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The role of activated protein C resistance in the pathogenesis of venous thrombosis

W C Hooper1, B L Evatt

  • 1Hematologic Disease Branch, Division of AIDS, STD, and TB Laboratory Research, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.

Insights

Venous thromboembolism (VTE), a common cardiovascular disease, often results from altered anticoagulant proteins. This review discusses the protein C system and clinical issues linked to activated protein C resistance.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Biochemistry

Background:

  • Venous thromboembolism (VTE) is a significant cardiovascular disease.
  • VTE pathogenesis involves acquired or inherited defects in hemostatic regulatory proteins.
  • The protein C/protein S pathway is crucial for natural anticoagulation.

Purpose of the Study:

  • To describe the pathobiology of the natural anticoagulant protein system.
  • To review the clinical implications of activated protein C resistance.

Main Methods:

  • Literature review of VTE and anticoagulant pathways.
  • Analysis of the protein C system's role in hemostasis.

Main Results:

  • Deficiencies in the protein C pathway, acquired or inherited, are linked to VTE.
  • Acquired deficiencies often stem from conditions like cancer, AIDS, or diabetes.
  • Inherited deficiencies can cause VTE in healthy individuals.

Conclusions:

  • Understanding the anticoagulant protein system is key to VTE management.
  • Activated protein C resistance has significant clinical implications for thrombosis risk.

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