INFECTION OF HELICOBACTER-PYLORI IN GASTRIC ADAPTATION TO CONTINUED ADMINISTRATION OF ASPIRIN IN HUMANS

Background & Aims: Involvement of Helicobacter pylori in aspirin-induc ed gastropathy and adaptation to aspirin remains unclear. The aim of t his study was to compare gastric damage and adaptation after repeated exposures to acetylsalicylic acid in the same subjects before and afte r eradication of H. pylori. Methods: Before and after H. pylori eradic ation, 8 volunteers were given aspirin, 2 g/day during 14 days. Mucosa l damage was evaluated by endoscopy and histological analysis of biops y samples. Gastric microbleeding, DNA synthesis, prostaglandin E-2 gen eration, and luminal contents of transforming growth factor alpha and its immunohistochemical expression were determined on days 0, 3, 7, an d 14 of aspirin course. Results: In all subjects, aspirin-induced gast ric damage that reached maximum on day 3. In H. pylori-positive subjec ts, this damage was maintained at a similar level up to day 14. After H. pylori eradication, the damage was significantly lessened both in e ndoscopy and histology at day 14 and accompanied by increased mucosal expression and luminal release of transforming growth factor alpha. Pr ostaglandin E-2 generation was significantly greater in H. pylori-posi tive subjects than after H. pylori eradication, but aspirin treatment resulted in >90% reduction of this generation independent of H. pylori status. Conclusions: Gastric adaptation to aspirin is impaired in H. pylori-positive subjects, but eradication of this bacterium restores t his process.