NSAID-induced gastric injury: its pathogenesis and management

Injury to the gastric mucosa associated with the use of aspirin and other NSAIDs appears to be principally attributable to impairment of mucosal defense mechanisms against damage by acid and pepsin, that are mediated largely by prostaglandins. Modification of the drug dose or delivery system and substitution of a less gastrotoxic agent, such as a nonacetylated salicylate, are among the initial approaches that have been used to reduce the risk of NSAID-induced gastric injury. Other recommended measures include the avoidance of cigarettes, concentrated alcohol, and combination therapy with multiple NSAIDs. In high-risk patients, especially those with previous peptic ulcer disease, prophylactic therapy with a cytoprotective or acid-secretion-reducing drug is indicated. Drugs often used in the treatment of NSAID-associated mucosal damage include H2-receptor blockers, which inhibit gastric acid secretion, and agents such as synthetic prostaglandins and sucralfate, which improve mucosal defense. More potent inhibitors of gastric acid, such as drugs which block H+/K+ ATPase, may offer improved results for healing NSAID-induced gastric ulcers resistant to other therapy. Because NSAID-induced gastric lesions are not always accompanied by symptoms, patients receiving these drugs must be closely monitored for signs of gastric injury. Small ulcers can generally be healed with antiulcer medications. In patients with larger ulcers, withdrawal of NSAID therapy is usually required, at least until healing has occurred.