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Anticardiolipin antibodies in patients with rheumatoid arthritis

A J de Brum-Fernandes1, W Cossermelli-Messina, C Bueno

  • 1Department of Rheumatology, University of Sao Paulo, School of Medicine, Brazil.

Clinical Rheumatology
|December 1, 1989
PubMed

Insights

Anticardiolipin antibodies (ACA) were found in 16.48% of rheumatoid arthritis patients. ACA presence correlated with disease systematization and antinuclear antibodies, suggesting a role in rheumatoid arthritis morbidity or pathogenesis.

Area of Science:

  • Rheumatology
  • Immunology
  • Serology

Background:

  • Rheumatoid arthritis (RA) is a chronic autoimmune disease.
  • Anticardiolipin antibodies (ACA) are associated with autoimmune conditions and thrombosis.
  • The role of ACA in RA pathogenesis and clinical manifestations requires further investigation.

Purpose of the Study:

  • To investigate the prevalence of anticardiolipin antibodies (ACA) in patients with rheumatoid arthritis (RA).
  • To explore the association between ACA positivity and specific clinical and laboratory features in RA patients.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) was used to measure ACA levels in 73 RA patients.
  • Patients were categorized as ACA-positive or ACA-negative based on control group values.
  • Clinical and laboratory data, including spontaneous abortions, CNS involvement, disease activity, platelet counts, antinuclear antibodies (ANA), and rheumatoid factor, were compared between groups.

Main Results:

  • ACA were detected in 16.48% of RA patients.
  • A significant association was found between ACA positivity (IgG, IgM, or both) and disease systematization.
  • ACA positivity also showed a significant association with the presence of antinuclear antibodies (ANA).

Conclusions:

  • Anticardiolipin antibodies may be present in a subset of rheumatoid arthritis patients.
  • ACA positivity in RA is associated with disease systematization and the presence of ANA.
  • These findings suggest a potential role for ACA in the morbidity or pathogenesis of rheumatoid arthritis.

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