Gastric adaptation to aspirin and Helicobacter pylori infection in man

The relationship between Helicobacter pylori infection and aspirin (ASA)-in duced gastropathy and gastric adaptation to ASA remains unclear. We compare d gastric damage and adaptation after repeated exposures to ASA in the same subjects without H. pylori infection and those infected by H. pylori befor e and after eradication of this H. pylori. Twenty-four volunteers in two gr oups (A and B), without H. pylori infection (group A) and with H. pylori in fection (group B) before and after H. pylori eradication, were given ASA 2 g/day or placebo for 14 days. Mucosal damage was evaluated by endoscopy and gastric microbleeding; mucosal prostaglandin (PG) E-2 generation and lumin al transforming growth factor (TGF)alpha were determined on days 0, 3, 7 an d 14 of the ASA course. In all subjects, ASA-induced gastric damage reached a maximum on day 3. In H. pylori-positive subjects this damage was maintai ned at a similar level up to the 14th day of observation. Following H. pylo ri eradication, the damage was significantly lessened at day 14, as reveale d by both endoscopy and microbleeding, and was accompanied by increased muc osal release of TGF alpha. Prostaglandin E-2 generation was significantly h igher in H. pylori-positive subjects than after H. pylori eradication, but ASA treatment resulted in greater than 90% reduction of this generation ind ependent of H. pylori status. Gastric adaptation to ASA is impaired in H. p ylori-positive subjects but eradication of this bacterium restores this pro cess.