EPIDEMIOLOGY AND PREVENTION OF NONSTEROIDAL ANTIINFLAMMATORY DRUG EFFECTS ITN THE GASTROINTESTINAL-TRACT

Lesions of the gastric, duodenal and intestinal mucosae are found in l arge numbers of patients using non-steroidal anti-inflammatory drugs ( NSAIDs); however, no markers have yet been isolated to identify patien ts at risk for developing gastrointestinal problems or to predict whic h patients with lesions are at risk for developing catastrophic compli cations. There appears to be a poor correlation between the presence o f ulcer disease and the appearance of symptoms while patients are usin g NSAIDs. The ideal treatment-namely, withdrawal from NSAIDs-may not a lways be practicable in patients who require the analgesic benefit of these otherwise generally innocuous agents. It is incumbent on the cli nician to identify the agent most appropriate for the needs of the ind ividual, and to supplement NSAID therapy, where appropriate, with a me ans of preventing or minimizing adverse effects. Four classes of drugs are used to prevent NSAID-related gastric mucosal damage: histamine ( H-2)-receptor antagonists (ranitidine, cimetidine, nizatidine, famotid ine); gastric acid-pump inhibitor (omeprazole); barrier agent (sucralf ate); and prostaglandin analogue (misoprostol). The current therapies (H-2 antagonists and barriers) have not lived up to their promise for preventing gastroduodenal erosion. Moreover, such protection as they p rovide is limited to the duodenal mucosa; they afford no protection to the gastric mucosa. Preliminary data indicate that an acid pump inhib itor may be useful, but large-scale studies have yet to be reported. A cute and long-term studies of the prostaglandin analogue misoprostol h ave shown that this agent has an important role as an adjunctive thera py to prevent both gastric and duodenal ulceration due to NSAIDs.