Terapevticheskii arkhiv · 2001
[Changes in hemostasis system in patients with hereditary thrombophilia caused by mutation of blood coagulation factor V ( factor V Leiden)].
Сравнительное исследованиеАннотация на английскомСтатьяНазвание и аннотация: Оригинал на русском
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Papaian L P, Kobilianskaia V A, Sheĭdina A M, Baranovskaia S S, Sirotkina O V, Kargin V D, Saltykova N B, Beliazo O E, Golovina O G, Papaian K A, Tarkovskaia L R
Аннотация
AIM: To study the incidence of mutation of Leyden's factor V in patients with venous thrombosis and the hemostatic system in carrier of this genetic defect.
MATERIALS AND METHODS: A hundred and one patients aged 15-69 years who had venous thrombosis and 10 individuals with mutation of Leyden's factor V without manifestations in the history of thrombosis were examined. Factor V gene mutations and the thrombocyte and plasma links of hemostasis were determined by routine methods.
RESULTS: The Leyden's factor V genotype Arg506-->Gln was detected in 17 of the 101 patients with venous thrombosis. Patients and asymptomatic individuals with this factor were found to have significant hypercoagulation, as evidenced by lower activated protein C-resistance index, higher factor VIII (von Willebrand's factor) activity, elevated von Willebrand's factor antigen levels, and enhanced intravascular platelet activation. In the presence of lupoid anticoagulant, hypercoagulation increased and protein C activity decreased.
CONCLUSION: Detection of signs of hypercoagulation in patients with inherited thrombophilia at recovery in carriers of Leyden's factor V without clinical manifestations of thrombosis shows it necessary to make a particularly careful monitoring of the hemostatic system in these subjects. This is especially important for hypercoagulation-predisposing situations, such as pregnancy, surgical interventions, long-term immobilization, use of contraceptives, etc. when preventive measures may be used to prevent thrombotic events.
MATERIALS AND METHODS: A hundred and one patients aged 15-69 years who had venous thrombosis and 10 individuals with mutation of Leyden's factor V without manifestations in the history of thrombosis were examined. Factor V gene mutations and the thrombocyte and plasma links of hemostasis were determined by routine methods.
RESULTS: The Leyden's factor V genotype Arg506-->Gln was detected in 17 of the 101 patients with venous thrombosis. Patients and asymptomatic individuals with this factor were found to have significant hypercoagulation, as evidenced by lower activated protein C-resistance index, higher factor VIII (von Willebrand's factor) activity, elevated von Willebrand's factor antigen levels, and enhanced intravascular platelet activation. In the presence of lupoid anticoagulant, hypercoagulation increased and protein C activity decreased.
CONCLUSION: Detection of signs of hypercoagulation in patients with inherited thrombophilia at recovery in carriers of Leyden's factor V without clinical manifestations of thrombosis shows it necessary to make a particularly careful monitoring of the hemostatic system in these subjects. This is especially important for hypercoagulation-predisposing situations, such as pregnancy, surgical interventions, long-term immobilization, use of contraceptives, etc. when preventive measures may be used to prevent thrombotic events.