Hypercoagulability in sickle cell disease and beta-thalassemia.

Abstract:

:Sickle cell disease (SCD) and beta-thalassemia (also referred to as beta-thalassemia) are common hereditary hemoglobinopathies with differing pathophysiologies and clinical courses. However, patients with both diseases exhibit increased platelet and coagulation activation, as well as decreased levels of natural anticoagulant proteins. In addition, they are characterized by thrombotic complications that may share a similar pathogenesis. The pathogenesis of hypercoagulability is likely multifactorial, with contributions from the abnormal red blood cell (RBC) phospholipid membrane asymmetry, ischemia-reperfusion injury, and chronic hemolysis with resultant nitric oxide depletion. More studies are needed to better define the contribution of hemostatic activation to the pathophysiology of SCD and beta-thalassemia. Furthermore, adequately controlled studies using anticoagulants and antiplatelet agents are warranted to define the role of hypercoagulability in specific complications of these diseases.

journal_name

Curr Mol Med

authors

Singer ST,Ataga KI

doi

10.2174/156652408786241366

subject

Has Abstract

pub_date

2008-11-01 00:00:00

pages

639-45

issue

7

eissn

1566-5240

issn

1875-5666

journal_volume

8

pub_type

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