cholecystokinin and Gastritis

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

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

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

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

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

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

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

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

Topics: Alkalosis; Anemia, Pernicious; Blood Glucose; Cholecystokinin; Duodenum; Fasting; Gastritis; Glucose; Histamine; Humans; Hydrochloric Acid; Insulin; Secretin

Gastric lipase is one of the prepancreatic lipases found in some mammalian species and in humans. Our knowledge of the hormonal regulation of gastric lipase secretion in children and adolescents is still very limited. The aim of this study was to compare the activity of human gastric lipase (HGL) in gastric juice in healthy adolescents and in patients with gastritis. The adolescents were allocated to three groups: the first including patients with Helicobacter pylori gastritis (HPG; n = 10), the second including patients with superficial gastritis caused by pathogens other than H. pylori (non-HPG; n = 14) and the control group including healthy adolescents (n = 14). Activity of HGL was measured in gastric juice collected during endoscopy. Plasma concentrations of cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) were measured in all adolescents. Activity of HGL in the non-HPG group was significantly lower than in the HPG group (p < 0.005) and the control group (p < 0.005). Mean plasma GIP levels in the control group were lower than in the non-HPG group (p < 0.003) and the HPG group (p < 0.01). We conclude that the regulation of HGL secretion by GLP-1 and CCK is altered in patients with gastritis. Moreover, GIP is a potent controller of HGL activity, both in healthy subjects and in patients with gastritis.

Topics: Adolescent; Body Mass Index; Body Weight; Case-Control Studies; Cholecystokinin; Fasting; Gastric Inhibitory Polypeptide; Gastritis; Gastrointestinal Tract; Glucagon-Like Peptide 1; Helicobacter Infections; Humans; Hydrogen-Ion Concentration; Lipase; Young Adult

Cholecystokinin (CCK) prevents macroscopic injury to the stomach from luminal irritants by an unknown mechanism. The present study was undertaken in conscious rats to ascertain what role gastric mucosal blood flow, sensory neurons, and endogenous somatostatin play in CCK-induced gastric protection. Subcutaneous administration of CCK (10-100 micrograms/kg) significantly reduced macroscopic injury to the acid-secreting portion of the stomach caused by 1 ml of orally administered acidified ethanol (150 mM HCl, 50% ethanol) and augmented gastric mucosal blood flow (fluorescent microspheres) in a dose-dependent fashion. However, although the protective response to CCK (100 micrograms/kg) was still present at 2 h, the blood flow response had returned to baseline by 45 min. Ablation of capsaicin-sensitive afferent neurons with capsaicin (125 mg/kg sc) did not negate CCK-induced protection. Pretreatment with exogenous somatostatin (1 pmol-1 nmol/kg sc) failed to prevent the damaging effects of acidified ethanol to gastric mucosa. Immunoneutralization of endogenous somatostatin with somatostatin monoclonal antibody (2 mg ip) did not reverse the protective actions of CCK. Thus the data suggest that although CCK may prepare the gastric mucosa to withstand a damaging insult by augmenting gastric mucosal blood flow, its protective mechanism is independent of intact sensory neurons and endogenous somatostatin.

Topics: Animals; Capsaicin; Cholecystokinin; Ethanol; Gastric Mucosa; Gastritis; Hydrogen-Ion Concentration; Neurotoxins; Rats; Rats, Sprague-Dawley; Regional Blood Flow; Sincalide; Somatostatin; Time Factors

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

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

Methods of endogenous stimulation of the exocrinous pancreatic function in chronic primary gastroduodenitis were used. It was expressed in parallel gastric hyperchlorhydria, hyperproduction of pancreatic hydrocarbonates at initial stages of chronic primary gastroduodenitis and reduction of their excretion with diverse changes of the activity of pancreatic enzymes in prolonged and persistent course of the disease.

Topics: Cholecystokinin; Chronic Disease; Duodenitis; Gastritis; Humans; Pancreas; Recurrence; Secretin; Stimulation, Chemical

A diffuse peptide microcarcinoidosis was observed both in a 56-year-old man with chronic atrophic gastritis and in a 33-year-old female with chronic atrophic gastritis and pernicious anaemia. Besides hyperplasia of endocrine cells at the base of gastric fundus and corpus mucosa with infiltration of the mucosal muscular layer multiple macro- and micropolyp carcinoids were present. In both cases serotonin was demonstrated immunohistochemically in the intestinal metaplastic mucosal changes, in the microcarcinoidosis foci and in the carcinoids. However, no appropriate clinical symptomatology was observed. The diagnosis can already be made by biopsy which must be deep enough and include gastric mucosa containing the mucosal muscular layer. Should gastric carcinoid be established histologically the other macroscopically normal mucosa must also be biopsied for exclusion of diffuse microcarcinoidosis as intermediate form of a multiple carcinoid. In such a case treatment consists of total gastrectomy.

Topics: Adult; Anemia, Pernicious; Cholecystokinin; Female; Gastrectomy; Gastric Mucosa; Gastritis; Gastritis, Atrophic; Humans; Hyperplasia; Male; Malignant Carcinoid Syndrome; Middle Aged; Serotonin; Somatostatin; Stomach Neoplasms

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

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

In order to evaluate if duodenogastric reflux (DGR) is associated with a different frequency of gastric dysplasia in comparison with the absence of DGR. 40 dyspeptic patients were studied. Nineteen of them had scintigraphic evidence of the DGR, while in 21 DGR was absent. The obtained results demonstrate a higher frequency of antral gastritis in presence of DGR, while fundic gastritis is similarly represented in the two studied groups. Dysplasia of the mild type is observed in 1 case of fundic atrophic gastritis without DGR and in 3 cases of atrophic gastritis with DGR (1 in fundus and 2 in antrum), thus demonstrating that reflux gastritis is not strictly correlated with dysplasia.

Topics: Adult; Biopsy; Cholecystokinin; Duodenogastric Reflux; Female; Gastric Mucosa; Gastritis; Humans; Imino Acids; Male; Middle Aged; Radionuclide Imaging; Technetium

99mTc-diethyl-IDA is completely excreted into the bile. When cholecystokinin is given after priming of the biliary tract with this tracer, gallbladder contraction leads to expulsion of bile into the duodenum. At the same time cholecystokinin causes contraction of the pylorus, which should normally prevent substantial reflux of tracer into the stomach. We have applied these physiological characteristics in a method to quantify biliary gastric reflux. Fourteen controls had a median reflux of 4.3% of the intravenous dose (93% of controls had values less than 9%). In 18 patients with Billroth II gastrectomies the median reflux was 46% (p less than 0.001). Patients with chronic gastritis (no. = 18) had also increased reflux (median 18.1%, p less than 0.001). The same was found in gastric ulcer (no. = 18, median 11.8%, p less than 0.003). In duodenal ulcer (no. = 7) increased reflux existed in only two patients with pyloric deformation. Patients with hiatal hernia did not show increased reflux (no. = 10, median 2.2%). Bilirubin measurements tended to underestimate reflux in pathological cases, whereas bile acid measurements and reflux percentages of tracer showed a close relationship (r = 0.87, p less than 0.001).

Topics: Bile Reflux; Biliary Tract Diseases; Cholecystokinin; Gastrectomy; Gastritis; Humans; Imino Acids; Methods; Stomach Ulcer; Technetium; Technetium Tc 99m Diethyl-iminodiacetic Acid

Twenty-six patients who had typical symptoms of biliary tract disease, e.g. postprandial right upper quadrant pain, nausea and vomiting, fatty food intolerance and flatulence and who had had two or more normal oral cholecystograms were subjected to cholecytokinin cholescystography. Ten patients showed a normal response to the intravenous administration of cholecystokinin, namely prompt and complete emptying of the gallbladder without producing any adverse reaction or symptoms. Sixteen patients demonstrated either no contraction or incomplete contraction of the gallbladder in response to cholecystokinin; several patients had moderate contraction of the gallbladder accompanied by symptoms of biliary colic. This latter group underwent cholecystectomy and operative cholangiography. Fifteen of the 16 patients are asymptomatic or improved, and only one patient continues to have symptoms. All removed gallbladders had histologic evidence of chronic cholecystitis. It is concluded that in some individuals with continuing symptoms suggesting gallbladder disease but normal oral cholecystograms, cholecystokinin cholecystography may be helpful in identifying physiologic dysfunction of the gallbladder.

Topics: Adult; Aged; Cholecystectomy; Cholecystitis; Cholecystography; Cholecystokinin; Diagnosis, Differential; Esophageal Achalasia; Esophageal Neoplasms; Female; Gallbladder; Gallbladder Diseases; Gastritis; Humans; Male; Middle Aged

Topics: Cholecystokinin; Cholelithiasis; Duodenal Ulcer; Esophageal Achalasia; Gastrins; Gastritis; Gastrointestinal Hormones; Humans; Pancreatic Diseases; Peptic Ulcer; Secretin; Stomach Neoplasms; Stomach Ulcer

Topics: Cholecystokinin; Gastric Acidity Determination; Gastritis; Humans; Pancreas; Pancreatitis; Peptic Ulcer; Secretin

Topics: Bicarbonates; Cholecystokinin; Enteritis; Gallbladder Diseases; Gastric Acidity Determination; Gastrins; Gastritis; Pancreas; Pancreatitis; Pyrazoles; Secretin; Stimulation, Chemical; Stomach Ulcer

Topics: Adult; Aged; Alcoholism; Amylases; Bicarbonates; Cholecystokinin; Chronic Disease; Feces; Female; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastritis; Humans; Lipids; Male; Middle Aged; Pancreas; Pancreatic Juice; Pancreatitis; Secretin

Topics: Biliary Dyskinesia; Cholecystitis; Cholecystokinin; Duodenum; Fats; Gastrins; Gastritis; Gastrointestinal Motility; Hepatitis A; Humans; Stomach

Topics: Amyloidosis; Biochemical Phenomena; Biochemistry; Cholangitis; Cholecystitis; Cholecystokinin; Colonic Neoplasms; Drug Therapy; Duodenum; Electrophoresis; Enteritis; Gastritis; Hemosiderosis; Humans; Intestinal Secretions; Leucyl Aminopeptidase; Liver Cirrhosis; Liver Diseases; Melanoma; Mucous Membrane; Nephrosis; Pancreatitis