Venous Thromboembolism
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
Therefore, more data are needed from various populations of patients with venous thromboembolism to help decide which patients will benefit from screening for resistance to APC.
|
8637344 |
1996 |
Venous Thromboembolism
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
We investigated the risk of recurrence of venous thromboembolism in APC resistant patients heterozygous for FV Leiden and compared these patient groups with a group of patients, who had a history of venous thromboembolism, but had neither APC resistance nor the FV Leiden mutation.
|
8815565 |
1996 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Resistance to activated protein C (APCR) has emerged as the most important hereditary cause of venous thromboembolism.
|
8868517 |
1996 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Here we have analysed 125 consecutive patients with incidental or recurrent venous thromboembolism for the presence of mutations at the cleavage sites for APC at amino acid positions Arg336 and Arg562 of factor VIII.
|
8616046 |
1996 |
Venous Thromboembolism
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
The HR2 haplotype was associated with significantly lower APC ratios both in patients with venous thromboembolism and in age- and sex-matched controls.
|
9269773 |
1997 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Resistance to activated protein C (APC) is the most common defect found in patients who have venous thromboembolism.
|
9128263 |
1997 |
Venous Thromboembolism
|
0.400 |
Therapeutic
|
phenotype |
CTD_human |
Tamoxifen-associated venous thrombosis and activated protein C resistance due to factor V Leiden.
|
9149031 |
1997 |
Venous Thromboembolism
|
0.400 |
Biomarker
|
phenotype |
CTD_human |
Tamoxifen-associated venous thrombosis and activated protein C resistance due to factor V Leiden.
|
9149031 |
1997 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
A single factor V gene G-A mutation (Arg506Gln) underlying activated protein C (APC) resistance is a common risk factor for venous thromboembolism.
|
9705241 |
1998 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Resistance to activated protein C (APC), which is almost exclusively caused by a point mutation in the factor V gene (FV:Q506 mutation or FV Leiden) is a recently discovered, prevalent risk factor for the occurrence of venous thromboembolism.
|
9763353 |
1998 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Activated protein C (APC) resistance is related to a single point mutation in the factor V gene (FV:Q506) and appears to be the most common inherited risk factor for venous thromboembolism.
|
9690807 |
1998 |
Venous Thromboembolism
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
High factor VIII plasma levels have been shown to represent a common increased risk for venous thromboembolism (VTE) and may cause an activated protein C (APC) resistance in the absence of the factor V Leiden mutation, but there are no studies specifically aimed to establish if high factor VIII and von Willebrand factor (vWF) concentrations may influence the APC sensitivity ratio (APC-SR) and increase the risk for VTE in the presence of the factor V Leiden mutation.
|
10695766 |
1999 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Activated protein C (APC) resistance, due to a point mutation in the factor V gene (FV:Q506), is a major risk factor for venous thromboembolism.
|
10235434 |
1999 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Participants with a reduced response to activated protein C were at higher risk even if they did not carry the mutation (odds ratio, 1.7 [CI, 1.0 to 2.7]); the attributable risk for venous thromboembolism was 5.1%.
|
10215560 |
1999 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
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.
|
10368524 |
1999 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
A total of 685 consecutive patients with at least one episode of VTE and 266 sex- and age-matched healthy controls were screened with regard to activated protein C resistance, protein C, protein S, and antithrombin deficiency, elevated serum levels of Lp(a), and the factor V G1691A, MTHFR C677T, and prothrombin G20210A mutations.
|
11071628 |
2000 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
The genetic defect of coagulation factor V known as factor V Leiden produces a resistance to degradation by activated protein C (APC) and increases the risk of venous thromboembolism.
|
10590188 |
2000 |
Venous Thromboembolism
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
Resistance to activated protein C (APC) is a risk factor for venous thromboembolism also in absence of the FV Leiden mutation.
|
11127861 |
2000 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
We conclude that a low level of circulating APC in individuals without any of the most recognized thrombophilic defects is a prevalent, independent risk factor for VTE, and that it predisposes to recurrent VTE.
|
11776301 |
2001 |
Venous Thromboembolism
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
We conclude that HRT diminishes the efficacy by which APC downregulates in-vitro thrombin formation in a similar fashion to that observed with low-dose oral contraceptives, but the increase in nAPCsr alone is not sufficient to explain the increased risk of VTE associated with use of HRT.
|
11703344 |
2001 |
Venous Thromboembolism
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
Because activated protein C resistance is a common risk factor for venous thromboembolism, we prospectively evaluated the activated protein C sensitivity ratio and factor V Leiden mutation in cancer patients with and without venous thromboembolism.
|
11165549 |
2001 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
The combination of the PROC mutation with a PROS deficiency in two family members triggered venous thromboembolism at age 31 and 6 years, respectively.
|
11434940 |
2001 |
Venous Thromboembolism
|
0.400 |
AlteredExpression
|
phenotype |
LHGDN |
Protein C, antithrombin, and venous thromboembolism incidence: a prospective population-based study.
|
12067914 |
2002 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
The activated protein C (APC) resistance phenotype associated with an abnormal factor V Leiden (FVL), and the G20210A prothrombin gene mutation are the most common findings in patients with venous thromboembolism (VTE).
|
12413582 |
2002 |
Venous Thromboembolism
|
0.400 |
Biomarker
|
phenotype |
BEFREE |
Activated protein C (APC) resistance is a common risk factor for venous thromboembolism (VTE) attributed to various mechanisms, including factor V Leiden (FVL) polymorphism.
|
12520697 |
2003 |