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Zohreh Rahimi
Abbas Parsian
(*) Corresponding Author:


Hemoglobin S in homozygous state or in combination with one of the structural variants of Hb D-Punjab, Hb O-Arab, Hb C or β-thalassemia mutation results in sickle cell disease (SCD) that is characterized by chronic hemolytic anemia and tissue injury secondary to vasooclusion. A chronic hypercoagulable state in SCD has been established with the increased risk of thromboembolic complications in these patients. The goal of present review is to survey of the literature related to thromboembolic events and genetic risk factors involved in the manifestation of these events in SCD patients with focus on studies from Mediterranean countries. Also, this review covers the pathogenesis of hypercoagulability and alteration in the components of hemostasis system.

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Author Biographies

Zohreh Rahimi

1. Medical Biology Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran 2. Department of Biochemistry, Medical School, Kermanshah University of Medical Sciences, Kermanshah, Iran

Abbas Parsian

Division of Neuroscience & Behavior, NIAAA, National Institutes of Health, Rockville, Maryland, USA