Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement
Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.
Acquired Resistance to Activated Protein C Is a Feature of Both Systemic Lupus Erythematosus (SLE) and Antiphospholipid Syndrome (APS) and Is More Marked in Patients with SLE and APS.
Wahl3, Denis, Zuily4, Stéphane, Brunette2, Agnès, Prestat-Tilly4, Marie, Regnault2, Véronique, Devignes1, Jean, Lecompte1, Thomas
Biological Haematology Department, Nancy University Hospital, Vandoeuvre les Nancy, France
INSERM U961, Nancy Université, Vandoeuvre les Nancy, France
Vascular Medicine Unit, Vandoeuvre les Nancy, France
Vascular Medicine Unit, Nancy University Hospital, Vandoeuvre les Nancy, France
Vascular manifestations of antiphospholipid syndrome (APS) include both venous (VTE) and arterial (ATE) thromboembolic events. However VTE are more frequent than ATE. Among the underlying mechanisms of VTE in APS, it has been suggested that acquired activated protein C (APC) resistance may be a candidate mechanism. However this is difficult to demonstrate with tests based on aPTT because of the effects of lupus anticoagulants on this parameter. In order to investigate APC resistance in APS we have conducted a study with a thrombin generation test (calibrated automated thrombography). APC resistance was determined with measurement of endogenous thrombin potential (ETP) at baseline and after addition of APC. The APC sensitivity ratio (sr) was defined as ETP with APC/baseline ETP.
We included 92 patients (37 with primary antiphospholipid syndrome, 15 with SLE without antiphospholipid antibodies PAPS, 11 with both APS and SLE and 29 with antiphospholipid antibodies (APA) but without APS) and 39 controls. APCsr was higher in all patient groups compared to controls indicating resistance to activated protein C: APCsr was 0.45 ± 0.20, p=0.005 in PAPS, 0.55 ± 0.16,p<0.001 in in SLE, 0.65 ± 0.16,p<0.0001 in patients with both PAPS and SLE and 0.53 ± 0.22,p<0.0001 in patients with APA without APS whereas controls 0.30 ± 0.11. Of note APCsr was also higher in patients with both SLE and APS than in patients with PAPS (p=0.009). Moreover APCsr in patients with venous thrombosis was higher than in controls: 0.47 ± 0.22 vs 0.30 ± 0.11, p< 0.001.
Overall these results suggest that acquired APC resistance is a potential risk factor for thrombosis in SLE and PAPS and is more marked when both conditions are present. Furthermore APC resistance seems to be more specifically associated with venous thromboembolism.
To cite this abstract, please use the following information:
Wahl, Denis, Zuily, Stéphane, Brunette, Agnès, Prestat-Tilly, Marie, Regnault, Véronique, Devignes, Jean, et al; Acquired Resistance to Activated Protein C Is a Feature of Both Systemic Lupus Erythematosus (SLE) and Antiphospholipid Syndrome (APS) and Is More Marked in Patients with SLE and APS. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :1