HELICOBACTER PYLORI-POSITIVE PEPTIC-ULCER PATIENTS DO NOT ADAPT TO ASPIRIN

Background: Recent studies indicate that eradication of Helicobacter p ylori might prevent peptic ulcer formation in patients treated with no n-steroidal anti-inflammatory drugs (NSAIDs), On the other hand, gastr ic adaptation after repeated exposures to aspirin (ASA) is well docume nted but the influence of H. pylori on this process remains to be eluc idated, Aim: To compare gastric damage and adaptation following repeat ed exposures to ASA in a group of patients with H. pylori infection, b efore and after eradication of the bacterium, and in H, pylori-negativ e controls. Methods: Eight healthy volunteers without H, pylori infect ion and eight patients with duodenal ulcer (DU) history and H. pylori infection before and after H. pylori eradication were given ASA 2 g/da y for a period of 14 days. Mucosal damage was evaluated by endoscopy a nd histology of biopsy samples. Gastric microbleeding, DNA synthesis i n the gastric mucosa and mucosal expression, as well as luminal conten t of transforming growth factor-alpha (TGF alpha) were determined on d ays 0, 3, 7 and 14 of the ASA course. Results: In all patients aspirin -induced gastric damage reached a maximum on day 3. In H, pylori-posit ive patients, this damage was maintained at a similar level up to day 14, whereas in H, pylori-negative controls and H, pylori-eradicated pa tients this damage significantly lessened on day 14 and was accompanie d by elevated DNA synthesis as well as increased mucosal expression an d luminal release of TGF alpha.