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APC resistance: biological basis and acquired influences
1Department of Biochemistry, Maastricht University, Maastricht, the Netherlands.
Journal of Thrombosis and Haemostasis : JTH
|December 17, 2009
Summary
Activated protein C (APC) resistance, a common condition impairing blood coagulation regulation, increases venous thrombosis risk. This review explores its varied causes and clinical significance.
Area of Science:
- Hematology
- Molecular Biology
- Thrombosis Research
Background:
- Blood coagulation is physiologically regulated by the proteolytic inactivation of factors Va and VIIIa by activated protein C (APC).
- Functional abnormalities in this pathway lead to APC resistance, a condition characterized by a poor anticoagulant response to added APC in vitro.
- APC resistance is prevalent and associated with an elevated risk of venous thrombosis.
Purpose of the Study:
- To review the multifactorial etiology of APC resistance.
- To discuss the clinical implications of APC resistance.
Main Methods:
- Literature review of studies on APC resistance, factor V (FV), FV(Leiden) mutation, and venous thrombosis.
- Analysis of genetic and acquired conditions contributing to APC resistance.
Main Results:
- APC resistance is linked to impaired inactivation of coagulation factors Va and VIIIa.
- The FV Arg506Gln (FV(Leiden)) mutation is a major cause of hereditary APC resistance by abolishing an APC-cleavage site.
- Multiple genetic and acquired factors beyond FV(Leiden) contribute to APC resistance.
Conclusions:
- APC resistance is a significant risk factor for venous thrombosis.
- Understanding the diverse causes of APC resistance is crucial for risk assessment and management.
- Further research into the multifactorial nature of APC resistance is warranted.
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