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- W3049236424 endingPage "2379" @default.
- W3049236424 startingPage "2368" @default.
- W3049236424 abstract "The genetic and molecular basis of sickle cell disease (SCD) has long since been characterized but the pathophysiological basis is not entirely defined. How a red cell hemolytic disorder initiates inflammation, endothelial dysfunction, coagulation activation and eventually leads to vascular thrombosis, is yet to be elucidated. Recent evidence has demonstrated a high frequency of unprovoked/recurrent venous thromboembolism (VTE) in SCD, with an increased risk of mortality among patients with a history of VTE. Here, we thoroughly review the molecular basis for the prothrombotic state in SCD, specifically highlighting emerging evidence for activation of overlapping inflammation and coagulation pathways, that predispose to venous thromboembolism. We share perspectives in managing venous thrombosis in SCD, highlighting innovative therapies with the potential to influence the clinical course of disease and reduce thrombotic risk, while maintaining an acceptable safety profile." @default.
- W3049236424 created "2020-08-21" @default.
- W3049236424 creator A5007450531 @default.
- W3049236424 creator A5008129268 @default.
- W3049236424 creator A5049700042 @default.
- W3049236424 date "2020-08-13" @default.
- W3049236424 modified "2023-10-16" @default.
- W3049236424 title "The molecular basis for the prothrombotic state in sickle cell disease" @default.
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