Traitements curatif et préventif des ulcères gastro-duodénaux induits par les AINS

Abstract

The use of treatments to heal or to prevent nonsteroidal anti-inflammatory drugs (NSAIDs) associated gastroduodenal lesions is based on replacement of mucosal prostaglandin deficiency or inhibition of acid secretion. Four-week acid suppression by proton pump inhibitors (PPI) with 7-day eradication triple therapy in Helicobacter pylori positive patients is effective in healing gastric and duodenal ulcer upon discontinuation of NSAIDs. In the event NSAIDs must be continued, PPIs (omeprazole 20 mg, lansoprazole 30 mg, pantoprazole 40 mg) are more effective than H2-blockers and cytoprotective agents (sucralfate, misoprostol) to heal mucosal lesions. In long-term prevention studies, omeprazole 20 mg, lansoprazole 15 mg, and pantoprazole 20 mg significantly reduce gastric and duodenal ulcer rates. Misoprostol 800 microg is as effective as PPIs for preventing symptomatic and complicated gastric ulcers, but less effective to prevent duodenal ulcer, with a high rate of adverse effects such as diarrhea. Helicobacter pylori eradication in infected patients decrease the risk of NSAIDs-associated lesions but is less effective than concomitant antisecretory treatment. Current data from comparative studies of PPIs vs ranitidine or misoprostol are in favor of the PPIs as well tolerated and effective drugs in the prophylaxis of NSAIDs-related gastroduodenal lesions in high-risk patients.