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 somatostain 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.

Key Words:

• Antral somatostatin
• Helicobacter pylori
• serum gastrin