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 |
Factor V Leiden thrombophilia is characterized by a poor anticoagulant response to activated protein C (APC) and an increased risk for venous thromboembolism (VTE).
|
29294595 |
2018 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Seven SNPs (F5 rs6025, F2 rs1799963, ABO rs514659, FGG rs2066865, F11 rs2289252, PROC rs1799810 and KNG1 rs710446) with four SNP-SNP interactions contributed to the genetic risk score for VTE, with an AUC of 0.66 (95% CI, 0.64-0.68).
|
25472531 |
2015 |
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 |
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 |
LHGDN |
These data indicate that individuals carrying the 4600AG genotype have high sEPCR levels but do not have an increased risk of thrombosis, whereas individuals carrying the 4678CC genotype have higher APC levels and lower risk of venous thromboembolism.
|
15116250 |
2004 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
We investigated in case-control studies both biological effects (FVIII levels and activated protein C sensitivity ratio) and clinical associations (venous thromboembolism) of the D1241E change.
|
15735794 |
2005 |
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 |
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 |
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 |
The p.R147W mutation, the c.C6152T in exon 7, causing a change in amino acid from arginine to tryptophan of the PROC gene has been reported as a common mutation in Taiwanese populations with venous thromboembolism (VTE).
|
28511552 |
2018 |
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 |
Biomarker
|
phenotype |
BEFREE |
These complexes as well as circulating APC were also measured in 121 patients with a history of venous thromboembolism (VTE) and 119 matched controls.
|
29448296 |
2018 |
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 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Several low-frequency genetic mutations, PROS1 p.Lys196Glu in Japanese and PROC p.Arg189Trp and p.Lys193del in Chinese, are significantly associated with increased risk for VTE, with odds ratio more than 2 through the reduced protein C anticoagulant activity.
|
24233386 |
2014 |
Venous Thromboembolism
|
0.400 |
AlteredExpression
|
phenotype |
BEFREE |
The THBD 1418T allele is associated with lower soluble TM, both in plasma and in HUVEC-conditioned medium, and with an increase in functional membrane-bound TM in HUVEC, which could explain the increased activated protein C levels and the reduced VTE risk observed in individuals carrying this allele.
|
23520161 |
2013 |
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 |
Biomarker
|
phenotype |
BEFREE |
The endogenous thrombin potential (ETP) showed a striking inter-individual variability among different FV Leiden carriers and, especially when measured in the presence of APC, correlated with VTE risk.
|
24226152 |
2014 |
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 |
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 |
Therapeutic
|
phenotype |
CTD_human |
Zymogen Protein C to prevent clotting without bleeding during invasive medical procedures.
|
21445774 |
2011 |
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 |
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 |
GeneticVariation
|
phenotype |
BEFREE |
Among them, the factor V (FV) Leiden mutation causes a reduced ability of activated protein C to inactivate activated FV and is the most frequent genetic predisposing factor for venous thromboembolism.
|
19932655 |
2010 |
Venous Thromboembolism
|
0.400 |
GeneticVariation
|
phenotype |
BEFREE |
Resistance to activated protein C (APC) has been demonstrated to be a risk factor for venous thromboembolism, but it is not known whether this phenotype is consistent over time.
|
15257714 |
2004 |