Abstract

The existence of two isoforms of the cyclo-oxygenase (COX) enzyme leads to the distinction between conventional non steroidal anti-inflammatory drugs (NSAIDs), which inhibit COX-2 and more or less COX-1, and coxibs, which are selective COX-2 inhibitors. The pathophysiological functions of COX-1 and COX-2 explain the similarities and differences between these two categories of NSAIDs. Both produce similar efficacy in symptomatic osteoarthritis and rheumatoid arthritis. Unfortunately, their dermatological and renal adverse events (sodium and water retention, acute renal failure) are very similar, as well as their drug-drug interactions. Furthermore, dyspeptic symptoms are virtually as common in patients receiving coxibs than in those taking conventional NSAIDs. On the other hand, gastroduodenal ulcers and ulcer complications (bleeding, perforation) are about twice less frequent with coxibs than with conventional NSAIDs. This benefit is wiped out in patients taking a coxib along with low-dose aspirin. Since coxibs may increase the risk of cardiovascular thrombotic events, they carry a contraindication for use in patients with ischaemic heart disease or stroke. Finally, coxibs should be prescribed to selected patients only, especially those suffering from osteoarthritis and rheumatoid arthritis with increased susceptibility to gastroduodenal ulcers, but without concomitant established arterial disease. Accordingly, conventional NSAIDs have more indications and they are intended for a larger population.

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