Adverse upper gastrointestinal effects of rofecoxib compared with NSAIDs.

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Abstract
Two isoforms of cyclooxygenase (COX), COX-1 and COX-2,1-4 catalyze human prostaglandin synthesis. Almost all currently available nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit both COX isoforms.5 COX-1 is constitutively expressed and generates prostaglandins believed to be involved in gastrointestinal (GI) mucosal protection,6 while COX-2 is induced at sites of inflammation throughout the body and generates prostaglandins that mediate inflammation and pain.7 Therefore, the anti-inflammatory effects of NSAIDs appear to be mediated via inhibition of COX-2,8 while the deleterious GI effects, a significant source of morbidity and mortality, are believed to occur primarily via inhibition of COX-1.5 These GI-related adverse effects (AEs)9-11 are estimated to be responsible for 107,000 hospitalizations and 16,500 deaths annually in the United States alone.12

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