gastrins and Chronic-Disease

The use of proton pump inhibitors (PPIs) over the last 30 years has rapidly increased both in the United States and worldwide. PPIs are not only very widely used both for approved indications (peptic ulcer disease, gastroesophageal reflux disease (GERD), Helicobacter pylori eradication regimens, stress ulcer prevention), but are also one of the most frequently off-label used drugs (25-70% of total). An increasing number of patients with moderate to advanced gastroesophageal reflux disease are remaining on PPI indefinitely. Whereas numerous studies show PPIs remain effective and safe, most of these studies are <5 years of duration and little data exist for >10 years of treatment. Recently, based primarily on observational/epidemiological studies, there have been an increasing number of reports raising issues about safety and side-effects with very long-term chronic treatment. Some of these safety issues are related to the possible long-term effects of chronic hypergastrinemia, which occurs in all patients taking chronic PPIs, others are related to the hypo-/achlorhydria that frequently occurs with chronic PPI treatment, and in others the mechanisms are unclear. These issues have raised considerable controversy in large part because of lack of long-term PPI treatment data (>10-20 years). Zollinger-Ellison syndrome (ZES) is caused by ectopic secretion of gastrin from a neuroendocrine tumor resulting in severe acid hypersecretion requiring life-long antisecretory treatment with PPIs, which are the drugs of choice. Because in <30% of patients with ZES, a long-term cure is not possible, these patients have life-long hypergastrinemia and require life-long treatment with PPIs. Therefore, ZES patients have been proposed as a good model of the long-term effects of hypergastrinemia in man as well as the effects/side-effects of very long-term PPI treatment. In this article, the insights from studies on ZES into these controversial issues with pertinence to chronic PPI use in non-ZES patients is reviewed, primarily concentrating on data from the prospective long-term studies of ZES patients at NIH.

Topics: Animals; Carcinoma, Neuroendocrine; Chronic Disease; Gastrinoma; Gastrins; Humans; Proton Pump Inhibitors; Risk Factors; Stomach Diseases; Time Factors; Treatment Outcome; 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

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

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

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

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

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

Helicobacter pylori is highly adapted to its unusual ecological niche in the human stomach. Urease activity permits H. pylori survival at a pH of <4 in vitro and is required for the organism to colonize in animal models. However, urease does not play an important role in the survival of the organism in a pH range between 4 and 7. Other mechanisms of pH homeostasis remain poorly understood, but preliminary studies indicate that novel proteins are produced when H.pylori cells are shifted from pH 7 to 3, and the gene encoding a P-type adenosine triphosphatase that may catalyze NH4+/H+ exchange across the cytoplasmic membrane has been cloned. Mechanisms of pH homeostasis in other enteric bacteria are reviewed and provide insight into additional pathways that may be used by H. pylori. An important adaptation of H. pylori to the gastric environment may be its ability to alter gastric acid secretion. Acute infection is associated with transient hypochlorhydria, whereas chronic infection is associated with hypergastrinemia and decreased somatostatin levels. Thus, the survival of H. pylori in the gastric environment may be attributed to both the development of specialized intrinsic defenses and the organism's ability to induce physiological alterations in the host environment.

Topics: Acute Disease; Chronic Disease; Cytoplasm; Duodenal Ulcer; Enterococcus faecalis; Escherichia coli; Gastric Acid; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Salmonella; Somatostatin; Urease

Topics: Chronic Disease; Duodenal Ulcer; Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Stomach Ulcer

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

In the Zollinger-Ellison syndrome, fundic argyrophil carcinoid tumors occur almost exclusively in the small subgroup of patients who also have multiple endocrine neoplasia type 1. In these patients, tumor development seems related to the same genetic alterations as those observed in other endocrine tumors related to multiple endocrine neoplasia type 1. We report here the second detailed case of a patient with sporadic Zollinger-Ellison syndrome who developed an argyrophil carcinoid tumor in nonatrophic fundic mucosa, suggesting that chronic hypergastrinemia may lead to fundic carcinoid development in nongenetically predisposed patients.

Topics: Aged; Biopsy; Carcinoid Tumor; Chronic Disease; Diagnosis, Differential; Female; Gastric Fundus; Gastric Mucosa; Gastrins; Humans; Multiple Endocrine Neoplasia Type 1; Silver Staining; Stomach Neoplasms; Zollinger-Ellison Syndrome

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

Serum gastrin levels were measured preoperatively and at several intervals postoperatively in 262 patients who underwent highly selective vagotomy for duodenal ulcer. An increase of serum gastrin levels was demonstrated postoperatively in all patients, irrespective of sex, length of history, acid secretion data or recurrence. At several years postoperatively, a highly significant secondary rise in serum gastrin levels was observed, which corresponded well to recent physiologic and morphologic data. The most suitable explanation appeared to be that the proximal gastric vagotomy (vagotomy of the fundus and corpus) abolished the vagally mediated inhibition of the G-cells in the antrum (disinhibition of the oxyntopyloric reflex). The serum gastrin values were always higher and the secondary postoperative increase was earlier for patients who had taken cimetidine preoperatively. Contrary to traditional expectations, no correlation at all was found between serum gastrin levels and acid secretion data. Recurrence could not be predicted on the basis of serum gastrin levels.

Topics: Adult; Chronic Disease; Cimetidine; Duodenal Ulcer; Evaluation Studies as Topic; Female; Follow-Up Studies; Gastrins; Humans; Male; Middle Aged; Premedication; Recurrence; Sex Factors; Vagotomy, Proximal Gastric

The action of acute and chronic administration of ethanol on pancreatic exocrine secretion in humans and several animal species is reviewed. If the data concerning the secretory action of ethanol on the pancreas are to the property assessed, several experimental variables have to be considered. Acute intravenous administration of ethanol inhibits basal and hormonally stimulated pancreatic secretion of bicarbonate and protein in nonalcoholic humans and most species of animals tested. Oral or intraduodenal ethanol causes moderate stimulation of pancreatic bicarbonate and enzyme secretion. Since anticholinergic agents and truncal vagotomy diminish the ethanol-induced inhibition of pancreatic secretion in the intact animal, it is possible that the action of ethanol on the pancreas is at least partly mediated by inhibitory cholinergic mechanisms. The action of ethanol on the pancreas may also be mediated by release of gastrointestinal hormones. Intravenous and oral administration of ethanol releases gastrin in dogs but not in humans. Pancreatic polypeptide is unlikely to be the hormonal mediator of the ethanol-induced inhibition of exocrine pancreatic secretion in humans and dogs, since ethanol does not release pancreatic polypeptide. The main secretory changes induced by chronic alcoholism in humans and dogs are increased basal secretion of pancreatic enzymes and decreased basal bicarbonate output, and these secretory changes may favour the occurrence of protein precipitates which are believed to be the first lesion of chronic pancreatitis in man. A decrease in the concentration of "pancreatic stone protein" in pancreatic juice may favour the development of protein precipitates in chronic alcoholic patients.

Topics: Acute Disease; Alcoholism; Animals; Calcium-Binding Proteins; Cholecystokinin; Chronic Disease; Dogs; Duodenum; Ethanol; Food; Gastric Juice; Gastrins; Gastrointestinal Hormones; Humans; Lithostathine; Nerve Tissue Proteins; Pancreas; Pancreatic Juice; Pancreatic Polypeptide; Pancreatitis; Secretin; Sphincter of Oddi; Stomach

Topics: Animals; Cholecystokinin; Chronic Disease; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Insulin; Insulin Secretion; Pancreatic Hormones; Pancreatic Polypeptide; Pancreatitis

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

Topics: Cholecystokinin; Chronic Disease; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Insulin; Pancreatic Hormones; Pancreatic Polypeptide; Pancreatitis; Secretin

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

Topics: Acute Disease; Alcoholism; Animals; Autoradiography; Bicarbonates; Chronic Disease; Dogs; Enzyme Inhibitors; Ethanol; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Humans; Pancreas; Pancreatic Juice; Pancreatitis; Proteins; Rabbits; Rats; Secretory Rate; Sphincter of Oddi

Topics: Anemia, Hypochromic; Body Weight; Bone Diseases; Chronic Disease; Diarrhea; Dumping Syndrome; Duodenal Obstruction; Duodenal Ulcer; Female; Follow-Up Studies; Gastrectomy; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Insulin; Male; Methods; Pentagastrin; Peptic Ulcer; Peptic Ulcer Hemorrhage; Peptic Ulcer Perforation; Postoperative Complications; Recurrence; Stomach Ulcer; Vomiting

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

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

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

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

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

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

Topics: Acute Disease; Adenoma, Islet Cell; Cholecystokinin; Chronic Disease; Gastrins; Humans; Methods; Pancreas; Pancreas Transplantation; Pancreatic Diseases; Pancreatic Neoplasms; Pancreatitis; Radiography; Secretin; Transplantation, Homologous; Zollinger-Ellison Syndrome

Topics: Animals; Chronic Disease; Dogs; Duodenal Ulcer; Gastric Acidity Determination; Gastric Juice; Gastrins; Histamine; Homocysteine; Humans; Liver Cirrhosis; Liver Diseases; Stomach

To observe the therapeutic efficacy of acupoint heat-sensitization moxibustion on chronic diarrhea patients as well as its effects on the levels of gastrointestinal neurotic mediators such as serum gastrin (GAS) and plasma motilin (MTL).. Sixty chronic diarrhea patients of Pi-Shen deficiency syndrome were randomly assigned to Group A (30 cases, treated with acupoint heat-sensitization moxibustion, once daily) and Group B (30 cases, treated with Changtai Oral Liquid, 10 mL each time, three times daily). The therapeutic course was 4 weeks. Another 20 healthy volunteers were recruited as the health control group. The levels of serum GAS and plasma MTL were detected using radioimmunoassay before and after treatment. The cured rate, the markedly effective case, the effective case, the ineffective case, and the total effective rate were calculated by the end of the treatment.. Before treatment the serum GAS level was lower and the plasma MTL level higher in the two patient groups than in the health control group with statistical difference (P<0.05). There was no statistical difference in the symptom integral between the two patient groups and the health control group (P>0.05). After treatment the serum GAS level increased, the plasma MTL level and the symptom integral decreased in the two patient groups, showing statistical difference when compared with the same group before treatment (P<0.05, P<0.01). After treatment the symptom integral was lower in the treatment group than in the control group with statistical difference (P<0.05). There was no statistical difference in the GAS and MTL levels between the two patient groups (P>0.05). The total effective rate for clinical symptoms was significantly higher in Group A than in Group B with statistical difference (93.3% vs 73.3%, P<0.05).. The therapy of acupoint heat-sensitization moxibustion was effective for chronic diarrhea patients of Pi-Shen deficiency syndrome. It could regulate the levels of serum GAS and plasma MTL and improve the patients' clinical symptoms.

Topics: Adult; Case-Control Studies; Chronic Disease; Diarrhea; Female; Gastrins; Humans; Male; Medicine, Chinese Traditional; Middle Aged; Motilin; Moxibustion; Single-Blind Method; Yang Deficiency; Yin Deficiency

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

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

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

After pylorus-preserving Whipple (PPW), delayed gastric emptying (DGE) is reported in up to 50% of these patients. We analyzed gastric emptying and hormonal adaptation of cholecystokinin (CCK), pancreatic polypeptide (PP), and gastrin following two surgical procedures for chronic pancreatitis (CP): the PPW and the duodenum-preserving pancreatic head resection (DPPHR).. Ten patients underwent DPPHR and 10 underwent PPW for CP. Preoperatively and 10 days and 6 months postoperatively, gastric emptying (paracetamol absorption test) and CCK, gastrin, and PP were measured using a test meal stimulation.. The area under the serum paracetamol time curve for 0 to 120 minutes (AUC) showed no preoperative difference. Ten days postoperatively, the AUC was significantly reduced (P <0.05) after PPW but not after DPPHR. Six months postoperatively, AUC was comparable with the preoperative findings in DPPHR and PPW. The integrated 180-minute PP release was significantly reduced 10 days and 6 months postoperatively in both groups. The integrated 180-minute CCK release was decreased 10 days after PPW, but failed to be significant (P = 0.053). Gastrin levels were postoperatively unchanged.. Following DPPHR we found no delay in gastric emptying. In contrast, DGE occurs early after PPW. Our data may help explain the slower recovery in PPW patients with regard to weight gain and relief from pain, which may be due to the functional alteration of gastric emptying and motility after this type of surgery.

Topics: Acetaminophen; Adult; Cholecystokinin; Chronic Disease; Female; Gastric Emptying; Gastrins; Humans; Male; Middle Aged; Pancreatic Polypeptide; Pancreaticoduodenectomy; Pancreatitis; Postoperative Complications

Sixty patients who presented with erosive/ulcerative refractory reflux esophagitis were randomized to receive a 4- to 8-week treatment with omeprazole 20 mg daily, or ranitidine 150 mg twice daily. Patients not healed after treatment were given the same drugs at doubled doses for a second period of equal duration. Patients still unhealed after this received open treatment with omeprazole 20 mg twice daily for a third period of 4 to 8 weeks. Endoscopic assessment and clinical and laboratory evaluation were performed every 4 weeks until there was complete esophageal mucosal repair. After 4 weeks, complete healing was observed in 50% of patients on omeprazole 20 mg daily, compared with 20.7% on ranitidine 150 mg twice per day (p < 0.01). After 8 weeks, the figures were 79.3% versus 34.5% (p < 0.5). With doubled doses after 4 weeks, complete healing was achieved in 96.6% of patients on omeprazole 40 mg daily, compared with 64.2% on ranitidine 300 mg twice per day (p < 0.05). The eight still "refractory" patients (one omeprazole, seven ranitidine) healed completely with 8 more weeks of omeprazole 20 mg twice daily. Patients treated with omeprazole experienced faster relief of heartburn, which disappeared in 60% of patients after 4 weeks, as compared to 21% of patients treated with ranitidine (p < 0.006). Apart from the mode of treatment, the only factor that proved to be related to healing at multivariate analysis was the pretreatment severity of gastroesophageal reflux, as measured by esophageal pH monitoring. Our study confirms that omeprazole, even at a low dosage, is the choice for refractory reflux esophagitis.

Topics: Adult; Chronic Disease; Double-Blind Method; Drug Administration Schedule; Drug Resistance; Esophagitis, Peptic; Esophagus; Female; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Omeprazole; Prognosis; Ranitidine; Time Factors; Treatment Outcome

Twenty-nine nongastrectomized and three partially gastrectomized patients with chronic reflux esophagitis resistant to 12 weeks' treatment with histamine H2-receptor antagonists were treated with a daily oral dose of 20-40 mg of omeprazole for 12-30 months. Basal serum gastrin, serum pepsinogen A, and serum pepsinogen C concentrations were monitored at regular intervals. Serum gastrin levels significantly (P less than 0.01) increased threefold to fourfold during the first 1-2 months of the study when all patients ingested 40 mg of omeprazole daily. Dose reduction to 20 mg did not significantly decrease gastrin levels. Serum gastrin levels showed a trend to further increase after the first 3 months of treatment, reaching statistically significant differences for values from the 3-12-month period (P less than 0.05) and from the 3-24-month period (P less than 0.005). Women and patients with high basal serum gastrin levels before omeprazole treatment were more likely to achieve higher serum gastrin levels during omeprazole treatment. Serum pepsinogen A and C levels were significantly (P less than 0.01) increased at all time intervals during long-term treatment with omeprazole. No significant tendency toward higher serum pepsinogen C levels in time was observed. However, serum pepsinogen A levels and the ratio of pepsinogen A to pepsinogen C further increased significantly (P less than or equal to 0.05) during the initial 3-12-month period. However, this trend was not observed anymore afterward. Antrectomized patients did not show increases in serum gastrin and serum pepsinogen A and C levels, suggesting that hypergastrinemia may be involved in the observed hyperpepsinogenemia.

Topics: Aged; Chronic Disease; Drug Administration Schedule; Esophagitis, Peptic; Female; Gastrectomy; Gastrins; Humans; Male; Middle Aged; Multicenter Studies as Topic; Omeprazole; Pepsinogens; Sex Factors

Zoujin pill (ZJP), a medication used to treat gastrointestinal disorders since the 15th Century in China, have been reported to exert anti-depressant effects in various models.. To assess the effects of ZJP on gastrointestinal function and depressive behavior in rats under chronic unpredictable mild stress (CUMS), and to examine the underlying mechanisms related to brain-gut axis.. The rats suffered the stressor once daily for 5 weeks. ZJP (0.6 and 1.2 g/kg) and fluoxetine (15 mg/kg) as positive control were administered to the rats through gastric intubation once daily for 5 consecutive weeks. The anti-depression effects were compared by performing sucrose preference tests and open field tests. Gastrointestinal motility was investigated by determining the gastrointestinal transit rate and by electrogastrogram. The serum levels of the gastrointestinal hormone (GAS, MOT, VIP, SP), inflammatory cytokine (IL-1β, IL-6; , TNFα) and glucagon-like peptide-1 (GLP-1) were assayed by enzyme-linked immunosorbent assay. For monoamine neurotransmitters (NE, 5-HT, DA), the levels were determined by high-performance liquid chromatography and electrochemical detection in conjunction, which was applied on the samples taken from the hypothalamus, hippocampus, and striatum.. The depression-like symptoms among rats under CUMS were significantly relieved by ZJP administration (0.6 and 1.2 g/kg). Gastrointestinal motility was also improved by restoring gastric electrical rhythm and promoting gastrointestinal propulsion. The ZJP at 0.6 g/kg dosage obviously up-regulated 5-HT and DA levels in hippocampus. The ZJP at 1.2 g/kg dosage could increase 5-HT and DA levels in hypothalamus, striatum, and hippocampus, while down-regulated the NE level in hypothalamus and hippocampus. ZJP also reversed the alterations in serum gastrointestinal hormones. Furthermore, treatment with ZJP significantly reduced levels of IL-1β, IL-6 and TNF-α and increased serum GLP-1 compared with the CUMS group. Fluoxetine also exerted similar anti-depressant effects in the absence of effects on gastrointestinal motility and the levels of serum hormone, inflammatory cytokine and GLP-1.. ZJP imposed anti-depressant and gastrointestinal regulating functions in rats under CUMS, suggesting potential clinical application. .

Topics: Animals; Antidepressive Agents; Behavior, Animal; Biogenic Monoamines; Brain; Chronic Disease; Cytokines; Depression; Drugs, Chinese Herbal; Gastrins; Gastrointestinal Transit; Glucagon-Like Peptide 1; Intestine, Small; Male; Motilin; Rats, Sprague-Dawley; Stress, Psychological; Substance P; Vasoactive Intestinal Peptide

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

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

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

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

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

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

To establish a rat model mimicking human bile reflux for studying the pathological effects of chronic bile reflux.. The duodenum of Sprague-Dawley rats was transected below the opening of the common bile duct, and a gastrojejunostomy was performed at the greater curvature of the forestomach. After the rats demonstrated bile reflux for 1 year, we studied the pathological features of the glandular stomach and forestomach mucosa. We also studied the effect of bile reflux on gastrin expression in the glandular stomach mucosa by using immunohistochemistry.. Chronic bile reflux caused significant hyperplasia and expansion of gastric glands in the glandular stomach. Dysplasia and cancer formation also developed, but the incidence was significantly lower than that reported in the literature. Intestinal metaplasia and ulceration in the glandular stomach were also rare. In the forestomach, the squamous epithelium showed significant hyperplasia and keratinization along with keratin pearls and keratocysts. Intestinal metaplasia was rare and no tumorigenesis was observed. Chronic bile reflux significantly increased gastrin expression in the glandular stomach mucosa.. When simulating the physiological bile reflux pathway, chronic bile reflux caused hyperplasia and expansion of gastric glands in the glandular stomach and squamous epithelial hyperplasia and keratinization in the forestomach.

Topics: Animals; Bile Reflux; Chronic Disease; Disease Models, Animal; Duodenum; Gastric Bypass; Gastric Mucosa; Gastrins; Hyperplasia; Male; Rats; Rats, Sprague-Dawley

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

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

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

A 26-year-old man was admitted to hospital with a 6-month history of diarrhea and abdominal pain. Before admission, upper and lower gastrointestinal endoscopy had shown a mild erosive duodenitis and the patient was started on a proton pump inhibitor. Physical examination and laboratory tests on admission were not constructive. In addition, repeated gastrointestinal endoscopy, cross-sectional imaging and neuroendocrine markers did not point to a specific etiology. Therefore, as a provocation test, the proton pump inhibitor therapy was discontinued. Discontinuation resulted in a progression of the patient's symptoms and an endoscopic detection of duodenal ulcers. Except for the normal serum gastrin levels, this constellation was suggestive of a gastrinoma, so that further investigations were initiated. Subsequently, the diagnosis could be confirmed and the gastrinoma located. After successful pancreaticoduodenectomy, the patient was symptom-free.. As part of a systematic investigation on chronic diarrhea, the work-up for neuroendocrine causes can play an important role. In this context, it should be kept in mind that some gastrinoma patients present without an elevation of serum gastrin levels. Regardless of a negative gastrin test, a typical symptom constellation should therefore prompt further investigations.

Topics: Abdominal Pain; Adult; Chronic Disease; Diagnosis, Differential; Diarrhea; Duodenal Ulcer; Duodenitis; Follow-Up Studies; Gastrinoma; Gastrins; Gastroscopy; Humans; Lymphatic Metastasis; Male; Pancreatic Neoplasms; Pancreaticoduodenectomy

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Candida albicans frequently inhabits the gastrointestinal tract of humans leading to gastrointestinal candidiasis, especially following suppression of gastric acidity, but studies on the relation between this fungal infection and gastric pathology are limited due to lack of convenient animal models resembling Candida infection in humans. MATERIAL AND METHODS. We compared the effects of C. albicans and vehicle inoculation on gastric secretion and healing of gastric ulcers induced by acetic acid in rats treated with 1) ranitidine (30 mg kg(-1) day(-1) s.c.) and 2) aspirin (ASA) (60 mg kg(-1) day(-1) i.g.) with or without probiotic bacteria Lactobacillus acidophillus. At day 0 and at 4, 15 and 25 days after ulcer induction, the ulcer area, the gastric blood flow (GBF), the quantitative gastric cultures of Candida and the expression of mRNAs for pro-inflammatory cytokines IL-1beta and TNF-alpha and growth factors EGF and TGFalpha were assessed in the gastric mucosa.. Gastric acid output was reduced by over 40% soon after Candida inoculation and this effect persisted during all time intervals tested. The area of ulcers in control rats significantly decreased at day 15 and the ulcers disappeared almost completely after 25 days of their induction. In contrast, the ulcers were present until day 25 in Candida-inoculated rats followed by a fall in GBF and a rise in plasma gastrin levels, these effects being significantly attenuated by the co-treatment with Lactobacillus. Candidiasis was accompanied by up-regulation of mRNA for IL-1beta, TNF-alpha, EGF and TGFalpha and a significant increment in plasma IL-1beta and TNF-alpha levels.. 1) Persistent colonization with Candida could be achieved in rats treated with antisecretory agents or non-steroidal anti-inflammatory drugs (NSAIDs) such as ASA; 2) candidiasis reduces gastric acid secretion, while delaying ulcer healing possibly due to the impairment in GBF in the ulcer area and enhanced expression and release of IL-1beta and TNFalpha and 3) probiotic therapy could be useful in the treatment against the deleterious action of fungal infection on the healing of pre-existing gastric ulcers.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Aspirin; Biopsy; Blood Flow Velocity; Candida albicans; Chronic Disease; Colony Count, Microbial; Cytokines; Disease Models, Animal; Electrophoresis, Agar Gel; Gastric Juice; Gastric Mucosa; Gastrins; Gene Expression Regulation; Lactobacillus acidophilus; Male; Microcirculation; Probiotics; Ranitidine; Rats; Rats, Wistar; RNA, Messenger; Stomach Ulcer

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

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

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

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

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

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

This study evaluates serum gastrin concentrations in dogs with chronic lymphocytic-plasmacytic enteritis, as well as its possible relationship with the severity of lesions present in the stomach. To achieve this aim, 5 dogs without gastrointestinal disease and 15 dogs with chronic lymphocytic-plasmacytic enteritis were included. Serum gastrin concentrations were significantly increased in dogs with chronic lymphocytic-plasmacytic enteritis compared with those in dogs without gastrointestinal disease. Also, there was a positive correlation between the severity of the gastric lesion and the serum gastrin concentration. Our findings indicate the possibility that gastrin plays a role in the etiology of an accompanying chronic antral gastritis in canine chronic lymphocytic-plasmacytic enteritis.

Topics: Analysis of Variance; Animals; Case-Control Studies; Chronic Disease; Dog Diseases; Dogs; Enteritis; Female; Gastrins; Male; Severity of Illness Index; Stomach

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

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

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

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

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

The therapeutic efficacy of tykveol was evaluated in 22 patients with chronic non-calculous cholecystitis and/or dyskinesia of the biliary tract (BT) concurrent with gallbladder deformity (GD). Supplementation of tykveol to the combined therapy in the patients with chronic non-calculous cholecystitis concurrent with GD was shown to exert a pronounced therapeutic effect. This caused positive changes in clinical symptoms and BT function, diminished the lithogenic propertes of bile. With the use of tykveol, recovery of neurohumoral regulation is an important factor that improves biliary tract function, as evidenced by decreased gastrin secretion.

Topics: Acalculous Cholecystitis; Adolescent; Adult; Bile; Biliary Dyskinesia; Biliary Tract; Chronic Disease; Cucurbita; Female; Gastrins; Humans; Male; Middle Aged; Phytotherapy; Treatment Outcome

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

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

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

The effect of chronic hypergastrinemia alone on gastric enterochromaffin-like (ECL) cells in humans is largely unknown because in the common chronic hypergastrinemic states (atrophic gastritis, chronic proton pump inhibitor use), it is not possible to separate the effect of hypergastrinemia and other factors, such as gastritis or atrophy. Studies of patients with sporadic Zollinger-Ellison syndrome (ZES) allow this separation.. In 106 patients with ZES, gastric biopsies were taken, and the qualitative ECL cell pattern/grade and the alpha-subunit of human chorionic gonadotropin (alpha-hCG) expression were determined.. In patients with active disease, 99% had ECL hyperplasia and abnormal alpha-hCG staining. Fifty percent had advanced changes in both of these, with 7% having dysplasia and 0% having carcinoids. Advanced ECL cell and alpha-hCG changes were most affected by the level of hypergastrinemia. For ECL cell changes, even mild hypergastrinemia had an effect. Advanced ECL change was also affected by the duration of drug treatment, cure status, and presence of atrophic gastritis, but not by sex or previous vagotomy. The alpha-hCG expression independently predicted dysplasia.. In humans, chronic hypergastrinemia alone causes advanced ECL cell change and abnormal expression of mucosal alpha-hCG. No threshold for this effect was detected, as reported by some, and in contrast to animal studies, sex and vagal tone did not play a major role. The long-term risk of developing gastric carcinoids with chronic hypergastrinemia is low in patients with sporadic gastrinomas (at least 100 times less than in patients with multiple endocrine neoplasia type 1 with ZES) for at least 15-20 years.

Topics: Adolescent; Adult; Aged; Child; Chronic Disease; Enterochromaffin Cells; Female; Gastric Mucosa; Gastrinoma; Gastrins; Glycoprotein Hormones, alpha Subunit; Humans; Hyperplasia; Male; Middle Aged; Pancreatic Neoplasms; Prospective Studies; Zollinger-Ellison Syndrome

The histopathology of Fibrocalculous Pancreatic Diabetes (FCPD) has been extensively studied, but there are no reports on alteration in patterns of hormone secreting cells using immunohistochemistry in islets of FCPD patients. In this study, we report on the histopathology and immunohistochemistry of islets of FCPD patients and its possible correlation with the clinical picture. Pancreatic biopsies were carried out in six patients with FCPD at the time of surgery for abdominal pain. Routine histopathology and immunohistochemistry studies were carried out with six primary antibodies namely insulin, glucagon, pancreatic polypeptide (PP), somatostatin, vasoactive intestinal peptide and gastrin. Histopathology of the pancreas showed a spectrum of changes ranging from moderate to severe atrophy, fibrosis of the parenchyma and degeneration of the ducts. Nesidioblastosis was present in three patients. Immunohistochemical studies showed a decrease in the number of islets but some patients showed evidence of hyperplasia. There was an overall decrease in the percent of insulin cells and the positivity in the islets correlated with plasma C-peptide levels and the duration of diabetes. There was no consistent relationship with glucagon with some patients showing increased and other decreased positivity. There was a marked decrease in PP and somatostatin positivity, the significance of which is not clear. The reduction, but partial preservation of insulin positivity is consistent with the ketosis resistance shown by patients with Fibrocalculous Pancreatic Diabetes.

Topics: Adolescent; Adult; Atrophy; Biopsy; Blood Glucose; Chronic Disease; Diabetes Mellitus; Female; Gastrins; Glucagon; Humans; Hyperplasia; Immunohistochemistry; Insulin; Islets of Langerhans; Male; Middle Aged; Pancreas; Pancreatic Ducts; Pancreatic Polypeptide; Pancreatitis; Vasoactive Intestinal Peptide

Prostaglandins (PG) derived from COX-1 are essential for the maintenance of mucosal integrity but COX-2 isoform synthesizes PG at a site of inflammation. Recently, COX-2 mRNA expression was demonstrated at the ulcer edge during healing of chronic gastric ulcers but the role for expression of COX-2 and its products such as PGE(2) and cytokines including interleukin (IL-1beta) and tumor necrosis factor alpha (TNFalpha) in ulcer healing remains unknown. In this study, Wistar rats with gastric ulcers produced by serosal application of acetic acid (ulcer area 28 mm(2)) received daily treatment either with: (1) vehicle (saline); (2) NS-398 (10 mg/kg-d i.g.) and Vioxx (5 mg/kg-d i.g.), both, highly specific COX-2 inhibitors; (3) meloxicam (5 mg/kg-d i.g.), a preferential inhibitor of COX-2; (4) resveratrol (10 mg/kg-d i.g.), a specific COX-1 inhibitor; (5) indomethacin (5 mg/kg-d i.g); and (6) aspirin (ASA; 50 mg/kg-d i.g.), non-selective inhibitors of both COX-1 and COX-2. At day 3, 7, and 14 after ulcer induction, the animals were sacrificed and the area of gastric ulcers was determined by planimetry and histology, gastric blood flow (GBF) at ulcer base and margin was measured by H(2) clearance technique, and blood was withdrawn for measurement of plasma IL-1beta and TNFalpha levels. The mucosal biopsy samples were taken for the determination of PGE(2) generation by RIA and expression of COX-1, COX-2, IL-1beta, and TNFalpha mRNA by RT-PCR. In vehicle-treated rats, gastric ulcers healed progressively and at day 14 the healing was completed, accompanied by a significant rise in the GBF at ulcer margin. The IL-1beta, TNFalpha, and COX-1 mRNA were detected in intact and ulcerated gastric mucosa, whereas COX-2 mRNA were upregulated only in ulcerated mucosa with peak observed at day 3 after ulcer induction. The plasma IL-1beta level was significantly increased at day 3 and 7 but then declined at day 14 to that measured in vehicle-controls. Indomethacin and ASA, which suppressed PGE(2) generation both in the non-ulcerated and ulcerated gastric mucosa, significantly delayed the rate of ulcer healing and this was accompanied by the fall in GBF at ulcer margin and further elevation of plasma IL-1beta and TNFalpha levels, which was sustained up to the end of the study. Treatment with NS-398 and Vioxx, which caused only a moderate decrease in the PGE(2) generation in the non-ulcerated gastric mucosa, delayed ulcer healing and attenuated significantly the GBF at ulcer marg

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Chronic Disease; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Dinoprostone; Gastric Mucosa; Gastrins; Indomethacin; Interleukin-1; Isoenzymes; Lactones; Male; Meloxicam; Membrane Proteins; Nitrobenzenes; Prostaglandin-Endoperoxide Synthases; Radioimmunoassay; Rats; Rats, Wistar; Resveratrol; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Stilbenes; Stomach Ulcer; Sulfonamides; Sulfones; Thiazines; Thiazoles; Tumor Necrosis Factor-alpha

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

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

The antigastrinic, antisecretory and antiulcer activities of CR 2945, (R)-1-naphthalenepropanoic acid,beta-[2-[[2-(8-azaspiro[4.5]dec-8-yl-carbonyl)-4,6-dimethylph enyl] amino]-2-oxoethyl], were investigated in vitro and in vivo in rats and cats. Its activities were compared with those of two gastrin/CCK(B) receptor antagonists, L-365,260 (3R(+)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4-benzodiazepin -3-yl)-N'-(3-methylphenyl)urea and CAM-1028 (4-[[2-[[3-(1H-indol-3-yl)-2-methyl-1-oxo-2-[[[1,7,7-trimethylbicyclo [2.2.1]hept-2-yl)oxy]carbonyl]amino]propyl]amino]-1-phenylethyl]amino -4-oxo-[1S-1alpha,2beta[S'(S')4alpha]]-butanoate -N-methyl-D-glucamine), of the histamine H2 receptor antagonist, ranitidine, and the proton pump inhibitor, omeprazole. Cytosolic Ca2+ elevation in rabbit parietal cells induced by gastrin (50 nM) was blocked by CR 2945 with an IC50 value of 5.9 nM. CAM-1028 and L-365,260 showed similar activity. CR 2945 antagonized pentagastrin-stimulated gastric acid secretion in rats (ED50 = 1.3 mg kg(-1) i.v. and 2.7 mg kg(-1) i.d.) and cats (1.6 mg kg(-1) i.v.). CR 2945 was slightly less potent than the reference compounds after i.v. administration, whereas after intraduodenal (i.d.) administration, it was more potent than both ranitidine and omeprazole. In the rat, the gastrin antagonism exhibited by CR 2945 was reversible and competitive, with a pA2 value of 7.33. CR 2945 had specific antigastrin activity, as it was unable to antagonize the gastric acid secretion stimulated by histamine or carbachol in rats up to the dose of 30 mg kg(-1). CR 2945 was about as efficacious as ranitidine against the indomethacin- and ethanol-induced gastric ulcers and the cysteamine-induced duodenal ulcer in rats. On the contrary, L-365,260 was only slightly effective. These results suggest that CR 2945 might be a promising compound for the therapy of acid-related disorders, and that its clinical use could help clarify the therapeutic potential of gastrin/CCK(B) receptor antagonists in the gut.

Topics: Animals; Anti-Anxiety Agents; Anti-Ulcer Agents; Benzodiazepines; Benzodiazepinones; Calcium; Cats; Chronic Disease; Cysteamine; Dose-Response Relationship, Drug; Ethanol; Gastric Acid; Gastric Fistula; Gastric Mucosa; Gastrins; Histamine H2 Antagonists; Indomethacin; Male; Omeprazole; Parietal Cells, Gastric; Pentagastrin; Perfusion; Phenylurea Compounds; Rabbits; Ranitidine; Rats; Receptors, Cholecystokinin; Stomach; Stomach Ulcer

Patients with chronic pancreatitis and exocrine insufficiency have lower intraduodenal pH compared to controls. It has been assumed that abnormal low intraduodenal pH in these patients not only results from impaired pancreatic bicarbonate secretion but also from an increased gastric acid load to the duodenum.. We have tested this hypothesis by combined intragastric and intraduodenal 24 h pH monitoring in nine chronic pancreatitis patients with exocrine pancreatic insufficiency and nine healthy control subjects during standardized test conditions. Postprandial gastrin and cholecystokinin release were also determined.. Median 24-h intraduodenal pH (5.90 vs. 6.00) and intragastric pH (1.60 vs. 1.70) were not significantly different between patients and controls. However, in the 2-h postprandial periods intraduodenal pH was below five for a significantly higher percentage of time in chronic pancreatitis patients compared to controls (lunch: 14.5% vs. 0.17%, P=0.011; dinner: 24.1% vs. 5.75%, P=0.05). The post-dinner intragastric pH was below three for a significantly higher percentage of time in chronic pancreatitis patients vs. controls (72.2 vs. 48.9%, P=0.04). Postprandial gastrin release was not significantly different between the two groups. Postprandial secretion of cholecystokinin (CCK), as enterogastrone, was significantly (P < 0.01) reduced in chronic pancreatitis patients (78 +/- 13 pmol/L, 120 min) compared to controls (155 +/- 14 pmol/L, 120 min).. Median intraduodenal and intragastric pH are not significantly decreased in patients with chronic pancreatitis and exocrine insufficiency but the postprandial time with an acidic pH in the duodenum (pH < 5) and in the stomach (pH < 3) is significantly (P

Topics: Adult; Case-Control Studies; Cholecystokinin; Chronic Disease; Duodenum; Exocrine Pancreatic Insufficiency; Female; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Pancreatitis; Postprandial Period; Time Factors

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

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

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

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

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

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

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

Whereas considerable experimental evidence suggests chronic hypergastrinemia can increase the occurrence of colonic neoplasia, the risks in man remain unclear. Zollinger-Ellison syndrome (ZES) is associated with marked plasma elevation of all forms of gastrin and, because of its prolonged course, has been shown to be an excellent model disease to study the effects of chronic hypergastrinemia in man. To determine whether profound chronic hypergastrinemia affects the occurrence of colonic dysplasia and neoplasia, 97 consecutive patients with ZES were studied. All patients underwent colonoscopic examination to the cecum, and the location, size, and type of polyps/tumors were determined. The patients had a mean fasting gastrin level 31 times above normal and a mean disease duration of 10 years; 17/97 (18%) had adenomatous polyps, 67/97 (69%) no adenomatous polyps, and 2/97 (2%) had colonoscopy and/or autopsy studies fo asymptomatic controls. Stratification by age or gender, presence of MEN-I, tumor extent, and duration of degree of hypergastrinemia did not increase prevalence. This study shows that despite prolonged, profound hypergastrinemia, no increased rate of colonic neoplasia (polyps or cancer) was noted. These data suggest that the development of hypergastrinemia secondary to continuous use of H+,K+-ATPase inhibitors for as long as 10 years is unlikely to cause an increased risk of developing colonic neoplasia in man.

Topics: Adenocarcinoma; Adenomatous Polyps; Age Distribution; Chronic Disease; Colonic Neoplasms; Colonic Polyps; Colonoscopy; Fasting; Female; Gastrins; Humans; Incidence; Male; Middle Aged; Risk Factors; Sex Distribution; Zollinger-Ellison Syndrome

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

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

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

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

We determined the relative contributions of endogenous gastrin, histamine and cholinergic tone to basal acid secretion in chronic fistula rats. Results were compared with those for acid secretion in pylorus-ligated rats. In chronic fistula rats, YM022 ¿(R)-1-[2,3-dihydro-1-(2'-methylphenacyl)-2-oxo-5-phenyl-1 H-1,4-benzodiazepin-3-yl]-3-(3-methylphenyl)urea¿ dose-dependently inhibited pentagastrin-stimulated acid secretion and abolished this secretion at 1 mumol/kg, s.c., but did not affect histamine- and carbachol-induced acid secretion even at 10 mumol/kg. In contrast, famotidine at 1 mumol/kg completely inhibited not only the acid secretion induced by histamine but also those by pentagastrin and carbachol. Furthermore, atropine abolished carbachol- and pentagastrin-stimulated acid secretion and significantly suppressed histamine-stimulated acid secretion at 0.1 mumol/kg. YM022 dose-dependently inhibited basal acid secretion. The YM022 dosage required to inhibit basal acid secretion is consistent with that required to suppress pentagastrin-induced acid secretion. Famotidine (1 mumol/kg) and atropine (0.1 mumol/kg) also abolished basal acid secretion. In pylorus-ligated rats, YM022 inhibited acid secretion in a dose-dependent manner; the inhibition at 1 mumol/kg, i.v. was 65%. No additional effect was observed when rats were dosed at 30 mumol/kg. Famotidine partially inhibited acid secretion in these rats, whereas atropine abolished this secretion. These results indicate that the major part of basal acid secretion in rats is attributable to endogenous gastrin via histamine- and cholinergic tone-dependent pathways. Moreover, pylorus ligation reduces the relative contribution of gastrin to acid secretion due to the activation of cholinergic tone.

Topics: Animals; Atropine; Benzodiazepines; Chronic Disease; Famotidine; Gastric Acid; Gastric Fistula; Gastrins; Histamine; Ligation; Male; Parasympathetic Nervous System; Pylorus; Rats; Rats, Sprague-Dawley

The effects of acid, infectious (Helicobacter pylori) and neuroendocrine factors on the course and outcome of chronic duodenitis were studied in 57 patients aged 15-35 years. Within 5-year follow-up ulcer emerged in 26% of duodenitis patients. Ulceration occurred as a result of high acid production in the basal and stimulated phases, contamination of pyloric-antral mucosa with Helicobacter pylori, unbalance of serum hormones T4, TTH, FSH, ACTH. In risk of ulcerogenesis there were psychological shifts with appearance of pathological reaction to the disease. Consideration of pathogenetic specificity of different duodenitis forms and basing on objective and subjective criteria allow identification of ulcer risk group and early start of optimal therapy.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Chronic Disease; Duodenal Ulcer; Duodenitis; Follicle Stimulating Hormone; Follow-Up Studies; Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Risk Factors; Stomach; Thyroid Hormones; Time Factors

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

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

Patients with the digestive form of chronic Chagas' disease exhibit abnormally increased gastrin release, possibly caused by antral gastrin cell (G cell) hyperfunction. In order to identify the mechanisms underlying this abnormality, we used an immunohistochemical method to assess the population of antral somatostatin-producing cells (D cells) in chagasic patients, since somatostatin is known to be the main inhibitory factor of gastrin secretion. Samples (N = 11) of endoscopic antral biopsies taken from 16 Chagas' disease patients and 13 control subjects were studied. Antral D and G cell populations were determined by an immunohistochemical technique using highly specific antibodies against somatostatin and gastrin. There was no significant difference between Chagas' disease and control groups regarding G cell population (number of cells/mm reported as median (range): 70.0 (23.7-247.0) vs 98.1 (52.7-169.4), P > 0.10). In contrast, the number of antral D cells in Chagas' disease patients was significantly lower than in controls (16.4 (6.9-54.4) vs 59.3 (29.6-113.8), P < 0.05). Chronic superficial gastritis and infection with Helicobacter pylori were more frequent in chagasic patients than in controls, but there was no demonstrable association between these factors and the reduction of the number of antral D cells. These data suggest that reduction in the number of antral somatostatin-producing cells, which should lead to reduced inhibition of gastrin cell activity, may play a role in the increased gastrin secretion observed in Chagas' disease patients.

Topics: Chagas Disease; Chronic Disease; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Pyloric Antrum; Somatostatin

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

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

It is not clear whether there is any association between metaplasia of the bronchial epithelium and changes in the distribution of neuroendocrine cells. This study examined, by immunohistological techniques, the distribution of neuroendocrine cells and juxtamucoscal nerve fibres in bronchial biopsies showing metaplastic changes.. Bronchial biopsies from 12 subjects with epithelial metaplasia associated with bronchiectasis and diffuse pulmonary fibrosis were examined by conventional light microscopy and immunohistological techniques for protein gene product 9.5 (PGP), chromogranin A and B (CAB), serotonin, vasoactive intestinal peptide (VIP), substance P (SP), calcitonin gene-related peptide (CGRP), calcitonin (CT), and gastrin releasing peptide (GRP).. Regions of non-metaplastic epithelium contained numerous PGP and serotonin immunoreactive cells. Sub-populations of these cells displayed CAB, CGRP, CT, and GRP immunoreactivity. Metaplastic epithelium contained only a few weakly stained PGP, serotonin, CAB, GRP, CT and CGRP immunoreactive cells in six cases. Metaplastic epithelium was characterised by a high number of CAB-containing cells in six cases and in these biopsies prominent PGP-containing nerve bundles were seen in the subepithelial layer beneath the metaplastic epithelium.. The distribution patterns of neuroendocrine cells and neuronal elements vary between areas of normal and metaplastic epithelium and within areas of metaplastic epithelium. Neuronal hyperplasia was associated with an increase in the number of CAB-containing cells within the metaplastic epithelium.

Topics: Adult; Aged; Bronchi; Calcitonin; Calcitonin Gene-Related Peptide; Chromogranin A; Chromogranins; Chronic Disease; Gastrin-Releasing Peptide; Gastrins; Humans; Immunohistochemistry; Lung Diseases; Middle Aged; Mucous Membrane; Neurosecretory Systems; Peptides; Serotonin; Substance P; Thiolester Hydrolases; Ubiquitin Thiolesterase

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

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

This study was designed to determine the efficacy of L-arginine in healing of gastric ulcers induced by acetic acid and to assess the role of nitric oxide (NO), prostaglandins, gastrin and polyamines in the healing process. Intragastric administration of L-arginine (32.5-300 mg/kg/day) enhanced the healing rate of these ulcers in a dose-dependent manner, while D-arginine (300 mg/kg/day) was not effective. The acceleration of healing by L-arginine was accompanied by a marked increase in gastric blood flow (GBF) at the ulcer margin, and an enhancement of serum gastrin level, mucosal DNA synthesis, and DNA and RNA contents and angiogenesis in the granulation tissue in the ulcer bed. A similar increase in ulcer healing associated with hyperemia at the ulcer margin and enhanced angiogenesis but without alteration in serum gastrin were observed after treatment with glyceryl trinitrate, an NO exogenous supplier. Treatment with NG-nitro-L-arginine (L-NNA), an inhibitor of NO synthase, delayed ulcer healing and this was accompanied by a reduction of GBF at the ulcer margin and in angiogenesis in granulation tissue and by a decrease in serum gastrin level and mucosal growth. Addition of L-arginine to L-NNA restored ulcer healing, hyperemia at the ulcer margin and angiogenesis and prevented the fall in serum gastrin and mucosal growth caused by L-NNA. Pretreatment with indomethacin also delayed ulcer healing and this was reversed by the coadministration of L-arginine. Inhibition of polyamine biosynthesis by difluoro-methyl-ornithine completely abolished the acceleration of the healing and the increase in mucosal growth induced by L-arginine. Our findings indicate that L-arginine accelerates ulcer healing due to its hyperemic, angiogenic and growth-promoting actions, possibly involving NO, gastrin and polyamines.

Topics: Animals; Arginine; Chronic Disease; Cyclooxygenase Inhibitors; Dose-Response Relationship, Drug; Eflornithine; Gastrins; Indomethacin; Nitric Oxide; Nitric Oxide Synthase; Nitroarginine; Nitroglycerin; Polyamines; Prostaglandins; Rats; Rats, Wistar; Regional Blood Flow; Stomach; Stomach Ulcer; Vasodilator Agents

Results of prognostic tests of vagotomy were studied in 365 patients with chronic duodenal ulcers (CDU). It was established that the atropin test can not be taken as the main criterion of prognosis of vagotomy. However, according to its results the patients can be divided into 2 groups: atropin sensitive (69.3%) and atropin-resistant (30.7%). According to the parameters of the atropin test and the night gastric secretion the patients were divided into 3 groups: favorable (45.7%), doubtful (31.0%) and unfavorable (23.3%) prognosis of effectiveness of vagotomy with draining operations of the stomach.

Topics: Atropine; Chronic Disease; Drug Resistance; Duodenal Ulcer; Gastric Acid; Gastrins; Humans; Nervous System Physiological Phenomena; Parasympatholytics; Phenylephrine; Prognosis; Recurrence; Reflex; Risk Factors; Sympathomimetics; Vagotomy

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

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

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

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

1. Patients with chronic Chagas' disease have abnormally low gastric acid secretion and increased gastrin release both during fasting and after different stimuli. Regardless of the relationship between intragastric acidity and gastrin secretion, it is uncertain whether hypergastrinemia in Chagas' disease is caused by an increased population of antral gastrin (G) cells (hyperplasia) or by enhanced cell activity (hyperfunction). 2. We therefore estimated G cell number in antral biopsies from 16 chagasic patients and 13 control subjects using a peroxidase-anti-peroxidase immunohistochemical technique. All subjects underwent a gastric secretion test to determine peak acid output following intravenous pentagastrin instillation. 3. Antral G cell number in Chagas' disease patients was not significantly different from that observed in the control group (number of cells/mm2, median and (range): 128 (44-284) vs 138 (65-285)). 4. In chagasic patients, peak acid output was significantly lower than in controls (mmol/h, median and (range): 9.819 (3.024-21.564) vs 17.490 (9.423-25.848)). 5. These results suggest that the increase in gastrin release associated with reduced gastric acid secretion in Chagas' disease is mediated by antral G cell hyperfunction rather than by hyperplasia.

Topics: Adult; Cell Count; Chagas Disease; Chronic Disease; Esophageal Achalasia; Female; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Male; Megacolon; Middle Aged; Pyloric Antrum

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

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

Evolution of gastrinoma tumoral mass, fasting serum gastrin concentrations, and gastric endocrine cells has been analyzed in 21 patients with the Zollinger-Ellison syndrome committed to long-term omeprazole treatment (up to 7.75 years, median 37 months). Gastrinoma growth was seen in eight patients. Significant increase in serum gastrin was only observed in the group of patients with gastrinoma growth. Fundic argyrophil cell densities were correlated with serum gastrin (r' = 0.68, P = 0.002). Argyrophil and antral gastrin cell densities significantly increased during the survey, but increases were greater in the group with gastrinoma growth (respectively, +136% and +131%) than in the other group (respectively, +34% and +43%). Progression in the degree of argyrophil cell hyperplasia, noted qualitatively, was observed in 11 patients. Fundic carcinoids developed in three of these 11 patients, all three having multiple endocrine neoplasia type 1 (MEN 1). Positive linear individual correlations (r > or = 0.85) between argyrophil cell densities and corresponding durations of omeprazole treatment were found in nine of the 10 patients studied at least three times and who had a clear-cut increase in those cell densities. Thus, increase in serum gastrin and fundic argyrophil cell densities appeared closely associated with gastrinoma growth; however, duration of drug-induced hypochlorhydria may also affect cell proliferation.

Topics: Adult; Aged; APUD Cells; Chi-Square Distribution; Chronic Disease; Female; Gastrinoma; Gastrins; Humans; Male; Middle Aged; Multiple Endocrine Neoplasia; Omeprazole; Pancreatic Neoplasms; Prospective Studies; Stomach; Time Factors; Zollinger-Ellison Syndrome

In the past five years 12 patients have been identified presenting with chronic duodenal ulcer (DU) disease and with no evidence of current or recent Helicobacter pylori (H pylori) infection. Four of them were taking regular non-steroidal anti inflammatory agents, one was subsequently found to have Crohn's disease of the duodenum, and one to have the Zollinger-Ellison syndrome. The remaining six patients with idiopathic DU disease were remarkable for their absence of the A1 blood antigen gene. Detailed studies of gastric function were performed in these six patients and compared with H pylori positive patients with DU and with healthy volunteers. The median integrated gastrin response in the patients with idiopathic DU (2810 (range 750-8750) ng/l min) was similar to that of the H pylori positive patients with DU (3355 (550-8725)) and higher than that of the H pylori negative healthy volunteers (560 (225-1125)). The median peak acid output in the patients with idiopathic DU (37 mmol/h, range 17-52) was similar to that of the H pylori positive patients with DU (40 (15-57)) and higher than that of the non-ulcer controls (22 (16-29)). The median percentage of a liquid meal retained in the stomach at 60 minutes was less in the patients with idiopathic DU (23 (15-33)) than in H pylori negative healthy volunteers (34 (30-53) p < 0.01). The median percentage of a solid meal retained at 60 minutes was less in the patients with idiopathic DU (54 (9-83)) than in either H pylori negative healthy volunteers (87 (49-95) p<0.01) or H pylori positive patients with DU (79 (51-100) p<0.01). In conclusion, three abnormalities of gastric function are prevalent in patients with H pylori negative idiopathic DU disease - hypergastrinaemia, increased acid secretion, and the one feature distinguishing them from H pylori positive patients with DU - rapid gastric emptying of both liquids and solids. Each of these abnormalities will increase the exposure of the duodenal mucosa to acid and thus explain its ulceration. The absence of the blood group A1 antigen gene is consistent with a genetic basis for the disturbed gastric function linked to the ABO blood group antigen genes.

Topics: ABO Blood-Group System; Adult; Chronic Disease; Duodenal Ulcer; Female; Gastric Acid; Gastric Emptying; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged

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

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

Information concerning the influence that gastrin may exert on the colon is fragmentary and somewhat controversial. This study analyzed the effect of chronic endogenous hypergastrinemia on cell proliferation and tumor occurrence in the human colonic mucosa.. Twenty-three consecutive hypergastrinemic patients presenting with the Zollinger-Ellison syndrome and 18 normogastrinemic subjects were studied. All had fasting serum gastrin determination, colonoscopy, and cell kinetic measurement in two colonic sites using in vitro 5'-bromodeoxyuridine incorporation.. Macroscopic tumors, one endocrine and five adenomas, were found in 5 of 23 hypergastrinemic patients, without apparent relationship with the level of gastrin. The labeling indices were significantly higher in hypergastrinemic than in normogastrinemic individuals in the right and left colon, (P < 0.002 to P < 0.001) without resulting in colonic cell hyperplasia. There was no correlation between labeling indices and serum gastrin concentrations or duration of hypergastrinemia. The DNA labeling distribution along the crypt was normal in the two groups, without expansion of the proliferative zone towards the surface.. These results showed for the first time that long-lasting endogenous hypergastrinemia is accompanied by increased in vivo cell proliferation in the human colonic mucosa. However, the prevalence of adenomas (17.4%) in patients, all more than 50 years old, may not be different from that in the general population.

Topics: Adenoma; Adult; Aged; Cell Division; Chronic Disease; Colon; Colonic Neoplasms; Colonoscopy; DNA; Female; Gastrins; Humans; Intestinal Mucosa; Male; Middle Aged; Zollinger-Ellison Syndrome

To find out if there was a correlation between hydrogen, potassium stimulated ATPase (H,K-ATPase) activity and gastric acid secretion in patients with duodenal ulcers after proximal gastric vagotomy.. Retrospective study.. Regional referral center.. 61 patients with chronic duodenal ulcers divided into three groups: patients who had not been operated on but had exacerbations of their symptoms (n = 39): those who had been treated successfully by proximal gastric vagotomy either less than 1 year ago (n = 7) or greater than or equal to 1 year ago (n = 9): and those patients who presented with recurrent ulceration after proximal gastric vagotomy (n = 6).. Measurement of H,K-ATPase activity and gastric acid secretion.. There was a decrease in H,K-ATPase activity after effective vagotomy, and enzyme activity was the lowest in patients who had been operated on 1 year ago. Both H,K-ATPase and gastric acid secretion were decreased by proximal gastric vagotomy.. There may be a gradual recovery of gastric H,K-ATPase activity with time after proximal gastric vagotomy.

Topics: Adenosine Triphosphatases; Adult; Chronic Disease; Duodenal Ulcer; Female; Gastric Acid; Gastric Mucosa; Gastrins; H(+)-K(+)-Exchanging ATPase; Humans; Male; Middle Aged; Vagotomy, Proximal Gastric

The authors provide the data on the hormonal spectrum (STH, gastrin, sex hormones) in patients with long unhealing duodenal ulcers. It is shown that changes in the concentrations and ratios of the concentrations of hypophyseal-gonadal hormones may serve as a defensive adaptation reaction of the body and may be due to activation of the adaptation systems that mediate the neurohumoral mechanisms of regulation. Such changes are more remarkable in patients with common peptic ulcer. Apparently, in patients with long unhealing ulcers, these mechanisms tend toward depletion, as a result of which the other mechanisms start prevailing (microcirculatory disorders, immunologic abnormalities, pathological microflora).

Topics: Adult; Chronic Disease; Cyclic AMP; Duodenal Ulcer; Female; Gastrins; Gonadal Steroid Hormones; Growth Hormone; Humans; Male; Ovary; Pituitary Gland; Testis; Wound Healing

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

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

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

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

We have investigated the relationship between cholecystokinin levels and abdominal pain in patients with chronic pancreatitis. The baseline and postprandial cholecystokinin levels were measured in 15 patients with chronic pancreatitis (8 with and 7 without abdominal pain) and in a reference group of 8 healthy subjects. The baseline, 30 and 60 min postprandial plasma cholecystokinin levels were significantly (p less than 0.05) higher in the patients with pain as compared with the other two groups. No correlation was observed between increased cholecystokinin levels and impairment of the exocrine pancreatic function as assessed by the NBT-PABA test. The increased cholecystokinin levels might be an important factor in the genesis of pain in chronic pancreatitis.

Topics: Abdominal Pain; Adult; Cholecystokinin; Chronic Disease; Female; Food; Gastrins; Humans; Male; Pancreatitis; Radioimmunoassay

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

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

Helicobacter pylori (previously Campylobacter pylori) is almost invariably associated with chronic duodenal ulcer disease. The relationship between H. pylori infection and duodenal ulcer in Zollinger-Ellison syndrome is unknown. We investigated the frequency of H. pylori infection in Zollinger-Ellison syndrome and also what effect H. pylori infection had on gastric function in patients with Zollinger-Ellison syndrome. H. pylori infection was diagnosed based on a specific serologic (ELISA) assay based on high-molecular-weight cell-associated proteins of H. pylori. We studied 20 patients with Zollinger-Ellison syndrome; 15 men and 5 women ranging in age from 24 to 71 years, median age 51. Six Zollinger-Ellison syndrome patients had H. pylori infection compared to 100 consecutive patients with chronic recurrent duodenal ulcer disease (P less than 0.05). Pretreatment basal acid output in Zollinger-Ellison syndrome patients ranged from 7.9 to 95.0 mmol/hr, median 35.2. Pentagastrin-stimulated maximal acid output ranged from 8.5 to 132 mmol/hr; median 52.7. Acid secretion was lower in the H. pylori-infected patients than the uninfected patients (BAO 24.5 +/- 6.5 vs 45.4 +/- 6.6, and MAO 44.3 +/- 11.8 vs 67.9 +/- 10.7, for H. pylori infected vs uninfected patients, respectively). The difference in BAO was statistically significant (P less than 0.05). The present results indicate that H. pylori is not a major contributing factor in duodenal ulcer associated with Zollinger-Ellison syndrome. The association of a reduced BAO with H. pylori suggests that these findings may be related.

Topics: Adult; Aged; Chronic Disease; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Prevalence; Recurrence; Zollinger-Ellison Syndrome

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

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

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 content of gastrin, beta-endorphin, insulin, C-peptide in 129 patients with chronic gastric and duodenal diseases was studied by standard radioimmunoassay during the acute phase of the disease and after routine treatment. It is concluded that normalization of the hormonal homeostasis is one the criteria of treatment efficacy.

Topics: Adolescent; Adult; Aged; beta-Endorphin; C-Peptide; Chronic Disease; Duodenal Diseases; Female; Gastrins; Humans; Insulin; Male; Middle Aged; Peptides; Stomach Diseases

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

We report a case of chronic diarrhea due to hypergastrinemia with achlorhydria but without gastritis in a five-year-old boy. Symptoms responded promptly to oral administration of hydrochloric acid and resolved completely after one year of treatment. The pathophysiologic situation in this patient closely resembled that normally seen in neonates, suggesting prolonged but nevertheless transient immaturity of gastric secretions.

Topics: Achlorhydria; Child, Preschool; Chronic Disease; Diarrhea; Gastrins; Humans; Male

Gastric acid secretion in response to a protein meal and to exogenously administered synthetic human gastrin 17-I was measured in patients with Barrett's esophagus, patients with uncomplicated gastroesophageal reflux, and normal age- and sex-matched controls. Acid secretion, both basally and in response to gastrin 17-I, was significantly greater in patients with Barrett's esophagus compared to normal individuals without reflux. Basal gastrin levels and meal-stimulated levels of the hormone were similar among all three groups. Sensitivity to gastrin, expressed as the concentration causing half-maximal acid secretion, was also similar among the study groups. It is speculated that elevated basal acid production in Barrett's esophagus may contribute to the pathogenesis of the disorder.

Topics: Barrett Esophagus; Chronic Disease; Cimetidine; Female; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastroesophageal Reflux; Humans; Male; Middle Aged; Monitoring, Physiologic; N-Methylscopolamine; Parasympatholytics; Scopolamine Derivatives

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

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

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

A disturbed intraduodenal milieu and pancreatic scarring in advanced chronic pancreatitis (CP) may lead to changes of gut and pancreatic hormones. In the present study, the gastroduodenal mucosal content of several regulatory peptides was determined in 8 patients with severe calcific CP and 8 healthy volunteers. In addition, hormone release into the bloodstream was estimated after intraduodenal acid/glucose stimulation in the control subjects and 8 CP patients each with or without secondary diabetes mellitus (DM), and in 8 patients with juvenile DM, so that disturbed gut hormone release could be attributed either to CP or DM. While VIP release into the circulation was similar in all participants, mucosal levels of VIP and substance P were significantly elevated in the duodenal bulb and descending duodenum of CP patients. The somatostatin content of gastroduodenal mucosa in CP was at least as high as in normals. Gastrin was significantly more abundant only in the duodenal bulb of CP patients, while plasma gastrin was normal. Duodenal CCK concentrations tended to be elevated in the duodenal bulb, but not significantly. The release of secretin seemed to be higher in type-1 diabetics than in CP patients. The mucosal pattern of GIP was nearly identical in CP patients and controls. Compatible with this finding, the GIP release did not show any peculiarities in CP with or without DM or in DM. Basal and stimulated plasma levels of motilin were abnormally high in CP. Pancreatic polypeptide plasma levels were normal in DM, but significantly reduced in CP, especially in CP with DM. Fasting PP and stimulated pancreatic enzyme outputs were linearly related.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Chronic Disease; Diabetes Mellitus; Female; Gastric Inhibitory Polypeptide; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Glucagon; Glucagon-Like Peptides; Humans; Intestinal Mucosa; Male; Middle Aged; Motilin; Neurotensin; Pancreatic Polypeptide; Pancreatitis; Secretin; Somatostatin; Substance P; Vasoactive Intestinal Peptide

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

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

Topics: Celiac Disease; Child, Preschool; Chronic Disease; Diarrhea, Infantile; Eating; Fasting; Female; Gastrins; Humans; Infant; Male; Reference Values

Duodenal acidification was studied in 53 peptic ulcer patients. Gastric and duodenal pH was studied using an electric probe with silver chloride and antimony electrodes. For a study of the mechanisms of changes of duodenal acidification gastrin was investigated using various exercise tests. Two types of disorders of duodenal acidification were established in the patients: related and unrelated to the vagus nerve. Characterization of the mechanism of disorders of duodenal acidification was provided. A study of duodenal acidification in peptic ulcer gave an opportunity for the development of effective pathogenetically substantiated therapeutic measures.

Topics: Adolescent; Adult; Atropine; Chronic Disease; Duodenal Ulcer; Duodenum; Fasting; Female; Gastric Acid; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Insulin; Male; Middle Aged; Stomach; Time Factors

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

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

This study describes the model of chronic gastric and duodenal ulcerations induced by the application of acetic acid on a strictly defined area of the serosal surface of the stomach and duodenum for 10 and 20 s, respectively. Acetic acid applied for longer (20-60 s) or on a larger area (28-64 mm2) resulted in the formation of severe ulcerations which penetrated into the surrounding organs and had very prolonged healing time. Ulcers induced by the application of acetic acid for 10-20 s on a smaller area (7-13.8 mm2) healed spontaneously within 2-3 weeks, thus constituting a model suitable for evaluation of drugs affecting the process of ulcer healing. Our preliminary results of 7- to 14-day treatment with certain drugs indicate that sucralfate and De-Nol, at the dose which does not affect gastric acid secretion, accelerated the healing rate of both gastric and duodenal ulcers so that the observed ulcer healing effect could be attributed to their ulcer healing property. In contrast, 16, 16-dimethyl PGE2 (dmPGE2) in cytoprotective dose was completely ineffective in enhancing ulcer healing. Higher, gastric inhibitory dose of dmPGE2 accelerated the healing of duodenal but not gastric ulcerations, indicating that the inhibition of gastric secretion rather that cytoprotective activity is responsible for ulcer healing effect of this prostaglandin.

Topics: Animals; Bismuth; Chronic Disease; Dinoprostone; Disease Models, Animal; Gastric Acid; Gastric Mucosa; Gastrins; Male; Pepsin A; Peptic Ulcer; Prostaglandins E; Rats; Rats, Inbred Strains; Sucralfate

Topics: Adolescent; Adult; Chronic Disease; Female; Gastric Emptying; Gastrins; Humans; Male; Middle Aged; Radionuclide Imaging; Spinal Cord Injuries; Stomach; Time Factors

We have established an experimental model of chronic gastric ulcer, in rats which transection of the lower horizontal portion of the duodenum and anastomosis of the forestomach to the upper part of the jejunum caused regurgitation of all duodenal juice into the stomach. After 3, 6, 12, and 30 wk, all treated rats developed an ulcer in the prepyloric region on the lesser curvature of the stomach. More than half of the antrum was finally involved in the ulcer. Histologic studies revealed chronic ulcers quite similar to human ones. As a control series, transection at the pylorus failed to produce an ulcer. Although many papers have appeared regarding the experimental production of chronic gastric ulcer, most of the studies reported have applied chemicals, drugs, or mechanical injury to the gastric mucosa. Our model produced chronic regurgitation of duodenal juice as a natural phenomenon, and uniformly resulted in ulcer formation. Intragastric total bile acid concentrations were significantly elevated in the reflux group. Serum gastrin levels, the thickness of the fundic mucosa, and the height of fundic gland were also significantly increased. Thus, the detergent action of bile acids and the increased acid secretion were assumed to play an important role in ulcer formation. Further studies using this model are warranted on the pathogenesis of chronic peptic ulceration.

Topics: Animals; Bile Acids and Salts; Chronic Disease; Disease Models, Animal; Duodenogastric Reflux; Gastric Mucosa; Gastrins; Hydrogen-Ion Concentration; Rats; Rats, Inbred Strains; Stomach Ulcer

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

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

Exocrine and endocrine stomach was studied serially in 13 patients who had gastrobulbar preserving pancreatoduodenectomy (GPPD). In most of them, acid output temporarily increased just after operation but recovered. Gastrin response level decreased transiently but returned to the preoperative level. A negative correlation was observed between the acid and gastrin levels, which suggests that the negative feedback mechanism between parietal cells and G cells was maintained. Acid and gastrin levels in GPPD were higher than those in conventional pancreatoduodenectomy (cPD) but not remarkably different from those of the controls. No peptic ulcer was detected after the operation. These findings indicated that GPPD poses little problem concerning offensive factors. Postoperative ulcer formation is considered to be prevented by the authors' procedure, which is devised to best preserve defensive mechanisms so that duodenectomy is minimized and the gastrointestinal continuity is reconstructed physiologically from mouth to anus by end-to-end duodenoduodenestomy, end-to-side pancreatojejunostomy, and end-to-side choledochojejunostomy.

Topics: Adult; Aged; Chronic Disease; Duodenal Neoplasms; Duodenum; Female; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Pancreatectomy; Pancreatitis; Postoperative Period

Topics: Adult; Chronic Disease; Duodenal Ulcer; Female; Gastric Mucosa; Gastrins; Histamine; Humans; Male; Middle Aged

In patients with hypercalcemia with abdominal symptoms, gastrin concentration is often measured to exclude the Zollinger-Ellison syndrome. We found that interpretation of such measurements is clouded by a contradictory literature. We therefore measured serum gastrin concentrations in 78 patients with primary hyperparathyroidism, 36 with nonparathyroid hypercalcemia, 13 with hypocalcemia, and 33 normocalcemic controls. Gastrin values above normal occurred in 22% of those with primary hyperparathyroidism and 28% of those with nonparathyroid hypercalcemia. Values above 250 pg/mL occurred only in those with hypochlorhydria or multiple endocrine neoplasia, type 1 (MEN 1). After parathyroidectomy, gastrin levels fell significantly, but elevated values tended to recur in those with MEN 1 if hypercalcemia recurred. Thus, chronic hypercalcemia of either parathyroid or nonparathyroid origin may elevate serum gastrin concentrations, but marked elevations suggest either achlorhydria or MEN 1.

Topics: Adult; Aged; Calcium; Chronic Disease; Creatinine; Diagnosis, Differential; Gastrins; Humans; Hypercalcemia; Hyperparathyroidism; Middle Aged; Multiple Endocrine Neoplasia; Parathyroid Hormone; Radioimmunoassay

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

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

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

Topics: Chronic Disease; Gastrins; Humans; Hypercalcemia

A patient with a calcifying chronic pancreatitis was found to have a neuroendocrine islet cell tumour (a previously unreported association). The tumour secreted both gastrin and ACTH leading to clinical manifestations of both the Zollinger-Ellison syndrome and Cushing's syndrome.

Topics: Adenoma, Islet Cell; Adrenocorticotropic Hormone; Aged; Calcinosis; Chronic Disease; Gastrins; Humans; Male; Pancreatic Neoplasms; Pancreatitis; Zollinger-Ellison Syndrome

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

Different food tests were used to study endocrine function of the pancreas in 75 persons with a history of brucellosis and in 30 patients with chronic acalculous cholecystitis. In persons with a history of brucellosis, the endocrine part of the pancreas was involved, which manifested itself in a decrease in the secretory response of B cells to stimulation with glucose and mixed food enriched with proteins and fat. The alterations described are likely to be caused by the infection itself.

Topics: Adolescent; Adult; Blood Glucose; Brucellosis; Cholecystitis; Chronic Disease; Enterochromaffin Cells; Female; Gastrins; Glucose Tolerance Test; Humans; Insulin; Islets of Langerhans; Male; Middle Aged; Pancreatic Function Tests; Time Factors

The authors describe the results of studying basal gastrin secretion in patients with peptic ulcer of the duodenum at different phases of disease treated in 3 stages. It was revealed that basal secretion of gastrin experienced substantial changes in the course of transition from the phase of exacerbation to the phase of disease remission. It was noted that the onset of the clinico-endoscopic remission of peptic ulcer did not correlate in all the cases with normalization of basal gastrin level. Patients who did not show normalization of basal gastrin level during treatment were more prone to the development of repeated exacerbations. Based on the data obtained the authors determined the prognostic importance of radioimmunoassay of gastrin basal concentration over time. The increment of gastrin concentration by more than 35 pg/ml of the level seen during peptic ulcer exacerbation is a prognostically unfavourable sign, for the probability of relapses rises up to 79% during a year.

Topics: Adult; Aged; Chronic Disease; Duodenal Ulcer; Duodenoscopy; Gastrins; Humans; Male; Middle Aged; Prognosis; Radioimmunoassay; Recurrence; Time Factors

Topics: Chronic Disease; Enterochromaffin Cells; Gastric Mucosa; Gastrins; Glomerulonephritis; Humans; Kidney Diseases; Nephrotic Syndrome; Pyelonephritis; Renal Dialysis

Acid secretory behavior as well as gastrin levels were evaluated in 38 cases of chronic duodenitis. Basal HCl secretion was normal in 39% of cases, hypochlorhydria was observed in 29%, and hyperchlorhydria in 32%. Maximal acid output was normal in 71% of patients with duodenitis, decreased in 19%, and increased in 10%. Fasting serum gastrin was always within normal limits. The secretory behavior correlated with age but not with the histological pattern of duodenal mucosa. In chronic duodenitis, normal secretion or hypochlorhydria is the prevailing finding. This does not exclude the possibility of a peptic pathogenetic mechanism which could be involved in the rare cases of chronic duodenitis with hyperchlorhydria. Acid-peptic disease is not etiopathogenetic in the causation of most cases of chronic duodenitis.

Topics: Adult; Aged; Chronic Disease; Duodenitis; Female; Gastric Acid; Gastrins; Humans; Male; Middle Aged; Monoamine Oxidase

Heterogeneity is the most important consideration in the pathophysiology of peptic ulcer disease. Acute ulcers and erosions present clinically with gastrointestinal bleeding or perforation. If they heal there is no predictable recurrence. Factors concerned with mucosal defense are relatively more important than aggressive factors such as acid and pepsin. Local ischemia is the earliest recognizable gross lesion. The gastric mucosa is at least as vulnerable as the duodenal mucosa and probably more so. Most drug-induced ulcers occur in the stomach. Chronic or recurrent true peptic ulcers (penetrating the muscularis mucosae) usually present with abdominal pain. Many duodenal ulcer patients report that the pain occurs when the stomach is empty or is relieved by food, and follows a pattern of relatively long periods of freedom from symptoms between recurrences. Approximately 50% of patients experience a recurrence within a year if anti-ulcer medication is stopped. In most western countries recurrent duodenal ulcer is more common than gastric ulcer. Peptic ulcer disease is also more common in men. Recent evidence indicates genetic and familial factors in duodenal ulcer and increased acid-pepsin secretion in response to a variety of stimuli. However, it is also becoming clear that of all the abnormal functions noted, few are present in all subjects and many are clustered in subgroups. In chronic gastric ulcer of the corpus, defective defense mechanisms, such as duodenogastric reflux and atrophic gastritis, seem to be more important than aggressive factors. Nevertheless, antisecretory medications accelerate the healing of such ulcers. It remains to be seen whether prostaglandins, mucus secretion, or gastric mucosal blood flow are impaired in chronic ulcer disease.

Topics: Acute Disease; Animals; Burns; Chronic Disease; Duodenal Ulcer; Gastric Acid; Gastric Emptying; Gastrins; Humans; Intestinal Mucosa; Peptic Ulcer; Recurrence; Spinal Cord Injuries; Stomach Ulcer; Stress, Physiological

The relation between gastric acid secretion and plasma concentrations of adrenaline, noradrenaline, dopamine and gastrin was investigated in normal volunteers, adrenalectomized subjects and patients with duodenal ulcer (DU) during digestion and in response to insulin and modified sham feeding (MSF). Basal plasma noradrenaline concentrations were significantly higher in DU patients than in normals whereas basal plasma adrenaline and dopamine concentrations were low in both groups. Basal acid output was similar in the two groups. Insulin markedly increased plasma adrenaline in controls but had no discernible effect in adrenalectomized subjects. Still, there was no difference between acid secretion in the two groups. Insulin, but not MSF, caused a marked increase in plasma catecholamine concentrations in DU patients whereas the acid responses were the same. The significantly increased plasma noradrenaline concentration in DU patients was normalized 6 weeks after highly selective vagotomy but tended to return to the preoperative value 1 year postoperatively. Our results suggest that endogenously released adrenaline might affect gastric function only when present in extremely high plasma concentrations. The pathophysiological role of noradrenaline in DU disease remains obscure.

Topics: Catecholamines; Chronic Disease; Duodenal Ulcer; Eating; Gastric Acid; Gastric Mucosa; Gastrins; Histamine H2 Antagonists; Humans; Hypoglycemia; Insulin; Vagotomy

Topics: Adolescent; Adult; Chronic Disease; Female; Furunculosis; Gastrins; Growth Hormone; Hormones; Humans; Hydrocortisone; Inflammation; Male; Middle Aged; Pyoderma; Radioimmunoassay; Recurrence; Sweat Gland Diseases; Thyroid Hormones

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

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

Topics: Adult; Chronic Disease; Female; Gastrins; Humans; Male; Middle Aged; Pancreatitis

The relationship between thyroid disorders and gastric pathophysiology has been studied mainly from standpoints of gastric histology and gastric acid output capacity. Though anti-gastric antibody has been thought to play a part in this relationship, there have been no clear conclusions obtained about that. Since blood gastrin levels are easily measurable by radioimmunoassay today, the relationship between thyroid disorders and gastric pathophysiology has drawn attention again from a standpoint of gastrin levels. Seino et al. have reported about hypergastrinemia in hyperthyroidism, speculating that beta-adrenergic hyperresponsiveness of gastrin-producing cells could be the mechanism of hypergastrinemia. However, there are other reports which mentioned feedback mechanism between gastrin and gastric acid or interaction of gastrointestinal hormones as the main mechanism of hypergastrinemia. In this study, the problem of gastrin in Graves' disease and chronic thyroiditis were studied by measurement of fasting serum gastrin levels and gastric juice excretion in view of feedback mechanism between gastrin-producing cells and parietal cells which are the target cells of gastrin. Following results were obtained. Fasting serum gastrin levels in Graves' disease were 236.2 +/- 39.1 (mean +/- SE) pg/ml for 39 hyperthyroid patients and 126.3 +/- 23.9 pg/ml for 35 euthyroid patients. These levels were significantly higher than those of sex and age-matched control subjects with P less than 0.001 and P less than 0.05, respectively. Fasting serum gastrin levels in serial studies of 13 patients with Graves' disease were 222.3 +/- 56.7 pg/ml before treatment and 167.3 +/- 56.6 pg/ml at the time of euthyroid state after a mean observation period of 6.6 +/- 1.1 months. Fasting serum gastrin levels at the time of euthyroid state decreased significantly when compared with fasting serum gastrin levels before treatment (P less than 0.05). Fasting serum gastrin levels in chronic thyroiditis were 160.7 +/- 51.1 pg/ml for 24 hypothyroid patients and 96.4 +/- 24.7 pg/ml for 31 euthyroid patients. Each of these levels had no significant differences when compared with sex and age-matched control subjects. Fasting serum gastrin levels in serial studies of 10 patients with chronic thyroiditis were 81.1 +/- 18.0 pg/ml at the time of hypothyroid state and 91.5 +/- 15.2 pg/ml at the time of euthyroid state after a mean observation period of 7.1 +/- 2.1 months. Fasting serum gastrin levels bef

Topics: Adolescent; Adult; Aged; Autoantibodies; Chronic Disease; Female; Gastric Juice; Gastrins; Graves Disease; Humans; Male; Middle Aged; Thyroglobulin; Thyroid Diseases; Thyroid Function Tests; Thyroid Gland; Thyroiditis, Autoimmune

A secretin provocative test was performed in 16 patients with chronic duodenal ulcer and in five patients with the Zollinger-Ellison syndrome. In four chronic duodenal ulcer patients a second secretin test was done during acute iv cimetidine administration. There were only slight variations of gastrin compared with the first test. A third test was done on the same four chronic duodenal ulcer patients after 1 month's po cimetidine treatment (1 g/day); gastrin at 0 time was significantly higher than in the previous two tests (p less than 0.01). Integrated gastrin response after secretin was significantly lower in the third test than in the first (p less than 0.05). In two Zollinger-Ellison syndrome patients treated with 1.0 and 1.4 g/day cimetidine for 3 months, gastrin at 0 time was not markedly increased, whereas compared with the first test gastrin levels were higher at each time after secretin. These data suggest that previous cimetidine treatment does not alter, and may even increase, the diagnostic sensitivity of the secretin test.

Topics: Adolescent; Adult; Chronic Disease; Cimetidine; Duodenal Ulcer; Female; Gastrins; Humans; Male; Middle Aged; Secretin; Zollinger-Ellison Syndrome

Topics: Adolescent; Adult; Chronic Disease; Duodenal Diseases; Female; Gastrins; Humans; Male; Middle Aged; Stomach Diseases

Secretin is known to inhibit gastric acid secretion but in some cases is able to stimulate both gastrin release and acid output. Different studies suggest that gastrin concentration at the parietal cell level modulates the acid response to secretin. Our purpose was to investigate in rats with chronic endogenous hypergastrinemia, as well as in control rats, the effect of an intravenous bolus of secretin GIH (from 0.25 to 4 clinical units (CU)/rat) on acid secretion. Both groups of rats were equipped with a chronic double gastric fistula allowing the collection of diluted gastric secretion every 2 min. We observed a dose-related inhibition of acid output (ID 50 less than 0.5 CU/rat) by secretin. In addition, in rats with hypergastrinemia; the acid response was phasic: an initial increase of acid output forewent its inhibition by 4 CU secretin. This phasic response suggests that secretin could act on acid secretion by releasing mediators which stimulate (as gastrin) and/or inhibit (as somatostatin) acid output.

Topics: Animals; Chronic Disease; Dose-Response Relationship, Drug; Gastric Acid; Gastrins; Parietal Cells, Gastric; Rats; Rats, Inbred Strains; Secretin

Topics: Acute Disease; Amylases; Animals; Cholangiopancreatography, Endoscopic Retrograde; Chronic Disease; Gastrins; Pancreas; Pancreatitis; Somatostatin; Swine

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

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

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

Topics: Animals; Cell Count; Chronic Disease; Colon; Duodenum; Esophagus; Female; Gastric Mucosa; Gastrins; Hyperplasia; Intestinal Mucosa; Intestine, Small; Intestines; Mast Cells; Organ Size; Rats; Splenomegaly; Stomach; Taeniasis

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

Controversial data have been reported on gastric acid secretion in patients with chronic pancreatitis. Moreover, studies on gastroduodenal morphological changes in patients with this disease and with other alcohol-related conditions have given different results. Basal and penta-gastrin-stimulated gastric secretion, histological changes of gastric and duodenal mucosa, and basal and meal-stimulated gastrin were measured in 21 patients with chronic alcoholic pancreatitis and in the following pair-matched groups: 21 chronic alcoholics and 21 control subjects (nonulcer dyspepsia), and in 19 patients with proven liver cirrhosis of alcoholic origin. No patient suffered from peptic ulcers. Moreover, gastric secretion was also measured in 51 patients with proven duodenal ulcers and in 34 healthy subjects. Basal acid output in patients with chronic pancreatitis was significantly higher (p less than 0.05) than in the other groups, except for the patients with duodenal ulcers. Peak acid output values in patient with chronic pancreatitis were similar to those measured in patients with duodenal ulcer, and they were higher than in the healthy subject group and in patients with liver cirrhosis, but statistical significance was not attained for patients with nonulcer dyspepsia. An increased frequency of duodenitis was found in patients with chronic pancreatitis, whereas an increased frequency of gastric metaplasia in the duodenal bulb was observed in all the patients with alcohol-related conditions considered. No relevant differences among the considered groups were found relating to gastric histological changes. Basal and meal-stimulated gastrin were similar in all the studied groups. This study suggests that in patients with chronic pancreatitis there is increased gastric secretion and probably an increased capacity for secretion of acid. Moreover, in patients with chronic pancreatitis, duodenitis seems to be frequent, but it probably is not directly related to chronic alcohol consumption.

Topics: Adult; Alcoholism; Chronic Disease; Duodenum; Female; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Pancreatitis; Stomach

Topics: Biopsy; Chronic Disease; Gastric Mucosa; Gastrins; Gastrointestinal Diseases; Humans; Nucleotides, Cyclic

Of 114 patients with chronic pancreatitis, 19 (16.7%) has gastric or duodenal ulcers. Patients with moderate pancreatic exocrine dysfunction tended to show high acid output and low serum gastrin levels, while those with severe dysfunction had slightly lower acid output and higher serum gastrin levels. The higher the degree of pancreatic fibrosis, the higher tended to be the acid output and serum gastrin levels. Not all patients with ulcers developed hypergastrinemia. The mechanism of acid hypersecretion and ulcer formation in patients with chronic pancreatitis cannot be explained solely by pancreatic deterioration, fibrosis or gastrin release; a decrease in the production and release of gastric inhibitory hormone should be taken into consideration.

Topics: Chronic Disease; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Humans; Male; Middle Aged; Pancreas; Pancreatitis; Stomach Ulcer

Topics: Adult; Chronic Disease; Female; Gastrins; Humans; Male; Middle Aged; Pepsinogens; Peptic Ulcer; Renal Dialysis; Uremia

In order to test tthe hypothesis that chronically elevated serum gastrin levels induce hypercalcitoninaemia, we have measured serum calcitonin levels in patients with chronic hypergastrinaemia. Basal serum calcitonin concentrations were found to be elevated in 2 of 23 patients with Zollinger-Ellison syndrome, but not in 16 patients with hypergastrinaemia due to achlorhydria or a single patient with primary hypergastrinaemia of antral origin. Both Zollinger-Ellison patients with hypercalcitoninaemia (0.31 and 0.79 ng/ml) had multiple endocrine adenomatosis type 1, but no medullary carcinoma of the thyroid. The hypercalcitoninaemia in these patients does not seem to be related to multiple endocrine adenomatosis type 1, since serum calcitonin was normal in 12 normogastrinaemic patients with hyperparathyroidism from families with multiple endocrine adenomatosis type 1. We conclude that chronically elevated serum gastrin levels do not result in hypercalcitoninaemia.

Topics: Calcitonin; Chronic Disease; Gastrins; Humans; Multiple Endocrine Neoplasia; Zollinger-Ellison Syndrome

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

Topics: Adult; Chronic Disease; Duodenal Ulcer; Gastrins; Humans; Middle Aged; Peptic Ulcer; Postgastrectomy Syndromes; Postoperative Period

Fasting serum gastrin and gastrin response to a protein meal were measured in a group of patients with chronic pancreatitis and in controls. No significant differences were found between the two groups of subjects. In patients with chronic pancreatitis no relation was found between gastrin release and the severity of pancreatic exocrine insufficiency.

Topics: Adult; Alcoholism; Chronic Disease; Fasting; Female; Food; Gastrins; Humans; Male; Middle Aged; Pancreatitis

Plasma gastrin levels were measured by radioimmunoassay before and after a test meal associated with 40 ml ethanol in 21 patients presenting with chronic calcifying pancreatitis, in 10 apparently normal subjects drinking since at least 5 years 100 g alcohol a day, in 14 subjects presenting hepatic alcoholic cirrhosis and in 18 apparently normal non alcoholic controls. Post-stimulation gastrin concentration were higher in chronic pancreatitis patients or in normal alcoholics (peak post-stimulation value: 74 +/- 41 and 74 +/- 43 pg/ml respectively) than in cirrhotics or non alcoholic controls (45 +/- 26 and 41 +/- 15 pg/ml respectively) (m +/- SD).

Topics: Adult; Alcoholism; Chronic Disease; Ethanol; Fasting; Food; Gastrins; Humans; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Pancreatitis

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

Topics: Adolescent; Child; Chronic Disease; Duodenal Ulcer; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Pepsin A; Peptic Ulcer

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

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

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

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

Thirteen patients with Zollinger-Ellison syndrome (ZES) were treated with cimetidine. This population could be divided into chronic forms, mostly presenting as a common duodenal ulcer, and acute forms resulting in critical problems requiring intensive medical care. Among the 7 patients with chronic ZES, cimetidine treatment was unsuccessful in 2; satisfactory clinical control was obtained in 3 others, but gastrinoma excision was the final treatment; cimetidine treatment has been prolonged for more than 15 months in the last 2 patients. If, in this condition, acute pharmacologic secretory inhibition were constantly obtained, therapeutic efficiency criteria are not sensitive enough to establish certainty in the patient's long-term follow-up. Total gastrectomy is still a valuable alternative if excision of the gastrinoma is not possible. Of the 6 patients with acute ZES, 4 were treated by pirenzepin (0.5 mg/kg intramuscularly 3 times a day) adjunctive to cimetidine infusion (2.4 mg/day), which resulted in increased antisecretory activity. However, total gastrectomy was the final outcome in every patient, with 1 immediate postoperative death. In conclusion, cimetidine in ZES treatment, although capable of inducing ulcer healing, diarrhea disappearance, and dramatic secretory inhibition, is still challenged by surgery, which allows either complete cure of the gastrinoma or definitive suppression of the secretory virulence.

Topics: Acute Disease; Benzodiazepines; Chronic Disease; Cimetidine; Duodenal Neoplasms; Gastrectomy; Gastrins; Guanidines; Humans; Peptic Ulcer; Piperazines; Zollinger-Ellison Syndrome

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

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

In order to investigate the frequency of fasting hypergastrinaemia in primary hyperparathyroidism (A) and in chronic hypercalcaemia (B), in 40 and 16 patients respectively gastrin, parathyroid hormone (PTH) and serum calcium levels were measured and compared with those of a control group (40 subjects) with similar distribution of sex and age. Moreover, possible linear relationships between these parameters were investigated. Notwithstanding significant differences in calcium and PTH levels between the three groups (A: high PTH, high Ca++; B: low PTH, high Ca++; C: normal PTH and Ca++ levels), no significant difference in gastrin levels were found. However, in the first group, a marked increase of gastrin was observed in one patient, very probably affected by a gastrin-secreting tumor (positive secretin test). While no linear relationship between PTH and gastrin values was present in all the three groups, a significant correlation between serum calcium and fasting gastrin was detectable in the group A, ruling-out the above mentioned patient. Present data suggest that PTH does not modify gastrin levels and that chronic moderate hypercalcaemia does not raise serum fasting gastrin, at least in clinical conditions. Moreover, the frequency of hypergastrinaemia in hyperparathyroidism is very low and it seems to be present only in patients with gastrin-secreting tumors.

Topics: Adult; Aged; Calcium; Chronic Disease; Fasting; Female; Gastrins; Humans; Hypercalcemia; Hyperparathyroidism; Male; Middle Aged; Parathyroid Hormone; Radioimmunoassay

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

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

Secretin releasing response to intraduodenal acid infusion was investigated in 15 cases of diseased control, 7 cases of duodenal ulcer, 5 cases of chronic pancreatitis, and 6 cases of diabetes mellitus. Plasma secretin levels in response to duodenal acidification were less in duodenal ulcer and the appearance of the maximal peak was delayed compared with that found in control. It is suggested that the secretin release was impaired in duodenal ulcer in spite of hypersecretion of gastric acids. In chronic pancreatitis, secretin releasing response to acidification was markedly impaired, in addition, inhibition of secretin release by bicarbonate was diminished due to a lack of bicarbonate flow from the pancreas. On the other hand, although the response of secretin release in diabetes mellitus was also lower compared with that in control group, the capacity of secretin response showed values in-between control subjects and chronic pancreatitis. This research was supported in part by grant from the Ministry of Education, Science and Culture in Japan.

Topics: Adolescent; Adult; Chronic Disease; Diabetes Mellitus; Duodenal Ulcer; Female; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Pancreatitis; Secretin

Topics: Adult; Cholecystitis; Chronic Disease; Duodenal Obstruction; Female; Gastrins; Humans; Male; Middle Aged; Pancreatitis; Peptic Ulcer

Topics: Chronic Disease; Esophageal Achalasia; Esophagus; Gastrins; Humans; Manometry

Topics: Acute Disease; Animals; Chronic Disease; Cysteamine; Disease Models, Animal; Duodenal Ulcer; Duodenum; Female; Gastric Juice; Gastrins; Male; Rats

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

1. In duodenal ulcer patients SPV results in an increase of basal and postprandial serum gastrin levels. There is no decrease of hypergastrinemia even five years after SPV. 2. After SPV there is a significant increase in basal serum GIP levels; postprandial GIP concentrations show a faster increase after food intake. 3. Serum insulin and blood glucose concentrations are not altered by SPV.

Topics: Chronic Disease; Digestion; Duodenal Ulcer; Follow-Up Studies; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Humans; Insulin; Vagotomy

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

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

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

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

In this study the effect of calcium infusion over 3 h without gastric aspiration on serum gastrin was determined in fifteen normal subjects, ten patients with duodenal ulcer, nine with stomal ulcer, five with total gastrectomy, six with achlorhydria and sixteen with proved or presumed Zollinger-Ellison (ZE) syndrome. Serum gastrin only rose significantly in the patients with ZE-syndrome or achlorhydria. An increase of above or below 50% of basal value seems to be a valuable criterion by which to differentiate between patients with and without ZE-syndrome. Serum gastrin levels in forty-four patients with chronic hypercalcaemia (72+/-24 pg/ml, mean+/-SD) were not significantly different from the levels in 100 normal subjects (66+/-18 pg/ml; P greater than 0.10). However, in one patient with ZE-syndrome and in two patients with achlorhydria serum gastrin values were markedly higher during chronic hypercalcaemia than during normocalcaemia. It is concluded that acute or chronic hypercalcaemia without gastric aspiration does not lead to hypergastrinaemia in the absence of ZE-syndrome or achlorhydria.

Topics: Acute Disease; Calcium; Chronic Disease; Gastrins; Humans; Hypercalcemia; Zollinger-Ellison Syndrome

Topics: Chronic Disease; Gastrins; Humans; Liver Diseases; Peptic Ulcer; Prednisone; Stimulation, Chemical

Fasting serum gastrin was determined in 35 Chinese patients with various types of chronic gastritis and in 23 Chinese control subjects. The mean (+/- S.D.) fasting serum gastrin levels for 13 patients with chronic atrophic gastritis, 16 patients with chronic gastritis and six patients with acute-on-chronic gastritis were 32.1 (+/- 38.9) pg./ml., 36.1 (+/- 23.2) pg./ml. and 33.7 (+/- 19.4) pg./ml., respectively. The mean (+/- S.D.) fasting serum gastrin levels for the whole gastritis group (35 patients) and the control group were 34.2 (+/- 28.8) pg./ml. and 24.6 (+/- 13.7) pg./ml., respectively. Statistical analysis showed that the mean basal serum gastrin levels of the three gastritis groups did not differ significantly from control subjects and with each other.

Topics: Adult; China; Chronic Disease; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Singapore

Topics: Animals; Chronic Disease; Dogs; Duodenal Ulcer; Gastrins; Histamine Release; Humans; Hydrogen-Ion Concentration; Polyps; Stomach Neoplasms

Angiographic findings in one giant cell carcinoma, one cystadenocarcinoma, one poorly vascularized mucinous cystadenocarcinoma, as well as in two avascular (gastrin- and glucagon-producing) islet-cell tumors of the pancreas are described. Two hypervascularized islet-cell tumors are presented for comparison and a case of tumorous chronic pancreatitis in a child is reported because ot its rarity. The aggressiveness of the giant cell carcinoma of the pancreas was demonstrated by its expansive growth. In the case of cystadenocarcinoma angiography revealed the tumor with hepatic metastases not diagnosed at explorative laparotomy. The relative hypovascularity in the case of mucinous cystadenocarcinoma was unusual. Both avascular islet-cell tumors simulated a pancreatic pseudocyst and the final diagnosis was made only by immunoassay. Chronic pancreatitis in a child presented with marked hypervascularization.

Topics: Adenoma, Islet Cell; Adult; Aged; Angiography; Carcinoma; Celiac Artery; Chronic Disease; Contrast Media; Cystadenoma; Diagnosis, Differential; Female; Gastrins; Glucagon; Hepatic Artery; Humans; Male; Middle Aged; Pancreatic Cyst; Pancreatic Neoplasms; Pancreatitis; Zollinger-Ellison Syndrome

The response of serum immunoreactive gastric inhibitory polypeptide (IR-GIP), gastrin (IRG) and insulin (IRI) to a mixed standard meal was measured in 15 controls, 6 patients with coeliac disease, 26 patients with chronic pancreatitis and partial duodenopancreatectomy (Whipple's procedure). Serum levels of IR-GIP, IRG and IRI were significantly reduced in patients with coeliac disease. The serum glucose increase was significantly smaller only during the first hour after the meal. Since small intestinal GIP- and G-cells are situated mainly in the glands of duodenal and jejunal mucosa their absolute number is not significantly reduced in coeliac disease. It is suggested that the release of IR-GIP and duodenal IRG is influenced by the rate of absorption of nutrients. In patients with chronic pancreatitis the IR-GIP release is significantly greater than in controls, the IRG release normal and the IRI response delayed. After Whipple's procedure the IR-GIP response is increased significantly while the IRG secretion is abolished. This demonstrates that the duodenum is not necessary for GIP release and that pancreatic and jejunal gastrin are without clinical significance.

Topics: Adult; Aged; Celiac Disease; Chronic Disease; Duodenum; Eating; Female; Gastrins; Gastrointestinal Hormones; Humans; Insulin; Insulin Secretion; Jejunum; Male; Middle Aged; Pancreatectomy; Pancreatitis

On the basis of some experimental observations of hypergastrinemia in animals chronically intoxicated with ethanol, both fasting and after meals serum gastrin were determined in patients affected by chronic alcoholic pancreatitis. A significant increase in serum gastrin levels was observed in patients with chronic pancreatitis compared with controls, both in basal conditions and following food stimulation. The physiopathological hypotheses and possible aetiopathogenetic implications suggested by such gastrin behaviour are discussed.

Topics: Adult; Aged; Alcoholism; Chronic Disease; Gastrins; Humans; Male; Middle Aged; Pancreatitis

Topics: Chronic Disease; Gastrins; Humans; Respiratory Insufficiency

Twenty-nine patients with chronic pancreatitis had a significantly greater IR-GIP response to a test meal than 15 controls. This increased response was not related to the degree of steatorrhoea or glucose intolerance. It was most marked in a group of patients with moderately impaired IRI release and medium steatorrhoea. From this is concluded that the IR-GIP response to a test meal is determined by at least two factors: 1. feedback control via insulin secretion, 2. assimilation of fat. In chronic pancreatitis endocrine insufficiency may induce an exaggerated GIP response and severe exocrine insufficiency may prevent fat induced GIP release. Gastrin is not involved in the different GIP response in patients with chronic pancreatitis.

Topics: Adult; Celiac Disease; Chronic Disease; Eating; Female; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Humans; Insulin; Male; Pancreatitis

Elevation in fasting serum gastrin levels was found in three patients being evaluated for persistent upper abdominal pain without radiographic evidence of peptic ulcer disease. Fiberoptic endoscopy of the upper gastrointestinal tract in each patient revealed characteristic changes of chronic atrophic gastritis. Gastric biopsies showed diffuse chronic inflammation in the lamina propria, a decrease in the number of parietal cells, and "intestinalization" of gastric mucosa. Total achlorhydria was demonstrated after a maximal histalog stimulus; however, serum levels of vitamin B12 and Schilling test values were normal in all three patients. Parietal cell antibodies were found in the serum in all patients in a dilution of 1:20 to 1:80. These cases represent autoimmune (type A) chronic atrophic gastritis and should be distinguished from chronic simple (type B) gastritis, in which serum gastrin levels are normal and no parietal cell antibodies are found in the serum. Patients with autoimmune gastritis should be observed at frequent intervals for the occurrence of pernicious anemia or gastric carcinoma.

Topics: Achlorhydria; Adult; Antacids; Atrophy; Autoantibodies; Autoimmune Diseases; Chronic Disease; Female; Gastrectomy; Gastrins; Gastritis; Humans; Middle Aged

Topics: Adult; Chronic Disease; Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Hepatitis; Humans; Liver; Liver Cirrhosis; Middle Aged; Peptic Ulcer; Stomach Ulcer

Topics: Adult; Chronic Disease; Gastrins; Glomerular Filtration Rate; Humans; Middle Aged; Nephritis; Pyelonephritis

Topics: Chronic Disease; Gastrins; Humans; Peptic Ulcer

Topics: Atrophy; Biopsy; Chronic Disease; Gastric Mucosa; Gastrins; Gastritis; Humans; Sodium; Stimulation, Chemical

Topics: Adult; Aged; Chronic Disease; Fasting; Gastrins; Gastritis; Humans; Middle Aged

Topics: Adolescent; Adult; Biopsy, Needle; Chronic Disease; Duodenal Diseases; Gastric Mucosa; Gastrins; Histocytochemistry; Humans; Middle Aged; Peptic Ulcer; Stomach Diseases

Gastirn blood levels after the ingestion of a meat meal, either alone or associated with ethanol (1.0 gm./kg.), are higher and better sustained in dogs treated chronically with alcohol than in control animals. This greater gastrin-releasing capacity of the dog gastric antrum would be responsible for the increased parietal cell mass and gastric acid secretion shown by animals subjected to chronic alcohol intoxication.

Topics: Alcoholism; Animals; Chronic Disease; Dogs; Ethanol; Fasting; Gastric Mucosa; Gastrins; Humans; Radioimmunoassay; Time Factors

The effects of somatostatin (growth hormone release inhibiting hormone) on basal gastrin were studied in patients suffering from pernicious anaemia and chronic renal and liver disease, and during sequential arginine/insulin-stimulated gastrin release in normal subjects. When basal gastrin concentrations were normal (10-50 pg/ml) in controls and in patients who were in renal and liver failure, somatostatin had no effect on gastrin levels. Raised basal gastrin levels in pernicious anaemia and in 2 cases of chronic renal disease, were significantly inhibited by somatostatin with a half-life (T 1/2) of 3-4 minutes. Arginine infusion caused an insignificant rise in serum gastrin which was unaffected by somatostatin, whereas insulin hypoglycaemia significantly stimulated gastrin release, which was inhibited by somatostatin.

Topics: Adult; Anemia, Pernicious; Arginine; Chronic Disease; Depression, Chemical; Gastrins; Humans; Insulin Antagonists; Kidney Failure, Chronic; Liver Diseases; Secretory Rate; Somatostatin; Stimulation, Chemical

Topics: Adult; Aged; Chronic Disease; Dumping Syndrome; Duodenal Ulcer; Female; Gastrectomy; Gastric Juice; Gastrins; Gastroscopy; Humans; Hypotension; Male; Middle Aged; Pain, Postoperative; Pentagastrin; Postgastrectomy Syndromes; Pyloric Antrum; Pylorus; Radiography; Stomach; Stomach Ulcer; Tachycardia; Vomiting

Topics: Animals; Atropine; Bicarbonates; Chronic Disease; Dogs; Dose-Response Relationship, Drug; Ethanol; Gastric Fistula; Gastrins; Lidocaine; Pancreas; Pancreatic Fistula; Pancreatic Juice; Proteins; Secretin

Topics: Animals; Blood Glucose; Chronic Disease; Depression, Chemical; Dogs; Dose-Response Relationship, Drug; Gastric Fistula; Gastric Juice; Gastrins; Insulin; Stimulation, Chemical; Time Factors

Topics: Animals; Chronic Disease; Gastrins; Gastritis; Humans; Mice

Topics: Anemia, Pernicious; Chronic Disease; Duodenal Ulcer; Epithelial Cells; Fluorescence; Gastric Mucosa; Gastrins; Gastritis; Humans; Immune Sera; Metaplasia; Methods; Stomach Neoplasms; Stomach Ulcer

Topics: Chronic Disease; Gastrins; Gastritis; Zollinger-Ellison Syndrome

The gastric antral mucosa was studied histologically in 22 patients with atrophic gastritis, of whom 11 had high levels and 11 had normal levels of serum gastrin. The antrum was graded histologically from normal to grade 3 gastritis. All patients with hypergastrinaemia (nine seropositive and two seronegative for parietal cell antibody) had either a normal antrum or minimal (grade 1) antral gastritis. In contrast all but one patient without raised serum gastrin (nine seronegative and two seropositive for parietal cell antibody) had severe (grades 2-3) antral gastritis. Thus circulating gastrin levels observed in patients with gastritis and achlorhydria can be directly related to the presence or absence of antral mucosal damage.Comparison of the histological appearances of the antral mucosa with serum gastrin and parietal cell antibody status has provided a basis for the separation of two distinctive forms of atrophic gastritis.

Topics: Achlorhydria; Anemia, Pernicious; Antibodies; Atrophy; Chronic Disease; Gastric Mucosa; Gastrins; Gastritis; Humans; Middle Aged; Postgastrectomy Syndromes; Radioimmunoassay; Stomach

Topics: Anemia, Aplastic; Animals; Antibodies; Chronic Disease; Gastrins; Gastritis; Guinea Pigs; Humans; Liver Diseases; Peptic Ulcer; Rabbits; Radioimmunoassay

Fasting gastrin levels in serum were measured in 49 patients with different types of chronic gastritis and in matched controls. In 15 patients with established pernicious anaemia the mean (+/- S.E. of mean) level of gastrin was greatly raised (699 +/- 99 pg/ml). In 17 patients with chronic atrophic gastritis, seropositive for parietal cell antibody but with adequate vitamin-B(12) absorption, the level was also raised (476 +/- 74 pg/ml). By contrast, in "simple" atrophic gastritis seronegative for parietal cell antibody the gastrin levels were significantly lower for both diffuse atrophic gastritis (129 +/- 31 pg/ml) and multifocal gastritis (14 +/- 4 pg/ml). These levels were similar to those in the controls (46 +/- 7 pg/ml).The mechanism of the raised gastrin levels remains uncertain, but neither achlorhydria nor in vivo action of the parietal cell antibody wholly accounted for the hypergastrinaemia.We conclude that hypergastrinaemia is characteristic of gastritis associated with autoimmune reactions to gastric antigens and pernicious anaemia and that a raised serum gastrin is a useful marker of the type of gastritis that tends to progress to the gastric lesion of pernicious anaemia. The findings suggest that this type of gastritis is an essentially different disease from "simple" atrophic gastritis, and the differences in gastrin levels may be due to sparing of the antral mucosa in the autoimmune type but not in "simple" gastritis.

Topics: Achlorhydria; Aged; Anemia, Pernicious; Antibodies; Antigens; Autoimmune Diseases; Chronic Disease; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Vitamin B 12

Topics: Achlorhydria; Chronic Disease; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Histamine; Humans; Hydrogen-Ion Concentration; Hypertrophy; Insulin; Intubation, Gastrointestinal; Protein-Losing Enteropathies; Stimulation, Chemical; Stomach; Stomach Diseases; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Adolescent; Adult; Aged; Chronic Disease; Female; Gastric Juice; Gastrins; Gastritis; Humans; Injections, Intramuscular; Male; Middle Aged

Topics: Adult; Aged; Cholecystokinin; Chronic Disease; Duodenal Ulcer; Duodenum; Female; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Injections, Intravenous; Male; Middle Aged; Pancreatitis; Secretin; Secretory Rate; Stomach

Topics: Biopsy; Chronic Disease; Duodenal Ulcer; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Injections, Subcutaneous; Time Factors

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

Topics: Adult; Chronic Disease; Duodenal Ulcer; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastritis; Humans; Male; Methods; Middle Aged; Nausea; Succinates

Topics: Afferent Loop Syndrome; Cholecystokinin; Chronic Disease; Gastrectomy; Gastrins; Humans; Methods; Recurrence; Secretin; Stomach Ulcer

Topics: Acetylcholine; Acute Disease; Amides; Amino Acids; Animals; Bethanechol Compounds; Blood Pressure; Chronic Disease; Dogs; Drug Synergism; Gastric Fistula; Gastric Juice; Gastrins; Gastrointestinal Motility; Guinea Pigs; Histamine; Ileum; Male; Methacholine Compounds; Pepsin A; Peptides; Perfusion; Pylorus; Rats; Stomach; Tachyphylaxis

Topics: Age Factors; Animals; Chronic Disease; Cystic Fibrosis; Depression, Chemical; Dogs; Gastrins; Injections, Intravenous; Pancreatitis; Secretin; Sex Factors; Vagus Nerve

Topics: Age Factors; Chronic Disease; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Glycyrrhiza; Humans; Male; Plants, Medicinal; Regeneration; Stomach Ulcer; Terpenes

Topics: Amylases; Bicarbonates; Bilirubin; Cholecystokinin; Chronic Disease; Duodenum; Gastrins; Humans; Lipase; Methods; Pancreatic Juice; Pancreatitis; Peptides; Secretin; Stimulation, Chemical; Stomach; Trypsin

Topics: Adolescent; Adult; Child; Chronic Disease; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastritis; Histamine; Humans; Middle Aged; Pyrazoles

Topics: Chronic Disease; Duodenal Ulcer; Gastric Juice; Gastrins; Humans; Injections, Intravenous; Intestinal Secretions; Pylorus; Vagotomy