Open AccessCongenital Thrombotic Risk Factors in β-Thalassemia
Author(s) -
Tansu Sipahi,
Aslıhan Kara,
Ayça Esra Kuybulu,
Yonca Eğin,
Nejat Akar
Publication year - 2008
Publication title -
clinical and applied thrombosis/hemostasis
Language(s) - English
Resource type - Journals
eISSN - 1938-2723
pISSN - 1076-0296
DOI - 10.1177/1076029608316170
Subject(s) - endothelial protein c receptor , medicine , protein c , methylenetetrahydrofolate reductase , factor v leiden , thalassemia , gastroenterology , thrombosis , thrombophilia , factor v , genetics , allele , venous thrombosis , biology , gene , platelet , thrombin
Thalassemia major patients have increased risk for thromboembolic complications because of the chronic hypercoagulable state. The question arising from this is whether thromboembolic complications are the result of genetic polymorphisms of prothrombotic factors. Here, we studied factor V 1691 G-A (FVL), factor II polymorphism (G20210A), methyltetrahydrofolate reductase mutation (MTHFR, C677T), and endothelial cell protein C receptor (EPCR) deletion polymorphism and their relationship with thromboembolic complications. We found significant decrements of protein C and protein S and a slight increased prevalence of congenital thrombophilic mutations when compared with controls. Although 5 of the patients had high soluble EPCR (sEPCR) levels, no significant change was found in sEPCR values between patients and controls.