Short-term/low-dose aspirin-induced duodenal erosions are not dependent on Helicobacter pylori infection, cyclooxygenase expression and prostaglandin E₂ levels

Abstract

Objective. The mechanisms of interaction between Helicobacter pylori infection and low-dose aspirin in the induction of duodenal erosions are not fully understood. The aim of this study was to investigate the effects of low-dose aspirin on the induction of duodenal erosions, the expression of cyclooxygenases and prostaglandin (PG)-E₂ levels in healthy subjects according to their H. pylori status. Material and methods. Twenty healthy volunteers (H. pylori-negative n=10, H. pylori-positive n=10) received 100 mg aspirin/day for 1 week. During esophagogastroduodenoscopy, duodenal biopsies were taken before and at days 1, 3, and 7 of medication. COX-1 and -2 expressions were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR), and immunohistochemistry; mucosal PGE₂ levels were determined by ELISA. Three months after successful eradication of infection, nine H. pylori-positive subjects repeated the protocol. Results. Aspirin-induced duodenal erosions occurred independently of whether H. pylori infection was present or not. There was no difference in duodenal COX-1 and COX-2 expression among the groups and expression was not affected by aspirin. Basal duodenal PGE₂ levels were similar among the different groups (H. pylori-negative 4.3±4.2, H. pylori-positive 5.2±1.3, following H. pylori eradication 5.2±1.4 ng/µg protein) and were not affected by low-dose aspirin. Conclusions. In healthy subjects, low-dose aspirin-induced duodenal erosions are not influenced by H. pylori status. Low-dose aspirin medication for one week does not affect either cyclooxygenase expression or duodenal PGE₂ levels and therefore is likely to induce duodenal damage mainly through topical toxicity.

• COX-1
• COX-2
• duodenal erosions
• H. pylori
• low-dose aspirin
• PGE₂