin (SST) levels than the control patients. The amount of gastrin and SST in the antral mucosa did not differ in the two groups of patients. In the fundic mucosa, the patients with PA had increased tissue concentrations of both gastrin and SST as compared with the tissue concentrations in the controls. These findings of hormone tissue concentrations were correlated to the number of argyrophilic cells. Thus, in the antral mucosa the number of argyrophilic cells did not differ in patients with PA and in the controls. In the fundic mucosa, however, the number of argyrophilic cells was significantly elevated in patients with PA as compared with the controls.

Topics: Aged; Anemia, Pernicious; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Somatostatin

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

Topics: Gastrins; Gastritis, Atrophic; Gastrointestinal Diseases; Humans; Peptic Ulcer; Radioimmunoassay; Stomach Neoplasms

Prior to a study of the pathophysiological significance of chronic atrophic gastritis and hypergastrinemia, we evaluated a new radioimmunoassay kit for serum total gastrin (Diagnostic Products Corp.). The mean intra-assay CV ranged from 2 to 5% (2386 patients' samples in 47 assay runs done during four months). Total CVs for two controls ranged from 4 to 10%. Within-assay bias was 5%. Oleate decreased the values, indicating that intravenous heparin, which releases endothelial lipase, causing in vitro lipolysis, should be avoided if indwelling catheters are used for sampling, e.g., during provocation tests for gastrin release. Of three other commercial kits examined, two were affected by oleate. Other anions such as heparin and EDTA also affected the assay. Values for gastrin in heparinized plasma from surgical patients representing a variety of disorders agreed well with results obtained by a reference laboratory. We confirm the usefulness of this assay for discriminating clinical situations and conclude that ligand assays, besides those for thyroid assessment, should be assessed for interference from nonesterified fatty acids. Preliminary data also suggest a marked age dependence of serum gastrin concentration.

Topics: Adult; Aged; Anticoagulants; Evaluation Studies as Topic; Fatty Acids, Nonesterified; Female; Gastrins; Gastritis, Atrophic; Gastrointestinal Diseases; Humans; Lipids; Male; Middle Aged; Radioimmunoassay; Reagent Kits, Diagnostic

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

The distribution of G-cells in the gastric glands was studied quantitatively using the indirect immunoperoxidase method in 37 resected stomachs: 11 for esophageal cancer, 14 for gastric cancer, 4 for gastric ulcer, 7 for duodenal ulcer, and 1 for atypical epithelium. G-cells were seen in the pyloric glands and in the pseudopyloric glands in the atrophic fundic gland area. No G-cells were found in the fundic glands or in the cardiac glands. There was a significant correlation between the number of G-cells and the pyloric and/or pseudopyloric glandular tubes (p less than 0.01). The number of G-cells per glandular tube was 1.9 +/- 0.5 in the pyloric glands and 1.2 +/- 0.4 in the pseudopyloric glands on the pyloric part of the atrophic fundic gland area. G-cells were rarely seen in the pseudopyloric glands on the cardiac part of the atrophic fundic gland area. It is suggested that the pseudopyloric glands without G-cells in the cardiac region are akin to cardiac glands.

Topics: Adult; Aged; Cell Count; Enterochromaffin Cells; Female; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Immunoenzyme Techniques; Male; Middle Aged; Pyloric Antrum

The serum values of PG I and gastrin have been established in a normal population and in several clinical diseases. The PG I is raised in duodenal, gastric, and pyloric ulcer even though the gastrin is normal. Both PG I and gastrin values are raised in renal insufficiency and the Zollinger-Ellison syndrome. The PG I is lowered in atrophic gastritis and alcoholic cirrhosis, and is at the limit of detection in Biermer anemia and total gastrectomy. Insulin and sham-feeding are stimulants for PG I release by patients with duodenal ulcer, but no correlation is observed between PG I output and PAO in the studied group. The results show that PG I is able to distinguish between associated hypergastrinemia and hypoacidity (Biermer anemia type) or a hyperacidity (Zollinger-Ellison syndrome type), and that PG I is a good indicator for gastric hypoacidity. Overlapping between normal and ulcer subjects is comparable to those obtained in acid output determinations.

Topics: Adolescent; Adult; Aged; Anemia, Pernicious; Duodenal Ulcer; Female; Gastrectomy; Gastrins; Gastritis, Atrophic; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Male; Middle Aged; Pepsinogens; Reference Values; Stomach Ulcer; Zollinger-Ellison Syndrome

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

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

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

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

Topics: Acupuncture Therapy; Adult; Aged; Duodenal Ulcer; Fasting; Female; Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Zollinger-Ellison Syndrome

Topics: Gastrins; Gastritis, Atrophic; Humans; Male; Middle Aged; Radionuclide Imaging; Sodium Pertechnetate Tc 99m; Stomach Neoplasms; Technetium; Tetragastrin

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

Topics: Adult; Aged; Female; Gastric Acid; Gastrins; Gastritis, Atrophic; Humans; Hydrogen-Ion Concentration; Male; Middle Aged

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

A histological and immunohistological investigation was performed on biopsy specimens from ten patients 3 to 35 years after antrectomy, to study the type of epithelium and the possible occurrence of gastrin-producing cells (G cells) in the distal stump of the stomach remnant. The study showed that parietal cells were present in all patients, whereas G cells could not be demonstrated, although areas of pyloric-type epithelium (pseudopyloric metaplasia, were seen in eight. We conclude that the pyloric-type metaplasia, which occurs in the fundic mucosa after antrectomy, does not involve the G cells. It is suggested that the normal levels of fasting serum gastrin in these patients originate from outside the gastric mucosa, presumably from the duodenal bulb.

Topics: Adenocarcinoma; Biopsy; Epithelium; Fibrosis; Follow-Up Studies; Gastrectomy; Gastric Acid; Gastrin-Secreting Cells; Gastrins; Gastritis, Atrophic; Gastroscopy; Humans; Postoperative Period; Pyloric Antrum; Radioimmunoassay; Stomach Neoplasms; Stomach Ulcer; Time Factors

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

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: Animals; Fasting; Female; Gastrins; Gastritis, Atrophic; Gastrointestinal Diseases; Humans; Kidney; Male; Rabbits; Radioimmunoassay

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