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Clinical Chemistry 50: 677-678, 2004; 10.1373/clinchem.2003.029314
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(Clinical Chemistry. 2004;50:677-678.)
© 2004 American Association for Clinical Chemistry, Inc.

Letters to the Editor

Factor V Leiden in Blood Donors in Baghdad (Iraq)

Nasir A. Al-Allawi1,a, Jaladet M.S. Jubrael2 and Ferial A. Hilmi1

1 Department of Pathology, College of Medicine, and 2 Department of Molecular Biology, College of Science, University of Baghdad, Baghdad, Iraq

aAuthor for correspondence: Department of Pathology, College of Medicine, University of Baghdad, Bab-Almuaddem, Baghdad, Iraq. E-mail nallawi@yahoo.com; secondary e-mail nasirallawi@hotmail.com.

The first 20% of the full text of this article appears below.


To the Editor:

Human coagulation factor V is a 330-kDa single-chain glycoprotein that plays an important role in the coagulation pathway. After its activation by thrombin and factor Xa, activated factor V (Va) forms an essential part of the prothrombinase complex, which catalyzes the conversion of prothrombin to thrombin in the presence of calcium and a phospholipid membrane (1). Activated protein C (APC) inactivates factor Va and requires factor V as a cofactor in the APC-mediated inactivation of factor VIII (1)(2). Resistance to APC action leads to increased risk of thrombosis and is mostly attributable to a single point mutation in the factor V gene (factor V Leiden) with a G-to-A substitution at nucleotide 1691 (3).

Several studies have demonstrated the high prevalence of factor V Leiden in some Middle Eastern countries, . . . [Full Text of this Article]






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