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I read with great interest the review article by Lipsky et al¹ dealing with unresolved issues in the role of cyclooxygenase (COX) isoforms in normal physiologic processes and disease. The authors inferred from the available data that COX-2–specific inhibitors may have new therapeutic targets, such as adenomatous polyposis and colon cancer, and new untoward effects, such as thromboembolic cardiovascular adverse events, as compared with conventional nonsteroidal anti-inflammatory drugs (NSAIDs), which block both COX-1 and COX-2 activity.

Another key issue is whether COX-2–specific inhibitors have similar analgesic efficacy to conventional NSAIDs in acute pain states.² In fact, celecoxib was reported to be somewhat less effective than traditional nonselective NSAIDs in patients with postsurgical dental pain.³ Furthermore, the Food and Drug Administration described the multiple dose studies (treatment for up to 7 days) in patients with other types of pain as inconclusive.³ On the other hand, rofecoxib was found to provide analgesic . . . [Full Text of this Article]