Chen Y, Stanford MR, Wallace GR et al: Factor V Leiden mutation
does not correlatewith retinalvascularocclusionin whitepatients with Behcet's disease.
Factor V Leiden mutation
and the risk for thromboembolic disease: a clinical perspective.
Activated protein C resistance, the factor V Leiden mutation
, and a laboratory testing algorithm.
The C [right arrow] T change at position 1690 would produce a factor V deficiency, whereas the factor V Leiden mutation
(G [right arrow]A at position 1691) causes a thrombophilic predisposition.
Patients with a lupus anticoagulant should be evaluated directly with a genetic assay to determine if the factor V Leiden mutation
Hyperhomocysteinaemia and factor V Leiden mutation
are associated with Budd-Chiari syndrome.
The Factor V Leiden mutation
is the most common genetic thrombophilia: the heterozygous form, found in 5%-8% of the normal population, increases the risk of VTE fivefold, whereas the rarer homozygous form confers an 18-fold risk increase.
People who have the factor V Leiden mutation
are at somewhat higher than average risk for a type of clot that forms in large veins in the legs (deep venous thrombosis) or a clot that travels through the bloodstream and lodges in the lungs (pulmonary embolism).
Individuals heterozygous for the factor V Leiden mutation
have a sevenfold higher risk to develop venous thrombosis than wild-type (WT) individuals (1).
Activated C-reactive protein resistance not related to a factor V Leiden mutation
is known to be a risk factor for venous thrombosis, and an elevated C-reactive protein level, as seen with the resistance in this study, is a predictor of cardiovascular events.
The factor V Leiden mutation
is a common cause of unprovoked venous thrombosis in the white population.
Inherited thrombophilia due to Factor V Leiden mutation
Both men and women with factor V Leiden mutation
face a 30% lifetime risk of venous thromboembolism (VTE), and the prevalence in Europeans ranges from 5% to 15%.
To date, the cross-linking technology has been applied to detection of bacterial pathogens (1), quantification of viral DNA (2), assessment of gene dosage and methylation status (3), and detection of single-nucleotide polymorphisms (SNPs), specifically the factor V Leiden mutation
, G1691A, and the two most common mutations that are linked to hereditary hemochromatosis, G845A and C187G (4,5).
Cushman was quick to note that any role of testing for factor V Leiden mutation
in making decisions about prescribing estrogen plus progestin in postmenopausal women "will require further study.