Abstract
Recent evidence suggests that sickle cell disease (SCD) can be consideced a hypercoagulable state, in which both platelet activation and thiombin generation are abnormally increased. Although chrombosis is now known to play an important role in at least one of the vasoccusive complications of SCD, namely stroke, the significance of hypercoagulabiliry in the pathogenesis of vascular occlusion in SCD remains unclear. This review summarizes current evidence regarding platelet, coagulation, and fibrinolytic abnormalities in SCD and their possible role in vascular occlusion. Potential implications for therapy are also discussed

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