BMJ  2006;332:1451-1452 (17 June), doi:10.1136/bmj.332.7555.1451-b

Letter

Life without COX 2 inhibitors

Risks and benefits are determined by dose and potency

The first 150 words of the full text of this article appear below.

EDITOR—The paper by Kearney et al on the risk of atherothrombosis with cyclo-oxygenase-2 (COX 2) inhibitors and traditional non-steroidal anti-inflammatory drugs (NSAIDs) supports the data of Hippisley-Cox et al, who revised the gastrointestinal risks of these drugs.1 2


Figure Removed (Available Only in the Full Text)
 

A clear picture is forming, that the risks and benefits are determined by doses and potencies more than by their selectivity to the cyclo-oxygenases, with the exception of low dose aspirin, which permanently inhibits platelet function without affecting endothelial prostacyclin, producing the useful antithrombotic effect. But in higher doses, aspirin is also toxic.

Over 20 years ago a report from England showed that all NSAIDs could produce some deaths per million prescriptions.3 The least potent, such as ibuprofen, had the lowest risk of death (1.5), the risk increasing with potency (naproxen 4.6, diclofenac 5.3, piroxicam 7.0, and indomethacin 7.1).

The cardiovascular risk of COX 2 inhibitors follows a similar pattern. The . . . [Full text of this article]

Enrique J Sánchez-Delgado, professor

Hospital Metropolitano Vivian Pellas, Managua, Nicaragua esanchez@metropolitano.com.ni


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Do selective cyclo-oxygenase-2 inhibitors and traditional non-steroidal anti-inflammatory drugs increase the risk of atherothrombosis? Meta-analysis of randomised trials
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