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 increase of prothrombinic factors (by gain-of-function mutation) such as thrombophilia factor V Leiden (resistant to activated protein C), mutation in prothrombine G20210A or polymorphisms of MTHFR in homocysteine 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 thrombosis 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.
Corresponding author:
Oana V. BADULESCU
Department of Pathophysiology, “Grigore T. Popa” University of Medicine and Pharmacy, Iasi, Romania
Address: Universitatii street, no 16, 700115, Iasi, Romania
Email: violabadulescu@yahoo.com; Phone +40 0722 242 397
