Anti-inflammatories and gastroduodenal damage: therapeutic options.

Abstract

The association between use of nonsteroidal anti-inflammatory drugs (NSAIDs) and the development of upper gastrointestinal (GI) damage is well established. Studies have indicated that 12-30% of NSAID users will develop gastric ulcers and that 2-19% will develop duodenal ulcers. Furthermore, many NSAID-induced ulcers are "silent" and are only discovered when complications occur. When possible, the most effective method of preventing NSAID-induced gastropathy is discontinuation of NSAIDs or a reduction in the NSAID dosage. For patients who require continued NSAID therapy, four classes of drugs have been evaluated for their potential protective effects against NSAID-induced gastroduodenal damage:H2-receptor antagonists (eg, ranitidine), proton pump inhibitors (eg, omeprazole), acid-barrier compounds (eg, sucralfate), and prostaglandin E1 analogues (eg, misoprostol). H2-receptor antagonists have not been shown to be effective in preventing NSAID-induced gastric ulcers, and sucralfate has not been shown to be effective in preventing NSAID-induced gastric or duodenal ulcers. Similarly, newer proton pump inhibitors, such as omeprazole, do not appear to protect the stomach against NSAID-induced damage. In contrast, misoprostol has proven its efficacy in preventing both gastric and duodenal ulcers in arthritis patients taking NSAID therapy.