Treatment of nonsteroidal anti-inflammatory drug-induced gastropathy

Abstract

The etiology, natural history, epidemiology, prevention, and treatment of nonsteroidal anti-inflammatory drug (NSAID)-induced gastrointestinal (GI) effects are reviewed. Current evidence suggests that NSAIDs cause acute cellular damage by a topical effect that is exacerbated by impaired healing. Although acute gastric injury from NSAIDs is rapid and almost uniform from patient to patient, not all patients develop serious chronic injury. Some adaptation to the effects of NSAIDs does occur. Endoscopic studies have found that 14-31% of long-term NSAID users have gastric or duodenal ulcers. Data on individual drugs are inconsistent, but they suggest that enteric-coated aspirin, salsalate, and ibuprofen cause the lowest incidence of GI hemorrhage. Preventive measures tested to date include reduction in gastric acid production (histamine H2-receptor antagonists) and attempts to increase mucosal defenses (sucralfate or misoprostol). Misoprostol is the only drug with FDA-approved labeling for prevention of NSAID-induced gastropathy. NSAID-related ulcers heal in most patients within two to three months when they are treated with H2-receptor antagonists with or without antacid, omeprazole, or misoprostol. In patients with multiple risk factors, prophylaxis with misoprostol would be appropriate unless the clinician is concerned solely about reactivation of a duodenal ulcer, in which case an H2-receptor antagonist would also be appropriate. Full-dose treatment with H2-receptor antagonists, omeprazole, or misoprostol will heal NSAID-induced ulcers, even when NSAID therapy is continued.