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Antirheumatic therapy is associated with reduced complement activation in rheumatoid arthritis
Thao H P Nguyen1,2, Ingrid Hokstad3, Morten Wang Fagerland4
1Lillehammer Hospital for Rheumatic Diseases, Lillehammer, Norway.
Plos One
|February 25, 2022
Summary
Rheumatoid arthritis patients show elevated complement activation, indicated by soluble terminal complement complex (TCC). Antirheumatic treatments like methotrexate (MTX) and tumor necrosis factor inhibitors (TNFi) reduce TCC, with TNFi±MTX achieving sustained reduction and improving cardiovascular biomarkers.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Rheumatology
Background:
- The complement system is implicated in cardiovascular disease (CVD) pathophysiology and rheumatoid arthritis (RA) associated atherogenesis.
- Limited data exists on complement activation during RA treatment and its link to premature CVD in RA patients.
Purpose of the Study:
- To investigate the impact of methotrexate (MTX) and tumor necrosis factor inhibitors (TNFi) on complement activation in RA patients.
- To assess associations between soluble terminal complement complex (TCC) levels and inflammatory/cardiovascular biomarkers.
Main Methods:
- Studied 64 RA patients on MTX monotherapy or TNFi±MTX.
- Measured TCC levels via ELISA at baseline, 6 weeks, and 6 months.
- Correlated TCC with inflammatory markers (CRP, ESR, IL-6) and lipid profiles.
Main Results:
- Elevated baseline TCC levels (89% above reference) were observed in RA patients.
- TCC significantly decreased after 6 weeks of treatment, with sustained reduction seen after 6 months of TNFi±MTX.
- Reduced TCC correlated with decreased inflammation and improved lipid profiles; higher baseline TCC was linked to endothelial dysfunction.
Conclusions:
- Active RA is associated with increased complement activation (elevated TCC).
- Antirheumatic treatments reduce TCC, with TNFi±MTX providing sustained effects over 6 months.
- Elevated baseline TCC in RA patients with endothelial dysfunction suggests complement's role in RA-related atherosclerosis.
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