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Updates on etiopathogenesis of primary hypercoagulable states

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ABSTRACT

Primary hypercoagulable states are quantitative and qualitative anomalies of coagulation-specific proteins. Many anomalies like these involve acquired mutations and polymorphisms leading to antithrombotic factor deficiency (thrombophilia by antithrombine deficit (III), -protein S-deficit and protein C deficit), or in- crease of prothrombinic factors (by gain-of-function mutation) such as thrombophilia factor V Leiden (re- sistant to activated protein C), mutation in prothrom- bine G20210A or polymorphisms of MTHFR in homo- cysteine metabolism. Each is a factor of individual risk to thrombosis. Hence, when multiple prothrombotic mutations interact, these primary hypercoagulable states associate to increase predisposition to throm- bosis for lifelong. Thromboembolic events in patients diagnosed with inherited or acquired thrombophilia are among the leading causes of mortality worldwide.

Keywords: thrombosis, protein C, protein S, anti- thrombin III, thrombophilia.

Abbreviations  list

APC = activated protein C

VTE = venous thromboembolism

SNP = single nucleotide polymorphism

aVF = activated V factor

PVT = profound venous thrombosis AT (III) = antithrombine (III)

aXF = activated X factor PC = protein C

WISN = Warfarin induced skin necrosis FL (PF) = fetal loss

CID = disseminated intravascular coagulation PS = protein S

MTHFR = methylenetetrahydrofolate reductase

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Oana Badulescu, Emanuel Cojocariu and Elena Dudu

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