Non steroidal anti-inflammatory drugs (NSAIDs) are used for their anti-inflammatory, analgesic and anti-pyretic properties. NSAIDs exert their effect by inhibiting the cyclooxygenase (COX) enzyme. All NSAIDs inhibit the isoenzyme COX-2, however non-selective NSAIDs also inhibit COX-1. Inhibition of COX-1 results in decreased production of prostaglandins and thromboxane, which are involved with gastroprotection and thrombotic effects.

Inhibition of COX-2 results in decreased production of prostaglandins and prostacyclins, which are involved with inflammation and decreased platelet aggregation. It is believed that the mechanism for increased cardiovascular adverse outcomes with the use of selective COX-2 inhibitors is due to the lack of inhibition of thromboxane production, in conjunction with inhibition of prostacyclins. The most likely theory for the differences between the NSAIDs in terms of cardiovascular risk is their degree of selectivity for COX-2 compared with COX-1.

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A joint initiative of the Patient Services Section and the Drug and Therapeutics Information Service of the Pharmacy Department, Repatriation General Hospital, Daw Park, South Australia. The RGH Pharmacy E-Bulletin is distributed in electronic format on a weekly basis, and aims to present concise, factual information on issues of current interest in therapeutics, drug safety and cost-effective use of medications.

Editor: Assoc. Prof. Chris Alderman, University of South Australia – Director of Pharmacy, RGH © Pharmacy Department, Repatriation General Hospital, Daw Park, South Australia 5041.

Tagged as: anti-inflammatories, cardiovascular, COX-1, COX-2, NSAID, prostaglandin, RGH E-bulletin, thromboxane

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