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Ann Rheum Dis 2005;64:299-302 doi:10.1136/ard.2004.023523
  • Concise report

Rheumatoid factor, but not anti-cyclic citrullinated peptide antibodies, is modulated by infliximab treatment in rheumatoid arthritis

  1. L De Rycke,
  2. X Verhelst,
  3. E Kruithof,
  4. F Van den Bosch,
  5. I E A Hoffman,
  6. E M Veys,
  7. F De Keyser
  1. Department of Rheumatology, Ghent University Hospital, Ghent, Belgium
  1. Correspondence to:
    Dr L De Rycke
    Department of Rheumatology, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium; leen.deryckeUgent.be
  • Accepted 16 May 2004
  • Published Online First 27 May 2004

Abstract

Objectives: To analyse the effect of infliximab on IgM rheumatoid factor (RF) and anti-cyclic citrullinated peptide (CCP) antibodies, and determine whether baseline autoantibody titres (IgM RF and anti-CCP antibodies) are associated with changes in acute phase reactants.

Patients and methods: 62 patients with refractory RA were treated with infliximab combined with methotrexate. At baseline and week 30, serum samples were tested for IgM RF by two agglutination assays, and for anti-CCP antibodies by an ELISA. Percentage change in C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) was calculated.

Results: At baseline and week 30 RF titres were reduced significantly during infliximab treatment (p<0.001 and p = 0.038, respectively), whereas anti-CCP antibodies were unchanged (p = 0.240). Baseline IgM RF titres, but not anti-CCP antibodies, correlated inversely with changes in CRP and ESR during treatment. Patients with a marked decrease in acute phase reactants had lower IgM RF titres than those with a smaller decrease in CRP and ESR; no significant differences were found for anti-CCP antibodies.

Conclusion: The differential effect of infliximab treatment on IgM RF and anti-CCP antibodies, and the different predictive value on changes in acute phase reactants during infliximab treatment support the existing evidence that RF and anti-CCP antibodies are independent autoantibody systems in RA.

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