Rheumatoid arthritis

Identification of circulating autoantibodies to non-modified proteins associated with ACPA status in early rheumatoid arthritis

Rheumatology (Oxford)Published Case-control study

Authors' conclusion

These four autoantibodies may be useful in diagnostics and in predicting clinical phenotypes of RA.

Study context

Population
Early RA from the Swedish population-based Epidemiological Investigation of RA (EIRA) cohort (screening 80 ACPA-negative and 80 ACPA-positive); 93 early-RA patients from the LURA cohort for high-resolution CT (HRCT) lung abnormalities
Participants
317 / 302 / 372
Comparison
ACPA-positive vs ACPA-negative RA vs matched controls
  • ACPA-positiven = 317
  • ACPA-negativen = 302
  • Controlsn = 372reference
Outcome
Autoantibodies to non-modified proteins associated with presence/absence of ACPAs in RA
Methodological detailsdiscovery screening and validation, suspension bead array, age- and sex-matched controls, logistic regression
  • Discovery screening and validation
  • Suspension bead array
  • Age- and sex-matched controls
  • Logistic regression

Main finding

As reported in the abstract

Autoantibody association with ACPA status

Anti-ANOS1 IgG associated with ACPA-positive status, OR

3.02

95% CI 1.87–4.89

Anti-MURC IgG associated with ACPA-positive status, OR

1.86

95% CI 1.16–2.97

Anti-TSPYL4 IgG associated with being ACPA negative, OR

0.41

95% CI 0.19–0.89

Observational data: associations, not effects.

Further findings

Association with smoking and shared-epitope genes

Anti-ANOS1 IgG associated with smoking habit, OR
2.11 (95% CI 1.22-3.69)
Anti-MURC IgG associated with MHC class II shared-epitope genes, OR
1.95 (95% CI 1.11-3.46)

HRCT-defined lung abnormalities (LURA)

Anti-MAP2K6 and anti-TSPYL4 IgG correlated negatively with HRCT-defined lung abnormalities

Original publication

Identification of circulating autoantibodies to non-modified proteins associated with ACPA status in early rheumatoid arthritis. Rheumatology (Oxford). Published 9 January 2024. doi:10.1093/rheumatology/keae007

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