We have analysed 3380 chromosomes (1690 unrelated individuals) from twenty-four populations for the presence of factor V Leiden, an important risk factor in venous thromboembolism.
Thus, factor V Leiden was associated with a fourfold to fivefold increase in risk of recurrent VTE (crude relative risk, 4.1; P = .04; age- and smoking-adjusted relative risk, 4.7; P = .047).
To assess their tendencies to venous thrombosis, we compared the median age of first venous thromboembolism in patients with factor V Leiden or protein C deficiency, who were identified either within unselected consecutive cases with a first deep venous thrombosis derived from a population-based case-control study, or identified by selection of patients with a deep venous thrombosis, who were referred for thrombophilIa work-up.
A recently discovered mutation in coagulation factor V (Arg506-->Gln, referred to as factor V Leiden), which results in resistance to activated protein C, is found in approximately one fifth of patients with venous thromboembolism.
Further clinical trials are also required to determine if a longer course of treatment is indicated for subgroups of patients based on clinical characteristics and laboratory features (such as those with idiopathic thrombosis versus postoperative thrombosis, and those with or without identifiable molecular markers of a high risk of recurrent venous thromboembolism such as the factor V Leiden gene mutation).
The odds ratio for the FII 20210G/A mutation in 504 patients with venous thromboembolism compared to controls was 2.0 (95% CI 1.0-4.0) and, for factor V Leiden, 5.8 (95% CI 3.3-10.3).
We estimated the risk of VTE associated with use of OCs with and without the presence of Factor V Leiden mutation, protein C-, protein S- or antithrombin deficiency.
Risk of recurrent venous thromboembolism in patients with the factor V Leiden (FVR506Q) mutation: effect of warfarin and prediction by precipitating factors. East Anglian Thrombophilia Study Group.
Trial endpoints will include recurrent VTE, major bleeding episodes and all-cause mortality in the total patient population and separately in those patients with factor V Leiden.
In patients with the factor V Leiden or the F2G20210A mutations there was no apparent increase in risk of venous thromboembolism due to the MTHFRC677T polymorphism.
Factor V Leiden carriers who had had a VTE episode during oral contraceptive intake were more frequently carriers of the G20210A mutation (14.3%, P = 0.03).
To investigate the possible role of factor XIII Val34Leu in the pathogenesis of venous thromboembolism (VTE) and potential interactions with factor V Leiden (FV:Q506) and prothrombin G --> A 20210, we studied 221 patients with a history of VTE and 254 healthy controls.
The frequency of carriers of the factor V Leiden polymorphism was 9.75% among patients with venous thromboembolism, compared with 3.5% among controls, and 3.4% in the patients with CAD.
Although the relative risk of VTE is very significantly increased in factor V Leiden positive women using contraceptive pills, the absolute incidence of venous thrombotic events is low and fatal pulmonary embolism is rare.
Factor V Leiden (Arg506Gln), a confounding genetic risk factor but not mandatory for the occurrence of venous thromboembolism in homozygotes and obligate heterozygotes for cystathionine beta-synthase deficiency.
The results concerning the risk of recurrent venous thromboembolism (VTE) in carriers of the G1691A mutation in the coagulation factor V gene are not consistent and this risk in carriers of the G20210A polymorphism in the prothrombin gene has hitherto not been reported.
Furthermore, the normalized activated protein C sensitivity ratio of 80% of the users of third-generation preparations fell within the 5th to 95th percentile of the normalized activated protein C sensitivity ratio of female carriers of factor V Leiden, a mutation that is associated with hereditary resistance to activated protein C and with an increased risk of venous thromboembolism.
The O blood group protects against venous thromboembolism in individuals with the factor V Leiden but not the prothrombin (factor II G20210A) mutation.