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APC resistance: biological basis and acquired influences

E Castoldi1, J Rosing

  • 1Department of Biochemistry, Maastricht University, Maastricht, the Netherlands.

Journal of Thrombosis and Haemostasis : JTH
|December 17, 2009
PubMed

Insights

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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