Epidemiology and prevention of non-steroidal anti-inflammatory drug effects in the gastrointestinal tract.

Lesions of the gastric, duodenal and intestinal mucosae are found in large numbers of patients using non-steroidal anti-inflammatory drugs (NSAIDs); however, no markers have yet been isolated to identify patients at risk for developing gastrointestinal problems or to predict which patients with lesions are at risk for developing catastrophic complications. There appears to be a poor correlation between the presence of ulcer disease and the appearance of symptoms while patients are using NSAIDs. The ideal treatment--namely, withdrawal from NSAIDs--may not always be practicable in patients who require the analgesic benefit of these otherwise generally innocuous agents. It is incumbent on the clinician to identify the agent most appropriate for the needs of the individual, and to supplement NSAID therapy, where appropriate, with a means of preventing or minimizing adverse effects. Four classes of drugs are used to prevent NSAID-related gastric mucosal damage: histamine (H2)-receptor antagonists (ranitidine, cimetidine, nizatidine, famotidine); gastric acid-pump inhibitor (omeprazole); barrier agent (sucralfate); and prostaglandin analogue (misoprostol). The current therapies (H2 antagonists and barriers) have not lived up to their promise for preventing gastroduodenal erosion. Moreover, such protection as they provide is limited to the duodenal mucosa; they afford no protection to the gastric mucosa. Preliminary data indicate that an acid pump inhibitor may be useful, but large-scale studies have yet to be reported. Acute and long-term studies of the prostaglandin analogue misoprostol have shown that this agent has an important role as an adjunctive therapy to prevent both gastric and duodenal ulceration due to NSAIDs.