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Serum complement activation on heterologous platelets is associated with arterial thrombosis in patients with systemic lupus erythematosus and antiphospholipid antibodies

Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, New York, USA; Department of Pathology, The Mount Sinai School of Medicine, New York, New York, USA ellinor.peerschke{at}mountsinai.org

W Yin

Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, New York, USA; Department of Mechanical and Aerospace Engineering, Oklahoma State University, Stillwater, Oklahoma, USA

DR Alpert

The Hospital for Special Surgery, Weill Medical College of Cornell University, New York, New York, USA; Jersey Shore University Medical Center, Neptune, New Jersey, USA

RAS Roubey

Department of Medicine and Thurston Arthritis Research Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA

JE Salmon

The Hospital for Special Surgery, Weill Medical College of Cornell University, New York, New York, USA

B Ghebrehiwet

Departments of Medicine and Pathology, Stony Brook University, Stony Brook, New York, New York, USA

Complement plays a major role in inflammation and thrombosis associated with systemic lupus erythematosus (SLE) and the antiphospholipid syndrome (APS). A cross-sectional retrospective analysis was performed to evaluate serum complement fixation on platelets and thrombotic incidence using banked sera and clinical data from patients with SLE (n = 91), SLE with antiphospholipid antibodies (aPL) or APS (n = 78) and primary aPL (n = 57) or APS (n = 96). In-situ complement fixation was measured as C1q and C4d deposition on heterologous platelets using an enzyme-linked immunosorbent assay approach. Platelet activation by patient serum in the fluid phase was assessed via serotonin release assay. Enhanced in-situ complement fixation was associated with the presence of IgG aPL and IgG anti-β2 glycoprotein 1 antibodies (P < 0.05) and increased platelet activation (P < 0.005). Moreover, enhanced complement fixation, especially C4d deposition on heterologous platelets, was positively associated with arterial thrombotic events in patients with SLE and aPL (P = 0.039). Sera from patients with aPL possess an enhanced capacity for in-situ complement fixation on platelets. This capacity may influence arterial thrombosis risk in patients with SLE.

Key Words: antiphospholipid syndrome • systemic lupus erythematosus • thrombosis

Lupus, Vol. 18, No. 6, 530-538 (2009)
DOI: 10.1177/0961203308099974


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