Helicobacter pylori infection is associated with low antral somatostatin content in young adults. Implications for the pathogenesis of hypergastrinemia

Abstract

Background: Recent studies on the role of Helicobacter pylori in the pathogenesis of duodenal ulcers have focused on the mechanism by which H. pylori infections cause exaggerated gastrin release.

Methods: We determined meal-stimulated serum gastrin concentrations and antral somatostatin content in 24 asymptomatic volunteers (6 H. pylori-infected, 18 H. pylori-uninfected). Somatostatin content was determined by radioimmunoassay in biopsy specimens obtained from the antrum.

Results: Fasting and integrated 2-h gastrin concentrations were significantly higher in H. pylori-positive volunteers than in H. pylori-negative volunteers (fasting, 111 +/- 16.3 pmol/l versus 53.4 +/- 3.5 pmol/l; p < 0.05; integrated 2-h, 267 +/- 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, respectively (p < 0.01).

Conclusions: Low antral somatostatin content may cause hypergastrinemia in asymptomatic healthy volunteers, and H. pylori may contribute to the pathogenesis of duodenal ulcer, through this mechanism.