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


MeSH Major

  • Antiphospholipid Syndrome
  • Arterial Occlusive Diseases
  • Blood Platelets
  • Complement Activation
  • Lupus Erythematosus, Systemic
  • Platelet Activation
  • Thrombosis


  • 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.

publication date

  • May 12, 2009



  • Academic Article



  • eng

PubMed Central ID

  • PMC2707931

Digital Object Identifier (DOI)

  • 10.1177/0961203308099974

PubMed ID

  • 19395455

Additional Document Info

start page

  • 530

end page

  • 8


  • 18


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