Background/Purpose: We and others have suggested that complement activation can serve as an initiating signal that increases the thrombosis risk in SLE patients with antiphospholipid antibodies. Generation of complement activation products can result in proinflammatory and/or prothrombotic responses providing a permissive environment for the pathological effects of antibodies to negatively charged phospholipid protein complexes.

Methods: We analyzed the NYU SLE SAMPLE Biorepository initiated in September 2013 which consists of 539 patients fulfilling ACR and/or SLICC criteria for systemic lupus erythematosus. We identified 91 patients whose criteria included the presence of one or more for the following APLS antibodies: lupus anticoagulant, IgG or IgM anti-β₂-glycoprotein-I, or IgG or IgM anticardiolipin antibodies and determined if these patients received SLEDAI points for hypocomplementemia during any encounter. We then reviewed each patient’s medical record to identify the prevalence of thrombosis defined as DVT, PE, CVA, arterial occlusion with gangrene or amputation, and obstetric events as well as noncriteria manifestation of thrombocytopenia or valvulitis. We then compared the prevalence of these APLS manifestations in the SLE patients with and without evidence of complement activation.

Results: The NYU SLE SAMPLE biorepository includes 539 patients (90% female, mean age 43.0 ± .9, and 10 % men, mean age 41.0 ± .3). 54% Caucasian, 31% African American, 15% Asian, 30% Hispanic White, and 5% Hispanic Black. 91 of the 539 SLE patients had APLS antibodies, 79 female and 12 male (mean age 43.0 ± .2, 56% Caucasian, 33% African American, and 11% Asian). 24 % Hispanic white and 4% Hispanic Black. The total number of patients with adverse events is 48 of 91 (53%) with 29/48 (60%) in the SLE patients with APLS and evidence of hypocomplementemia and 19/43 (44%) in the patients without evidence of hypocomplementemia. The most common thrombotic event was DVT followed by CVA.

Conclusion: The prevalence of APLS as a criteria in the NYU SLE registry is 91 of 539 and adverse events were more common in the patients with evidence of hypocomplementemia (29/48, 60%) as compared to the patients without complement activation (19/43, 44%).These findings can inform decisions regarding which patient subsets may benefit from the prophylactic use of low-dose aspirin for primary prevention in asymptomatic lupus patients. Moreover, future clinical trials should be stratified on the basis of complement consumption to be sure that equal numbers of these patients appear in both the experimental and comparator treatment arms. Finally, future prospective studies should explore the interaction between complement activation products, platelets, neutrophils, mononuclear cells, endothelial cells, coagulation cascade, etc. in the adverse events that constitute antiphospholipid syndrome.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/complement-activation-as-a-marker-for-increased-thrombosis-risk-in-sle-patients-with-antiphospholipid-antibodies/