Complications digestives de l'aspirine

Abstract

This review focuses on aspirin-related gastrointestinal side-effects and the mechanism by which aspirin causes gastrointestinal damage. Aspirin causes direct gastric damage by topical irritant effects and indirect damage via systemic inhibition of cyclooxygenase synthesis and microcirculation injury. The question of a possible synergistic relation between the presence of Helicobacter pylori infection and aspirin use on gastric damage is not resolved. The pathogenesis of small intestinal and colonic damage is less well understood; an increase in intestinal permeability and free radical synthesis are suggested. Gastric damage predominates. Gastroduodenal lesions from aspirin have been documented in endoscopy studies. The lesions occur rapidly, even for low-dose aspirin. The association of aspirin consumption with upper gastrointestinal bleeding has been well established. The main risk factors are advanced age, concomitant use of nonsteroidal antiinflammatory drugs and history of ulcer. Low-dose aspirin are associated with increased risk of gastrointestinal bleeding and this risk is dose-dependant. Chronic aspirin consumption can cause iron deficiency anaemia. Uncomplicated gastric ulcer (but not uncomplicated duodenal ulcer) is associated with aspirin use, with relative risk 3. Other upper gastrointestinal complications have been reported: stenosis and perforation. Aspirin can also damage other areas of the gastrointestinal tract. Oesophageal injuries (oesophagitis and stricture) have been reported. Aspirin is associated with variceal bleeding episodes in patients with cirrhosis. The adverse effects of aspirin on the small bowel are perforation, bleeding, increasing permeability. The adverse effects of aspirin on the large intestine are perforation, bleeding, collagenous colitis and anorectal stenosis with suppositories containing aspirin. Direct clinical data regarding prophylaxis with co-administration of a protective drug are not yet available for aspirin. Patients should be made aware of adverse gastrointestinal effects due to aspirin. Further studies regarding prophylactic therapy of low-dose aspirin induced gastroduodenal lesions, which identify a subset of patients who may be at higher risk than the low-dose aspirin population as a whole, are warranted.