[Campylobacter pylori colonization of the antrum: effect of gastrin, somatostatin, pancreatic polypeptide and neurotensin].

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