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Summary

Background  The mechanisms by which Helicobacter pylori and low-dose aspirin induce gastric damage are not completely elucidated.

Aim  To evaluate the effects of low-dose aspirin on gastric damage, mucosal prostaglandin-E2 levels and cyclooxygenase-enzyme expression in relation to the H. pylori status.

Methods  Twenty healthy volunteers (H. pylori positive, n = 10; H. pylori negative, n = 10) received aspirin 100 mg/die for 1 week. At days 0, 1, 3 and 7, gastric mucosal lesions were studied by oesophagogastroduodenoscopy and histology. COX-1 and COX-2 were determined by immunohistochemistry and reverse-transcriptase polymerase chain reaction, and mucosal prostaglandin-E2 levels by enzyme-linked immunosorbent assay. Nine H. pylori-positive subjects repeated the protocol after H. pylori eradication.

Results  All groups developed a similar number of erosions. COX-1 and COX-2 expression, as well as mucosal prostaglandin-E2 levels were not influenced by H. pylori status and aspirin medication. Helicobacter pylori-negative and H. pylori-eradicated subjects who developed aspirin-induced erosions had significant lower pre-treatment antral prostaglandin-E2 levels than those without erosions (3.6 ng/μg vs. 6.3 ng/μg protein and 3.6 ng/μg vs. 6.0 ng/μg protein, respectively, P < 0.01 Mann–Whitney U-test).

Conclusions  In healthy subjects, low-dose aspirin for 1 week does neither affect cyclooxygenase expression nor mucosal prostaglandin-E2 levels. Antral prostaglandin-E2-basal levels appear to be critical for development of aspirin-induced gastric damage in subjects without H. pylori infection.