منابع مشابه
FACTOR V AND VIII INHIBITOR IN PATIENTS WITH COMBINED FACTOR V AND VIII DEFICIENCY
Patients with coagulation factor(s) deficiency who use coagulation therapy are susceptible to forming inhibitors against coagulation factor(s). In this survey we detected factor V and VIII inhibitor in ten patients with combined deficiency of factors V and VIII from north east of Iran (Khorassan province). It was revealed in our survey that eight patients had both factor V and factor VIII i...
متن کاملFactor V and thrombotic disease: description of a janus-faced protein.
The generation of thrombin by the prothrombinase complex constitutes an essential step in hemostasis, with thrombin being crucial for the amplification of blood coagulation, fibrin formation, and platelet activation. In the prothrombinase complex, the activated form of coagulation factor V (FVa) is an essential cofactor to the enzyme-activated factor X (FXa), FXa being virtually ineffective in ...
متن کاملCombined Factor V and VIII Deficiency
This review summarizes current data on the pathomechanisms and new genetic findings of combined factor V and VIII deficiency (CF5F8D). Congenital haemorrhagic disorders characterized by deficiency of two clotting factors comprise an interesting group. Among dual coagulation disorders, CF5F8D is the most common type. For the first time combined factor V and VIII deficiency (F5F8D) was reported b...
متن کاملFactor V Leiden and other coagulation factor mutations affecting thrombotic risk.
Five genetic defects have been established as risk factors for venous thrombosis. Three are protein C, protein S, and antithrombin deficiencies, defects in the anticoagulant pathways of blood coagulation. Together they can be found in approximately 15% of families with inherited thrombophilia. Their laboratory diagnosis is hampered by the large genetic heterogeneity of these defects. The other ...
متن کاملHomocysteine and thrombotic disease.
amino acid whose metabolism is at the intersection of The more severe cases of hyperhomocysteinemia are two metabolic pathways: remethylation and transsulfuration caused by homozygous defects in genes encoding for en(Fig 1). In remethylation, homocysteine acquires a methyl zymes of homocysteine metabolism. In such cases, a defect group from N-5-methyltetrahydrofolate (MTHF) or from bein an enzy...
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ژورنال
عنوان ژورنال: Arteriosclerosis, Thrombosis, and Vascular Biology
سال: 2002
ISSN: 1079-5642,1524-4636
DOI: 10.1161/01.atv.0000012665.51263.b7