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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Cyclooxygenase-2 inhibition and coagulation.

Selective inhibitors of cyclooxygenase-2 ( COX-2) have come under scrutiny because of a possibly increased thrombotic risk observed in retrospective studies and comparatively small cancer trials. Indeed, inhibition of COX-2 may favor a prothrombotic environment by suppressing endothelial prostacyclin synthesis while leaving COX-1-dependent platelet thromboxane (TX) A2 synthesis unopposed. However, in vitro studies have shown that the effect of coxibs on coagulation is dependent on several variables; for example, the coxib celecoxib reduces endothelial tissue factor expression, a key initiator of the coagulation cascade. Furthermore, animal studies are inconclusive as some studies investigating the effect of COX-2 inhibition in atherosclerosis imply a detrimental effect of coxibs, whereas others suggest a beneficial effect on plaque progression and stability. In healthy human subjects and in patients with atherosclerotic vascular diseases, the effect of COX-2 inhibition on coagulation is equally unclear as no prospective, randomized, double-blinded studies sufficiently powered to investigate cardiovascular endpoints have been performed to directly investigate a potentially cardiotoxic effect of coxibs. Here, we review the effect of COX-2 inhibition on the coagulation system; we discuss the molecular mechanisms involved and summarize important clinical trials in which an increased frequency of thrombotic complications coxibs was observed.[1]

References

  1. Cyclooxygenase-2 inhibition and coagulation. Steffel, J., Lüscher, T.F., Ruschitzka, F., Tanner, F.C. J. Cardiovasc. Pharmacol. (2006) [Pubmed]
 
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