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Publication Detail
Prevalence of anti-protein C antibodies and acquired activated protein C resistance and in systemic lupus erythematosus
  • Publication Type:
    Conference presentation
  • Publication Sub Type:
  • Authors:
    Ramirez G, Cohen H, Mackie I, Isenberg D, Efthymiou M
  • Date:
  • Name of Conference:
    British Society for Haemostasis and Thrombosis
  • Conference place:
  • Conference start date:
  • Conference finish date:
  • Notes:
BACKGROUND: Systemic lupus erythematosus (SLE) patients have a higher risk for venous thromboembolism (VTE), often associated with antiphospholipid antibodies (aPL). The protein C (PC) pathway regulates haemostasis and inflammation. Acquired resistance to protein C (APCr) is associated with a high prevalence of anti-PC antibodies (anti-PC) and a more severe clinical phenotype in VTE patients with antiphospholipid syndrome, but their potential role in SLE is unknown. AIM: To determine the prevalence of anti-PC and associations for APCr and thrombosis in patients with SLE. METHODS: Sixty-one patients with SLE have been enrolled and categorised by presence (+) or absence (-) of aPL and thrombotic history (aPL+/T+, n=15; aPL+/T-, n=17; aPL-/T+, n=8; aPL-/T-, n=21). Patients with heritable thrombophilia were excluded. Anti-PC levels were determined by ELISA and APCr by thrombin generation (TG) in the presence and absence of exogenous recombinant human activated PC (rhAPC) or Protac (to activate endogenous PC). RESULTS: 44% of all patients had anti-PC (aPL+/T+: 53%, aPL+/T-: 47%, aPL-/T-: 48%, aPL-/T+-: 25%; p=NS). aPL+ patients had higher median anti-PC levels than aPL- (37 vs 26U/mL, p=0.04). Anti-PC was associated with resistance to both rhAPC (p=0.01) and Protac (p<0.001). APCr prevalence was similar in aPL+ (54%) and aPL- (45%) patients. Resistance to rhAPC was associated with resistance to Protac (p=0.02), but was less frequently detected (30% vs 48% of all cases), especially in aPL- patients (14% vs 44% in aPL+; p=0.01). Resistance to rhAPC was higher in aPL+ compared to aPL- (p=0.02). CONCLUSION: anti-PC were detected in patients with SLE even if aPL-. Resistance to activation of PC was more frequently detected than resistance to exogenous APC, suggesting a possible defect in PC activation. Predictive clinical-pathophysiological models based on anti-PC-profile and APCr assays might offer aPL independent tools for the identification and management of SLE patients at increased risk of thrombosis.
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