Thrombophilia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Recently, a poor anticoagulant response to activated protein C (APC), due to a mutation of factor V (FV Leiden), has been identified as the most frequent hereditary disorder associated with venous thrombophilia.
|
12221665 |
2002 |
Thrombophilia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Protein C deficiency is a heritable thrombophilia caused by numerous different genetic alterations in the protein C (PROC) gene.
|
31821907 |
2020 |
Thrombophilia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Analysis of PROC and PROS1 single nucleotide polymorphisms in a thrombophilia family.
|
31295762 |
2019 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Resistance to activated protein C (APC) is the most common cause of familial thrombophilia.
|
8701918 |
1996 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Inherited activated protein C (APC) resistance is a newly described pathological condition associated with familial thrombophilia.
|
8603014 |
1996 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Resistance to activated protein C (APC) is a major cause of familial thrombophilia, and can be corrected by an anticoagulant activity expressed by purified factor V. We investigated linkage between APC resistance and the factor V gene in a large kindred with familial thrombophilia.
|
7911873 |
1994 |
Thrombophilia
|
0.200 |
AlteredExpression
|
disease |
BEFREE |
As a result, inactivation of factor-activated factor V by APC is impaired, which leads to a hypercoagulable state and a lifelong increased risk of thrombosis.
|
9107093 |
1997 |
Thrombophilia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
It was recently found that aPL may cause the acquired activated protein C resistance phenotype, whereas in familial thrombophilia, activated protein C resistance frequently results from a point mutation in the factor V gene (replacing arginine 506 with a glutamine) that leads into the (R-506-Q), the so-called Leiden mutation, that produces a mutated factor V, resistant to the catalytic action of activated protein C, otherwise normal in its procoagulant properties.
|
8970058 |
1996 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Whether APC dysfunction occurs in other Asian countries is an important aspect of mapping thrombophilia among Asians.
|
23301217 |
2013 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Mutated factor V (FVR506Q, FV:Q506 or FV Leiden) is partially resistant to APC which results in a hypercoagulable state conferring a life-long increased risk of thrombosis.
|
9198201 |
1997 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Inherited resistance to activated protein C (APC) has been recently recognized as a novel cause underlying venous thrombophilia.
|
9763354 |
1998 |
Thrombophilia
|
0.200 |
AlteredExpression
|
disease |
LHGDN |
Cigarette smoke dose-dependent hypercoagulability due to acquired activated protein C deficiency could contribute to the increased risk of thrombosis in smokers.
|
12482406 |
2003 |
Thrombophilia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
This mutation, defined as factor VLEIDEN, results in activated protein C (APC) resistance and is the most common genetic risk factor for familial thrombophilia.
|
11914653 |
2002 |
Thrombophilia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
The cause of the BCS still being unknown, in October 1996 we performed extensive laboratory investigations concerning states of thrombophilia and found moderately elevated IgG anticardiolipin antibodies (19.7 U/ml) and a resistance against activated protein C caused by heterozygosity for a point mutation of the factor V gene (1691G-->A; factor V Leiden).
|
10378363 |
1999 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
The situation changed with the discovery of inherited resistance to activated protein C (APC) as a novel mechanism for familial thrombophilia.
|
7632412 |
1995 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
The median age at the first thrombotic event for 28 APC-resistant members of thrombophilia families was 29 years and for 50 protein C-deficient members of thrombophilia families 31.5 years.
|
8943855 |
1996 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Complexes between activated protein C and protein C inhibitor measured with a new method: comparison of performance with other markers of hypercoagulability in the diagnosis of deep vein thrombosis.
|
11776306 |
2001 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Plasma hypercoagulability in the presence of thrombomodulin but not of activated protein C in patients with cirrhosis.
|
27421039 |
2017 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Thrombin generation assays sensitive to the APC- and TFPI-cofactor activities of protein S revealed similar hypercoagulable states in type I and type III protein S-deficient plasma.
|
20378562 |
2010 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Venous thrombosis due to poor anticoagulant response to activated protein C: Leiden Thrombophilia Study.
|
7902898 |
1994 |
Thrombophilia
|
0.200 |
AlteredExpression
|
disease |
BEFREE |
Conclusions FVBonn induces hypercoagulability via a combination of increased activation/procoagulant activity, decreased susceptibility to APC-mediated inactivation, and slightly reduced APC cofactor activity.
|
27090446 |
2016 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
HPO |
|
|
|
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Using an activated partial thromboplastin time (APTT) assay, Dahlback et al. recently reported that some individuals with thrombophilia show a poor in vitro anticoagulant response to activated protein C (APC-Resistance).
|
8873345 |
1996 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
We compare results of factor V DNA analysis with three different clotting-based assays designed to detect activated protein C (APC) resistance (APCR), using samples from 958 patients undergoing assessment for thrombophilia.
|
10492912 |
1999 |
Thrombophilia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
The factor V Leiden gene mutation decreases the sensitivity of factor V to the anticoagulant activity of activated protein C, and has been shown to be the most common inherited defect associated with a hypercoagulable state.
|
9625586 |
1998 |