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Professor John Vane won the Nobel Prize for elucidating the mechanism of action of aspirin. He reported that this was accomplished by blocking the enzyme called cyclooxygenase (COX-1) that was responsible for the conversion of arachidonic acid to prostaglandins. Prostaglandins liberated from arachidonic acid by cyclooxygenase are short-lived substances that act as local hormones (autocoids) important in normal physiology and pathologic conditions. Prostaglandins E2 (PGE2) is the principal eicosanoid in inflammatory conditions. Since that discovery, more than 30 nonsteroidal anti-inflammatory drugs (NSAIDs) have come on the market, and they represent the most widely prescribed class of drugs in the world. Along with their benefits, several side effect involving the gastrointestinal, renal, and hemopoietic systems have emerged that have limited their usefulness. Recently, a second cyclooxygenase enzyme system that appears to be only upregulated in inflammation has been described. Inhibition of this second enzyme (COX-2) appears to confer anti-inflammatory effects without inhibiting the prostaglandins that are important for normal physiologic function of the gastrointestinal, renal, and hemopoietic systems.

Clinical Implications of Cyclooxygenase Enzymes: COX-1/COX-2 Role of the New NSAIDs