Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
To assess the patterns of abnormal neuroradiologic findings in patients with a hypercoagulable state related to activated protein C (APC) resistance.
|
9530303 |
1998 |
Thrombophilia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
We compared clinical findings from patients with resistance to APC with or without the presence of factor V R506Q, and found that as a group, those with factor V R506Q had a higher incidence of hypercoagulability, but fewer additional risk factors for hypercoagulability.
|
9648899 |
1998 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
A novel genetic defect in factor V allowing for resistance to its cleavage by activated protein C has recently been implicated in a significant number of cases of familial thrombophilia.
|
9841693 |
1998 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Recently APCR has been shown to account for up to 50% of cases of thrombophilia.
|
9499670 |
1998 |
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 |
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 |
A single point mutation in the gene coding for coagulation factor V results in a form of factor Va that is resistant to degradation by activated protein C and leads to a relative hypercoagulable state.
|
9382368 |
1997 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Accordingly, the activated form of mutated factor V (FVa:Q506) is more slowly degraded by activated protein C than normal FVa (FVa:R506) is, resulting in hypercoagulability and a lifelong 5- to 10-fold increased risk of venous thrombosis.
|
9046944 |
1997 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Resistance to activated protein C (APC) is a frequent cause of thrombophilia.
|
9383024 |
1997 |
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 |
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 |
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 |
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 |
Mutated factor V (FV:Q506) is activated by thrombin or factor Xa in normal way, but impaired inactivation of mutated factor Va by APC results in life-long hypercoagulability.
|
8624369 |
1996 |
Thrombophilia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Therefore, by measuring F1+2 and TAT a state of biochemical hypercoagulability has been identified in about one-third of APC-resistant individuals.
|
8725708 |
1996 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Our results agree with the hypothesis that individuals with APC-resistance or protein S deficiency have an imbalance between pro- and anti-coagulant forces leading to increased thrombin generation and a hypercoagulable state.
|
8815575 |
1996 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Inherited resistance to activated protein C (APC) is a common disorder associated with hypercoagulability and lifelong risk of venous thrombosis.
|
8772620 |
1996 |
Thrombophilia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Resistance to activated protein C (APC) is the most frequent cause of inherited thrombophilia.
|
8637344 |
1996 |
Thrombophilia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
A point mutation in the factor V gene (FV Q506) renders factor V resistant to inactivation by activated protein C. The frequency of this mutation is known to be significantly increased in patients with thrombophilia.
|
8872815 |
1996 |
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 |
After activation, mutated factor V, FV:Q506, is less efficiently degraded by APC than normal factor V, which results in increased thrombin generation and a hypercoagulable state.
|
8578447 |
1995 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Mutated factor V is activated by thrombin or factor Xa in the normal way, but impaired inactivation of mutated factor Va by activated protein C results in a life-long hypercoagulability.
|
8839395 |
1995 |
Thrombophilia
|
0.200 |
Biomarker
|
disease |
BEFREE |
Inherited resistance to activated protein C (APC) was recently recognized as a novel cause underlying venous thrombophilia.
|
7590506 |
1995 |
Thrombophilia
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
As a result, the activated protein C-mediated cleavage and inhibition of mutated Factor V (FV:Q506) is impaired, which leads to increased thrombin generation, a hypercoagulable state, and a life-long increased risk of thrombosis.
|
9372020 |
1995 |