Few prospective studies have examined the factor V paradox: factor V Leiden (FVL) is a stronger risk factor for deep venous thrombosis (DVT) than for pulmonary embolism (PE).
Coagulation factor V gene 1691G>A polymorphism as an indicator for risk and prognosis of lower extremity deep venous thrombosis in Chinese Han population.
Logistic regression analyses were conducted in order to correlate indexes and lower extremity DVT. miR-495 overexpression, t-PA, PAF, and protein C were confirmed to be protective factors, while Stat3 overexpression, PT, ET-1, FIB, D-Dimer, blood coagulation factor V, and VIII were all ultimately considered to be risk factors of lower extremity DVT.
One patient received thrombolysis and stenting at 14 weeks of pregnancy for deep venous thrombosis (DVT) and May-Thurner syndrome, three for a previous postpartum DVT (2, 4, and 6 weeks postpartum), three for DVT before any pregnancy with a history of factor V Leiden, and the remaining five for unprovoked DVT.
A novel and deleterious single nucleotide variation in exon 11 of coagulation factor V (c.1631A>G) causing Gln544Arg exchange in factor V was identified in a 29 years old Somali female with DVT.
Prothrombotic polymorphisms were detected in 16 of 63 (25.4%) patients who were tested for factor V Leiden and prothrombin G20210A mutation (OR=3.47, p=0.002) in comparison to 49% in DVT patients (OR=9.95, p<0.0001).
The absolute 10-year risk of DVT in a high-risk group (i.e. those aged >60 years and homozygous for Factor V Leiden) was 35% in obese individuals and 18% in normal-weight individuals.
To determine if the deep vein thrombosis was of genetic origin, a peripheral blood DNA sample was analysed for the presence of the three most frequent mutations associated with thrombotic events: factor V Leiden (1691G>A), prothrombin (20210G>A) and methylene tetrahydrofolate reductase (677C>T).
It was our aim to assess whether factor V Leiden (FVL) and G20210A prothrombin (FII) mutation are associated with the presence of residual vein obstruction (RVO) after a standard course of anticoagulation for a first episode of idiopathic proximal deep-vein thrombosis (DVT) of the lower limbs, with or without symptomatic pulmonary embolism (PE).
We describe a 29-year-old man, heterozygous for factor V Leiden, who developed extensive pulmonary emboli with concomitant bilateral deep venous thrombosis, likely provoked by prolonged immobility during a car trip.
The prevalence of prothrombin G20210A polymorphism and of elevated factor VIII levels was significantly higher in patients with DVT and DVT/PE than in controls, but not in those with isolated PE, whereas factor V Leiden polymorphism was associated with isolated DVT but not with DVT/PE or isolated PE.
Women carrying the factor V Leiden (F5 rs6025) polymorphism, or who had reduced sensitivity to activated protein C (aPC) in the absence of F5 rs6025, had increased risk for DVT, with unadjusted ORs 7.7 (95% CI 4.7-12.7) and 3.5 (95% CI 2.2-5.4), respectively.
If the proband had VTE and factor V Leiden (FVL) and/or prothrombin (PT)20210A, the HR for DVT was 2.77 (95%CI 1.21-4.82) in the carriers overall, and 5.54 (95%CI 3.20-187.00) in those homozygous or double heterozygous for FVL and PT20210A.
The PlA1/A2 polymorphism of the GpIIIa gene was associated with DVT in our Italian BD patients, but does not seem to increase the risk of DVT due to factor V Leiden or prothrombin gene G20210A mutations.
Different risk of deep vein thrombosis and pulmonary embolism in carriers with factor V Leiden compared with non-carriers, but not in other thrombophilic defects. Results from a large retrospective family cohort study.
A case of an 18-year-old man with deep venous thrombosis of the lower limbs caused by hypoplasia of the inferior vena cava in combination with heterozygous factor V Leiden is presented.
Symptomatic PE complicated the first DVT in 242 patients (26%); the risk of PE was increased in patients with AT deficiency (relative risk [RR] 2.4, 95% confidence interval [CI] 1.6-3.6) or with PT-GA (RR 1.5, 95%CI 1.1-2.0) and decreased in those with FVL (RR 0.7, 95%CI 0.5-1.0) in comparison with those with unknown inherited defect.