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Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
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Published on: January 29, 2014

Complement activation in patients with primary antiphospholipid syndrome

K Oku1, T Atsumi, M Bohgaki

  • 1Department of Medicine II, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

Annals of the Rheumatic Diseases
|July 16, 2008
PubMed

Insights

Hypocomplementaemia, or low complement levels, is common in primary antiphospholipid syndrome (APS). This indicates complement activation and consumption, and correlates with anticoagulant activity in APS patients.

Area of Science:

  • Immunology
  • Rheumatology

Background:

  • Primary antiphospholipid syndrome (APS) is an autoimmune disorder characterized by blood clots and pregnancy complications.
  • The role of complement activation in APS pathogenesis is not fully understood.

Purpose of the Study:

  • To investigate the significance of complement activation in patients with primary APS.
  • To explore the relationship between complement activation and clinical manifestations in APS.

Main Methods:

  • Retrospective analysis of 36 primary APS patients, 42 non-SLE connective tissue disease controls, and 36 healthy volunteers.
  • Measurement of serum complement levels (C3, C4, CH50), anaphylatoxins (C3a, C4a, C5a), and complement regulatory factors (factor H, factor I).
  • Assessment of plasma anticoagulant activity using activated partial thromboplastin time.

Main Results:

  • Patients with primary APS exhibited significantly lower serum complement levels (C3, C4, CH50) compared to controls and healthy volunteers.
  • Elevated serum C3a and C4a levels were observed in most primary APS patients, indicating complement activation.
  • Hypocomplementaemia was more prevalent in primary APS patients with high anticoagulant activity.

Conclusions:

  • Hypocomplementaemia is a common finding in primary APS, reflecting complement activation and consumption.
  • Complement activation in APS may be linked to anticoagulant activity, potentially through antiphospholipid antibody-mediated activation of monocytes and macrophages via anaphylatoxins.
Abstract

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