Scandinavian journal of gastroenterology · 2008
Short-term/low-dose aspirin-induced duodenal erosions are not dependent on Helicobacter pylori infection, cyclooxygenase expression and prostaglandin E2 levels.
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Venerito Marino, Treiber Gerhard, Wex Thomas, Kuester Doerthe, Roessner Albert, Mönkemüller Klaus, Malfertheiner Peter
Аннотация
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)-E(2) 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 PGE(2) 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 PGE(2) 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/microg 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 PGE(2) levels and therefore is likely to induce duodenal damage mainly through topical toxicity.
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 PGE(2) 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 PGE(2) 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/microg 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 PGE(2) levels and therefore is likely to induce duodenal damage mainly through topical toxicity.