The "aspirin" of the new millennium: cyclooxygenase-2 inhibitors.

Abstract

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin synthesis via the cyclooxygenase (COX) enzyme, the key to both therapeutic benefits and toxicity. COX enzyme exists in 2 isoforms, COX-1 and COX-2. COX-1 enzyme is thought to mediate "housekeeping" or homeostatic functions, and COX-2 is considered an inducible enzyme in response to injury or inflammation. COX-2 inhibitors are the "next-generation" NSAIDs that may selectively block the COX-2 isoenzyme without affecting COX-1 function. This may result in control of pain and inflammation with a lower rate of adverse effects compared with older nonselective NSAIDs. Rapidly evolving evidence suggests that COX-2 enzyme has a diverse physiologic and pathologic role. This article addresses the role of COX-2 enzyme in health and disease as well as the potential therapeutic value and safety issues related to COX-2 inhibition.