HELICOBACTER-PYLORI INFECTION IS ASSOCIATED WITH LOW ANTRAL SOMATOSTATIN CONTENT IN YOUNG-ADULTS - IMPLICATIONS FOR THE PATHOGENESIS OF HYPERGASTRINEMIA

Background: Recent studies on the role of Helicobacter pylori in the p athogenesis of duodenal ulcers have focused on the mechanism by which H. pylori infections cause exaggerated gastrin release. Methods: We de termined meal-stimulated serum gastrin concentrations and antral somat ostain content in 24 asymptomatic Volunteers (6 H. pylori-infected, 18 H. pylori-uninfected). Somatostatin content was determined by radioim munoassay in biopsy specimens obtained from the antrum. Results: Fasti ng and integrated 2-h gastrin concentrations were significantly higher in H. pylori-positive volunteers than in H. pylori-negative volunteer s (fasting, 111 +/- 16.3 pmol/l Versus 53.4 +/- 3.5 pmol/l; p < 0.05; integrated 2-h, 2.67 +/- 41.2 pmol/l versus 70.1 +/- 2.1 pmol/l; p < 0 .01). Antral somatostatin content was 0.764 +/- 0.173 ng/mg and 2.931 +/- 0.414 ng/mg in H. pylori-positive and -negative volunteers, respec tively (p < 0.01). Conclusions: Low antral somatostatin content may ca use hypergastrinemia in asymptomatic healthy volunteers, and H. pylori may contribute to the pathogenesis of duodenal ulcer, through this me chanism.