Journal
ARTHRITIS & RHEUMATOLOGY
Volume 72, Issue 12, Pages 2025-2029Publisher
WILEY
DOI: 10.1002/art.41424
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Funding
- Department of Defense Congressionally Directed Medical Research Program [PR180230]
- National Center for Advancing Translational Sciences, NIH (Clinical and Translational Science Award) [UL1-TR-001082]
- VA Biomedical Laboratory Research and Development Merit grant [BX004790]
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Objective To examine serum autoantibodies to malondialdehyde-acetaldehyde (MAA) prior to rheumatoid arthritis (RA) diagnosis. Methods Concentrations of anti-MAA antibody isotypes, anti-cyclic citrullinated peptide 2 (anti-CCP-2), and IgM rheumatoid factor (IgM-RF) were evaluated before and after RA diagnosis in samples from cases (n = 214) and controls (n = 210). The timing of elevations in autoantibody concentrations relative to RA diagnosis was explored using separate mixed models for each antibody and/or isotype. Associations between prediagnosis autoantibody concentrations in RA patients were examined using mixed effects linear regression models. Results Concentrations of IgG (log(2)difference 0.34) and IgA (log(2)difference 0.43) anti-MAA antibodies in RA patients diverged from controls at 3.0 years and 2.3 years prior to diagnosis, respectively (P< 0.05 for both). There was no evidence of case-control divergence for IgM anti-MAA antibody concentration. Anti-CCP-2 and IgM-RF concentrations diverged between RA patients and controls beginning at 17.6 years and 7.2 years prior to RA diagnosis, respectively. All 3 anti-MAA antibody isotypes (IgA, IgM, and IgG) were significantly associated with anti-CCP-2 antibody and RF concentrations prior to diagnosis (beta = 0.22-0.27 for IgM-RF; beta = 0.44-0.93 for anti-CCP-2) (P< 0.001). Conclusion IgG and IgA anti-MAA autoantibodies are elevated prior to RA diagnosis but appear later in the preclinical course than anti-CCP-2 or RF. These findings suggest that MAA formation and anti-MAA immune responses could play a role in the transition from subclinical autoimmunity to clinically apparent arthritis.
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