NONSTEROIDAL ANTI-INFLAMMATORY drugs (NSAIDs) are among the most widely used medications in the world.1 NSAIDs inhibit cyclooxygenase-1 (COX-1) and COX-2 isoenzymes. Inhibition of COX-1 isoenzymes inhibits the production of thromboxane and thus inhibits platelet aggregation. In addition, inhibition of COX-1 isoenzymes compromises the gastrointestinal mucosa. As a result, the major limitation of NSAIDs is gastrointestinal toxicity, resulting in upper gastrointestinal events in 2% to 4% of patients per year.1
Selective COX-2 Inhibitors, NSAIDs, Aspirin, and Myocardial Infarction. Arch Intern Med. 2002;162(10):1091–1092. doi:10.1001/archinte.162.10.1091
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