Complement component 3 as biomarker of disease activity and cardiometabolic risk factor in rheumatoid arthritis and

Iván Arias de la Rosa1, Pilar Font1, Alejandro Escudero-Contreras2

  • 1Medicine Department, University of Cordoba, Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), Reina Sofia University Hospital, Cordoba, Spain.

Insights

Complement component 3 (C3) is linked to increased cardiometabolic risks in rheumatoid arthritis and spondyloarthritis. Elevated C3 levels indicate higher disease activity and insulin resistance in these conditions.

Area of Science:

  • Rheumatology and Immunology
  • Cardiovascular Medicine
  • Metabolic Syndrome

Background:

  • Rheumatic diseases like rheumatoid arthritis (RA), psoriatic arthritis (PsA), and axial spondyloarthritis (axSpA) are associated with high cardiovascular morbidity and mortality.
  • Understanding the factors contributing to cardiovascular risk in these inflammatory conditions is crucial for patient management.

Purpose of the Study:

  • To investigate the association between complement component 3 (C3) levels and cardiometabolic risk factors.
  • To explore the relationship between C3 and disease activity in RA, PsA, and axSpA patients.

Main Methods:

  • A cross-sectional study involving 200 RA, 80 PsA, 150 axSpA patients, and 100 healthy controls.
  • Analysis of cardiometabolic risk factors, serum C3 levels, and inflammatory markers.
  • Phenotypic classification using cluster analysis and biomarker accuracy assessment via ROC curve analysis.

Main Results:

  • Significantly elevated C3 levels were observed in RA, axSpA, and PsA patients.
  • Higher C3 levels correlated with an increased prevalence of cardiometabolic risk factors and higher disease activity.
  • Complement C3 levels effectively identified insulin-resistant patients, independent of obesity.

Conclusions:

  • Complement C3 is associated with increased cardiometabolic risk factors in RA and spondyloarthritis.
  • C3 serves as a valuable biomarker for assessing insulin resistance and disease activity in these rheumatic diseases.
Abstract

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