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Serotyping for an extended anti-citrullinated peptide autoantibody panel does not add value to CCP2 testing for diagnosing RA in an early undifferentiated arthritis cohort
  1. Arthur G Pratt1,2,
  2. Peter J Charles3,
  3. Muslima Chowdhury3,
  4. Gillian Wilson2,
  5. Patrick J Venables3,
  6. John D Isaacs1,2
  1. 1Musculoskeletal Research Group, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK
  2. 2Musculoskeletal Unit, The Freeman Hospital, Newcastle upon Tyne, UK
  3. 3The Kennedy Institute for Rheumatology, Imperial College, London, UK
  1. Correspondence to Professor John D Isaacs, Musculoskeletal Research Group, Institute of Cellular Medicine, Newcastle University, Floor 4 Cookson Building, The Medical School, Framlington Place, Newcastle upon Tyne NE2 4HH, UK; j.d.isaacs{at}ncl.ac.uk

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The now widely employed CCP2 assay, which detects circulating autoantibodies to a panel of synthetic, cyclic citrullinated peptides, carries a positive predictive value of 0.93 for rheumatoid arthritis (RA) among early undifferentiated arthritis (UA) patients,1 thus providing a cornerstone of recently evolved scoring systems that predict and classify early RA.2 However, approximately 80% of newly presenting UA patients are anti-CCP2-negative3 and a quarter of these evolve into RA within 3 years,1 thus experiencing diagnostic delay. The peptides used in the CCP2 assay do not necessarily correspond to in vivo generated proteins, yet citrullinated antigens of putative pathophysiological relevance have recently been described in association with specific circulating autoantibodies in RA.4 Therefore, we hypothesised that the detection of one or any such autoantibodies, as well as those against filaggrin components of the CCP1 assay,5 IgA or IgM rheumatoid factor (RF), might add to the diagnostic utility of CCP2 testing alone in predicting RA progression among early UA patients.

Consecutive adult UA patients with …

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