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Wando Mount Pleasant Library
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Hypercoagulability in sickle cell disease and beta-thalassemia.
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- Author(s): Singer ST;Singer ST; Ataga KI
- Source:
Current molecular medicine [Curr Mol Med] 2008 Nov; Vol. 8 (7), pp. 639-45.- Publication Type:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review- Language:
English - Source:
- Additional Information
- Source: Publisher: Bentham Science Publishers Country of Publication: Netherlands NLM ID: 101093076 Publication Model: Print Cited Medium: Print ISSN: 1566-5240 (Print) Linking ISSN: 15665240 NLM ISO Abbreviation: Curr Mol Med Subsets: MEDLINE
- Publication Information: Original Publication: Hilversum, The Netherlands ; Boca Raton, FL : Bentham Science Publishers, c2001-
- Subject Terms:
- 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.
- Number of References: 109
- Grant Information: HL7076 United States HL NHLBI NIH HHS; RR00046 United States RR NCRR NIH HHS
- Publication Date: Date Created: 20081111 Date Completed: 20090204 Latest Revision: 20190923
- Publication Date: 20221213
- Accession Number: 10.2174/156652408786241366
- Accession Number: 18991650
- Source:
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