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Related Concept Videos

Complement System01:27

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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
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Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
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Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
06:29

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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
Summary

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.

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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.