Kory Tray, MD

For over 25 years, NSAIDs have been used to treat a variety of pain syndromesand inflammatory diseases. More than 50 million Americanstake these drugs. Unfortunately, control of pain and inflammation is notachieved without an associated cost-namely, GI complications and, to a lesserextent, nephrotoxicity.In an attempt to reduce drug-related toxicity, a new class of selectiveNSAIDs-the COX-2 inhibitors-was introduced in 1999. These selectiveNSAIDs are as effective as and pose less risk of gastric toxicity than nonselectiveNSAIDs.1,2The COX-2 inhibitors are thought to reduce end-organ injury, such as GIulceration, by sparing homeostatic or “constitutive” COX-1 enzyme function.1,2 Incontrast, therapeutic effects result from the inhibition of the “inducible” COX-2enzyme.1,2 Such drug effects target the production of proinflammatory prostaglandinsby COX-2 without interrupting normal cell function mediated by COX-1.2,3