cholecystokinin and Gastritis--Atrophic

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

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

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

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