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In RA, becoming seronegative over the first year of treatment does not translate to better chances of drug-free remission
  1. Emma C de Moel1,
  2. Veerle F A M Derksen1,
  3. Leendert A Trouw1,
  4. Holger Bang2,
  5. Yvonne P M Goekoop-Ruiterman3,
  6. Gerda M Steup-Beekman1,4,
  7. Tom W J Huizinga1,
  8. Cornelia F Allaart1,
  9. René E M Toes1,
  10. Diane van der Woude1
  1. 1 Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands
  2. 2 Orgentec Diagnostika, Mainz, Germany
  3. 3 Department of Rheumatology, Haga Hospital, The Hague, The Netherlands
  4. 4 Department of Rheumatology, Haaglanden Medical Center, The Hague, The Netherlands
  1. Correspondence to Dr Emma C de Moel, Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands; e.c.de_moel{at}

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In rheumatoid arthritis (RA), it is becoming common to attempt to taper or stop medication, aiming for sustained drug-free remission (SDFR). Autoantibody seropositivity is a poor prognostic factor for this treatment goal. However, autoantibody levels may change and patients may become seronegative, sometimes termed ‘immunological remission’.1 Understanding how often this occurs and whether it is favourable for achieving SDFR is important to determine whether becoming seronegative is a meaningful prognostic marker for drug tapering decisions. Furthermore, it will elucidate pathways that lead to long-term resolution of the pathophysiology underlying RA.

To that end, we investigated the relationship between seroconversion and SDFR. In baseline and 1-year serum of 381 patients with seropositive RA, we measured 14 RA-associated autoantibodies by ELISA2: anti-CCP2 IgG, IgM and IgA; rheumatoid factor IgM and IgA; anti-CarP IgG, IgM and IgA; anti-acetylated   lysine vimentin IgG and anti-acetylated ornithine vimentin IgG (Orgentec Diagnostika , Germany); and anti-citrullinated vimentin 59–74 IgG, anti-citrullinated fibrinogen β 36–52 and α 27–43 IgG, anti-citrullinated enolase 5–20 IgG. Patients originated from the IMPROVED study,3 a randomised controlled treat-to-target trial …

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  • Handling editor Josef S Smolen

  • Contributors ECM, VFAMD and DW designed the research. ECM and VFAMD performed the experiments. HB kindly provided assays for anti-acetylated peptide antibodies. YPMGR, GMSB and CFA were responsible for design and clinical data collection of the IMPROVED study. ECM analysed the data and drafted the manuscript. All authors contributed to the interpretation of the data and preparation of the manuscript.

  • Funding This project was funded by the ZonMw (the Netherlands Organisation for Health Research and Development)-consortium MOlecular DIagnostics in RA (MODIRA), project number 436001001.

  • Competing interests None declared.

  • Patient consent Obtained

  • Ethics approval This study was conducted with the approval of the regional ethics committee at Leiden University Medical Center. The IMPROVED study was approved by the medical ethics committees of all participating hospitals.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement Details concerning data analysis and ‘data not shown’ are available upon request.