NSAIDs are a structurally varied group of compounds with common therapeutic effects (T§bl§.,16§:2)- NSAIDs inhibit the enzyme cyclooxygenase (COX), which is responsible for the production of prostaglandins from arachidonic acid. NSAIDs mediate inflammation through inhibition of prostaglandin production but may also inhibit neutrophils via nonprostaglandin mechanisms. NSAIDs work as antipyretics through inhibition of prostaglandin E 2 (PGE2) in the hypothalamus. The mechanism of NSAID-mediated analgesia is less clear than anti-inflammatory and antipyretic effects, but NSAIDs appear to attenuate prostaglandin-mediated hyperalgesia and local pain-fiber stimulus.
There are at least two forms of cyclooxygenase: COX I and II. COX I is found predominately in blood vessels, stomach, and kidneys at steady levels. COX II is not usually found at significant levels in human tissue; rather, production of the enzyme is induced by local inflammatory mediators. Most NSAIDs inhibit both COX I and COX II. Inhibition of COX I is believed to be responsible for much of the unwanted side effects of NSAIDs. Work is currently under way to develop selective inhibitors of COX II, which may be better anti-inflammatory agents and have fewer ill effects on the renal/GI and vascular system.
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