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  • Studying associations between variants in TRAF1-C5 and TNFAIP3-OLIG3 and the progression of joint destruction in rheumatoid arthritis in multiple cohorts

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Studying associations between variants in TRAF1-C5 and TNFAIP3-OLIG3 and the progression of joint destruction in rheumatoid arthritis in multiple cohorts
  1. R Knevel1,
  2. D P de Rooy1,
  3. P K Gregersen2,
  4. E Lindqvist3,
  5. A G Wilson4,
  6. G Gröndal5,
  7. A Zhernakova1,
  8. J A van Nies1,
  9. R E Toes1,
  10. R Tsonaka6,
  11. J J Houwing-Duistermaat6,
  12. K Steinsson5,
  13. T W Huizinga1,
  14. T Saxne3,
  15. A H van der Helm-van Mil1
  1. 1Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands
  2. 2Robert S Boas Center for Genomics and Human Genetics, Feinstein Institute for Medical Research and North Shore–Long Island Jewish Health System, Manhasset, New York, USA
  3. 3Department of Rheumatology, Lund University, Lund, Sweden
  4. 4School of Medicine and Biomedical Sciences, The University of Sheffield, Sheffield, UK
  5. 5Department of Rheumatology, Landspítali hospital, Reykjavik, Iceland
  6. 6Department of Medical Statistics, Leiden University Medical Center, Leiden, The Netherlands
  1. Correspondence to Dr Rachel Knevel, Department of Rheumatology, Leiden University Medical Center, Albinusdreef 2, 2333 ZA, Leiden, The Netherlands; r.knevel{at}lumc.nl

https://doi.org/10.1136/annrheumdis-2012-201289

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    The severity of joint destruction in rheumatoid arthritis (RA) is highly variable between patients. Recent twin and population studies indicated that the severity of joint destruction is influenced by genetic factors.1 ,2 Previously, we reported the association of rs10818488 (TRAF1-C5) and rs675520 (TNFAIP3-OLIG3) with progression of joint destruction.3 ,4 The genes near these loci encode for tumour necrosis factor receptor-associated factor-1 (TRAF1), complement component-5 (C5) and tumour necrosis factor α-induced protein-3 (TNFAIP3; a protein that inhibits NF-κ B activation). A basic principle in genetic association studies is to evaluate multiple cohorts to validate observed findings. We therefore studied both single-nucleotide polymorphisms in several RA cohorts with radiological follow-up data.

    Six thousand two hundred and eighty-two x-rays of 2666 RA patients were studied: 147 patients from Lund (Sweden), 385 patients from Sheffield (UK), 285 patients from Iceland, 384 patients from the North American Rheumatoid Arthritis Consortium (NARAC), 756 patients from the National Databank of Rheumatic Diseases (NDB), 113 patients from Wichita and 596 patients from the Leiden Early Arthritis Clinic (Leiden-EAC) cohort (table 1). Detailed information on these datasets is provided elsewhere.2 ,5,–,10 …

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    Footnotes

    • Funding This research was funded by the European Community's Seventh Framework Program (Masterswitch; FP7 Health-F2-2008-223404).

    • Competing interests None.

    • Ethics approval For each cohort the local ethical committee approved the data collection and patients signed informed consent.

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

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      Correction
      BMJ Publishing Group Ltd and European League Against Rheumatism
      Annals of the Rheumatic Diseases 2012; 71 2064-2064 Published Online First: 02 Nov 2012. doi: 10.1136/annrheumdis-2012-201289corr1