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REVIEW ARTICLE
Year : 2021  |  Volume : 6  |  Issue : 1  |  Page : 1-5

Hemostatic alteration in sickle cell disease: Pathophysiology of the hypercoagulable State


Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Saud bin Abdulaziz University for Health Sciences; King Abdullah International Medical Research Center, Riyadh, Saudi Arabia

Correspondence Address:
Naif Mohammed Alhawiti
Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Saud bin Abdulaziz University for Health Sciences, P.O. Box 22490, Riyadh 11481
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/KKUJHS.KKUJHS_7_21

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Sickle cell disease (SCD) is a monogenic genetic disease inherited in an autosomal recessive manner and distinguished by the presence of defective hemoglobin, known as homozygous sickled hemoglobin disease (HbSS). Sickled red blood cells lead to blood vessel obstruction, hemorrhage, and critical hemostatic function alterations. Defective hemoglobin that associated with serious health problems, such as thromboembolism among SCD patients, is clearly documented. Empirical evidence indicates that hypercoagulability states and proinflammatory phenotypes in patients with SCD are a substantial contribution of thromboembolic complications, with promoting morbidity and mortality. This review discusses the involvement of vascular endothelial cell, platelet, and coagulation cascade in the thrombogenesis of SCD.


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