Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) block the enzyme cyclo-oxygenase (COX), thereby reducing the synthesis of prostaglandins from arachidonic acid. This blockade is believed to be responsible for both the therapeutic (anti-inflammatory) and many of the unwanted effects of NSAIDs.1 It is now recognised that COX exists in two functionally distinct isoforms: COX-1 is active continuously and catalyses the synthesis of prostaglandins with physiologically protective effects (e.g. on the gastric mucosa), while COX-2 is induced during inflammation.2^,3 ▼Meloxicam (Mobic - Boehringer Ingelheim), which has been available in the UK for 2 years, is marketed as an NSAID with "COX-2 selectivity" in vitro, and so one which "in theory...should have a better GI side-effect profile". Is meloxicam an advance on traditional NSAIDs?