the contribution of cyclooxygenase1 and 2 to persistent thromboxane biosynthesis in aspirintreated essential thrombocythemia implications for antiplatelet therapy we tested whether cyclooxygenase 2 cox2 expression and unacetylated cox1 in newly formed platelets might contribute to persistent thromboxane tx biosynthesis in aspirintreated essential thrombocythemia et fortyone patients on chronic aspirin 100 mgday and 24 healthy subjects were studied platelet cox2 expression was significantly increased in patients and correlated with thiazole orangepositive platelets r 071 p 001 the rate of txa2 biosynthesis in vivo as reflected by urinary 11dehydrotxb2 txm excretion and the maximal biosynthetic capacity of platelets as reflected by serum txb2 were higher in patients compared with aspirintreated healthy volunteers serum txb2 was significantly reduced by the selective cox2 inhibitor ns398 added in vitro patients were randomized to adding the selective cox2 inhibitor etoricoxib or continuing aspirin for 7 days etoricoxib significantly reduced by approximately 25 txm excretion and serum txb2 fourteen of the 41 patients were studied again 21 7 months after the first visit serum txb2 was consistently reduced by approximately 30 by adding ns398 in vitro while it was completely suppressed with 50 microm aspirin accelerated platelet regeneration in most aspirintreated et patients may explain aspirinpersistent txa2 biosynthesis through enhanced cox2 activity and faster renewal of unacetylated cox1 these findings may help in reassessing the optimal antiplatelet strategy in et