Anti-protein C antibodies are associated with resistance to endogenous protein C activation and a severe thrombotic phenotype in antiphospholipid syndrome

J Thromb Haemost. 2014 Nov;12(11):1801-9. doi: 10.1111/jth.12722. Epub 2014 Oct 3.

Abstract

Background: Antiphospholipid antibodies may interfere with the anticoagulant activity of activated protein C (APC) to induce acquired APC resistance (APCr).

Aims: To investigate the frequency and characteristics of APCr by using recombinant human APC (rhAPC) and endogenous protein C activation in antiphospholipid syndrome (APS).

Methods: APCr was assessed in APS and non-APS venous thromboembolism (VTE) patients on warfarin and normal controls with rhAPC or Protac by thrombin generation. IgG anti-protein C and anti-protein S antibodies and avidity were assessed by ELISA.

Results: APS patients showed greater resistance to both rhAPC and Protac than non-APS patients and normal controls (median normalized endogenous thrombin potential inhibition): APS patients with rhAPC, 81.3% (95% confidence interval [CI] 75.2-88.3%; non-APS patients with rhAPC, 97.7% (95% CI 93.6-101.8%; APS patients with Protac, 66.0% (95% CI 59.5-72.6%); and non-APS patients with Protac, 80.7 (95% CI 74.2-87.2%). APS patients also had a higher frequency and higher levels of anti-protein C antibodies, with 60% (15/25) high-avidity antibodies. High-avidity anti-protein C antibodies were associated with greater APCr and with a severe thrombotic phenotype (defined as the development of recurrent VTE while patients were receiving therapeutic anticoagulation or both venous and arterial thrombosis). Twelve of 15 (80%) patients with high-avidity anti-protein C antibodies were classified as APS category I.

Conclusion: Thrombotic APS patients showed greater APCr to both rhAPC and activation of endogenous protein C by Protac. High-avidity anti-protein C antibodies, associated with greater APCr, may provide a marker for a severe thrombotic phenotype in APS. However, in patients with category I APS, it remains to be established whether anti-protein C or anti-β2 -glycoprotein I antibodies are responsible for APCr.

Keywords: Protac; activated protein C resistance; antibodies; antiphospholipid syndrome; protein C; venous thromboembolism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Activated Protein C Resistance / blood
  • Activated Protein C Resistance / diagnosis
  • Activated Protein C Resistance / drug therapy
  • Activated Protein C Resistance / immunology*
  • Adult
  • Aged
  • Antibodies, Antiphospholipid / blood*
  • Anticoagulants / therapeutic use
  • Antiphospholipid Syndrome / blood
  • Antiphospholipid Syndrome / complications*
  • Antiphospholipid Syndrome / diagnosis
  • Antiphospholipid Syndrome / drug therapy
  • Antiphospholipid Syndrome / immunology
  • Biomarkers / blood
  • Blood Coagulation Tests
  • Case-Control Studies
  • Cross-Sectional Studies
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Fibrinolytic Agents / therapeutic use
  • Humans
  • Intercellular Signaling Peptides and Proteins
  • Male
  • Middle Aged
  • Peptides / therapeutic use
  • Phenotype
  • Protein C / immunology*
  • Protein C / therapeutic use
  • Recombinant Proteins / therapeutic use
  • Severity of Illness Index
  • Venous Thromboembolism / blood
  • Venous Thromboembolism / diagnosis
  • Venous Thromboembolism / immunology*
  • Venous Thromboembolism / prevention & control
  • Warfarin / therapeutic use

Substances

  • Antibodies, Antiphospholipid
  • Anticoagulants
  • Biomarkers
  • Fibrinolytic Agents
  • Intercellular Signaling Peptides and Proteins
  • Peptides
  • Protein C
  • Recombinant Proteins
  • snake venom protein C activator
  • Warfarin