Open AccessSerum complement activation on heterologous platelets is associated with arterial thrombosis in patients with systemic lupus erythematosus and antiphospholipid antibodies
Author(s) -
Ellinor I.B. Peerschke,
Wei Yin,
Deborah Alpert,
Robert Roubey,
Jane E. Salmon,
Berhane Ghebrehiwet
Publication year - 2009
Publication title -
lupus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.069
H-Index - 103
eISSN - 1477-0962
pISSN - 0961-2033
DOI - 10.1177/0961203308099974
Subject(s) - medicine , platelet , antiphospholipid syndrome , immunology , heterologous , complement fixation test , antibody , complement system , thrombosis , systemic lupus erythematosus , lupus erythematosus , biology , disease , serology , biochemistry , gene
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-beta2 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.