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Thrombosis is a multi-factorial disorder with congenital and acquired risks. There are many genet- ic abnormalities causing an increasing in the risk of thrombophilia, and the presence of more than one abnormality gives rise to an additional increase in thrombotic risk. Haemostasis is a collection of biological processes as the blood coagulation, having the purpose of stopping the bleeding con- sequent to the rupture of a vessel. Various cellular and biochemical factors of haemostasis have implications in different physiological processes like inflammation.
In the haemostasis there is a balance between the procoagulant factors and anticoagulant proteins. The first genetic thrombotic disorders described were the deficiencies of natural procoagulant, such as antithrombin, protein C and protein S, but these abnormalities are rare and are caused by many different mutations. More recently, relatively common individual polymorphisms in the population have been described in procoagulant factors, such as factor V and prothrombin that cause an increased risk of venous thrombosis. Analyzing the haemostatic system, other polymor- phisms have come to light, such as genetic polymorphisms associated with thrombosis and arterio- vascular disease were found in many procoagulant proteins, including factor V, prothrombin, fi- brinogen, Factor VII, Factor XI and factor XIII. Moreover, polymorphisms of platelet glycopro- teins, fibrinolytic proteins, and enzymes in the metabolic pathway of transulfuration leading to high levels of homocysteine, have been described in association with thrombotic vascular disease. In general, the risk factors that promote venous thrombosis are abnormalities via anticoagulant, while polymorphisms of procoagulant proteins and metabolic pathway of transulfuration are main- ly associated with arterial disease. So it is useful to examine the association between polymor- phisms recently discovered for the evaluation of thromboembolic risk.