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BMJ 2006;332:1451-1452 (17 June), doi:10.1136/bmj.332.7555.1451-b
| The first 150 words of the full text of this article appear below. |
EDITORThe 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
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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
Enrique J Sánchez-Delgado, professor
Hospital Metropolitano Vivian Pellas, Managua, Nicaragua esanchez@metropolitano.com.ni
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