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The PTPN22 susceptibility risk variant is not associated with the rate of joint destruction in anti-citrullinated protein antibody-positive rheumatoid arthritis
  1. J A B van Nies1,
  2. R Knevel1,
  3. N Daha1,
  4. M P M van der Linden1,
  5. P K Gregersen2,
  6. M Kern2,
  7. S le Cessie3,4,
  8. J J Houwing-Duistermaat3,
  9. T W J Huizinga1,
  10. R E M Toes1,
  11. A H M van der Helm-van Mil1
  1. 1Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands
  2. 2The Feinstein Institute for Medical Research, North Shore LIJ Health System, Manhasset, New York, USA
  3. 3Department of Medical Statistics, Leiden University Medical Center, Leiden, The Netherlands
  4. 4Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands
  1. Correspondence to Dr R Knevel, Department of Rheumatology, Leiden University Medical Center, Albinusdreef 2, Leiden 2300, The Netherlands, r.knevel{at}

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A missense single-nucleotide polymorphism in the protein tyrosine phosphatase non-receptor 22 (PTPN22) gene, which encodes a negative regulator of T-cell activation, is an important genetic risk factor for rheumatoid arthritis (RA) susceptibility.1 The association of the PTPN22 susceptibility risk allele and the severity of joint destruction is unclear as a result of contradictory observations.2,,6 To determine an individual patient's rate of joint destruction accurately, it is required that radiological measurements are collected by means of standard procedures, scored quantitatively and sensitively and are repeated in time. Consequently, differences in used measurements and analysis methods may contribute to the occurrence of contrasting findings. Second, although the effect of PTPN22 on RA susceptibility is confined to the anti-citrullinated protein antibody (ACPA)-positive group,2 6 most studies on PTPN22 and joint destruction did not analyse the ACPA-positive subset.2,,5 The present study studied the effect of the PTPN22 susceptibility risk variant on the rate …

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  • The first two authors contributed equally.

  • Funding The work of AHMvdH-vM is supported by The Netherlands Organisation for Health Research and Development and the Dutch Arthritis Association. The NARAC collection was supported by NIH grants NO1-AR-2-2263 and RO1 AR44422 to PKG.

  • Competing interests None.

  • Patient consent Obtained.

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