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Clinical and epidemiological research
Extended report
Evidence to support IL-13 as a risk locus for psoriatic arthritis but not psoriasis vulgaris
  1. John Bowes1,
  2. Steve Eyre1,
  3. Edward Flynn1,
  4. Pauline Ho1,2,
  5. Salma Salah1,
  6. Richard B Warren3,
  7. Helena Marzo-Ortega4,
  8. Laura Coates4,
  9. Ross McManus5,
  10. Anthony W Ryan5,
  11. David Kane6,
  12. Eleanor Korendowych7,8,
  13. Neil McHugh7,8,
  14. Oliver FitzGerald9,10,
  15. Jonathan Packham11,12,
  16. Ann W Morgan4,
  17. Christopher E M Griffiths3,
  18. Ian N Bruce1,2,
  19. Jane Worthington1,
  20. Anne Barton1,2
  1. 1Arthritis Research UK Epidemiology Unit, Manchester Academic Health Science Centre, The University of Manchester, Manchester, UK
  2. 2The Kellgren Centre for Rheumatology, Central Manchester Foundation Trust, NIHR Manchester Biomedical Research Centre, Manchester, UK
  3. 3Dermatological Sciences, Salford Royal NHS Foundation Trust, Manchester Academic Health Science Centre, The University of Manchester, Manchester, UK
  4. 4NIHR-Leeds Musculoskeletal Biomedical Research Unit, Leeds Institute of Molecular Medicine, University of Leeds, Leeds, UK
  5. 5Department of Clinical Medicine, Institute of Molecular Medicine, Trinity College Dublin, Dublin, Ireland
  6. 6Adelaide and Meath Hospital and Trinity College Dublin, Dublin, Ireland
  7. 7Royal National Hospital for Rheumatic Diseases, Bath, UK
  8. 8Department of Pharmacy and Pharmacology, University of Bath, Bath, UK
  9. 9Department of Rheumatology, St Vincent's University Hospital, Dublin, Ireland
  10. 10UCD School of Medicine and Medical Sciences and Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland
  11. 11Haywood Hospital, Stoke on Trent, Staffordshire, UK
  12. 12Arthritis Research UK Primary Care Centre, Keele University, Staffordshire, UK
  1. Correspondence to Professor Anne Barton, Arthritis Research UK, Stopford Building, The University of Manchester, Manchester, UK; anne.barton{at}manchester.ac.uk

Abstract

Objective There is great interest in the identification of genetic factors that differentiate psoriatic arthritis (PsA) from psoriasis vulgaris (PsV), as such discoveries could lead to the identification of distinct underlying aetiological pathways. Recent studies identified single nucleotide polymorphisms (SNPs) in the interleukin 13 (IL-13) gene region as risk factors for PsV. Further investigations in one of these studies found the effect to be primarily restricted to PsA, thus suggesting the discovery of a specific genetic risk factor for PsA. Given this intriguing evidence, association to this gene was investigated in large collections of PsA and PsV patients and healthy controls.

Methods Two SNPs (rs20541 and rs1800925) mapping to the IL-13 gene were genotyped in 1057 PsA and 778 type I PsV patients using the Sequenom genotyping platform. Genotype frequencies were compared to those of 5575 healthy controls. Additional analyses were performed in phenotypic subgroups of PsA (type I or II PsV and in those seronegative for rheumatoid factor).

Results Both SNPs were found to be highly associated with susceptibility to PsA (rs1800925 ptrend = 6.1×10−5 OR 1.33, rs20541 ptrend = 8.0×10−4 OR 1.27), but neither SNP was significantly associated with susceptibility to PsV.

Conclusions This study confirms that the effect of IL-13 risk locus is specific for PsA, thus highlighting a key biological pathway that differentiates PsA from PsV. The identification of markers that differentiate the two diseases raises the possibility in future of allowing screening of PsV patients to identify those at risk of developing PsA.

This paper is freely available online under the BMJ Journals unlocked scheme, see http://ard.bmj.com/info/unlocked.dtl

https://doi.org/10.1136/ard.2010.143123

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    Footnotes

    • Funding JB, IB and AB are funded by Arthritis Research UK (arc grant; 17552). EF is supported by the European Community's Sixth Framework Programme AutoCure funding. This study makes use of data generated by the Wellcome Trust Case–Control Consortium. A full list of the investigators who contributed to the generation of the data is available from http://www.wtccc.org.uk. Funding for the project was provided by the Wellcome Trust under award 076113 and 085475.

    • Competing interests None.

    • Ethics approval This study was conducted with the approval of the MREC 99/8/84.

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