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HLA-A 31:01 is not associated with the development of methotrexate pneumonitis in the UK population: results from a genome-wide association study
  1. James Bluett1,
  2. Sally-Ann Owen1,
  3. Jonathan Massey1,
  4. Ana Alfirevic2,
  5. Munir Pirmohamed2,
  6. Darren Plant3,
  7. Suzanne M M Verstappen4,
  8. Anne Barton1,3
  9. on behalf of The Pneumonitis Study Consortium
  1. 1Arthritis Research UK Centre for Genetics and Genomics, Centre for Musculoskeletal Research, The University of Manchester, Manchester, UK
  2. 2Department of Molecular and Clinical Pharmacology, The Wolfson Centre for Personalised Medicine, Institute of Translational Medicine, University of Liverpool, Liverpool, UK
  3. 3NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK
  4. 4Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal Research, The University of Manchester, Manchester, UK
  1. Correspondence to Dr James Bluett, Arthritis Research UK Centre for Genetics and Genomics, Centre for Musculoskeletal Research, The University of Manchester, Manchester, UK; james.bluett{at}manchester.ac.uk

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We read with interest the article by Furukawa et al1 suggesting an association between HLA-A 31:01 and methotrexate (MTX)-induced interstitial lung disease (ILD) in Japanese patients with rheumatoid arthritis (RA). MTX-ILD or MTX-pneumonitis (MTX-P) is an idiosyncratic hypersensitivity reaction to MTX that usually occurs within the first year of MTX therapy, inducing inflammation, cytokine release and the activation of CD4+ T-lymphocytes within the lung parenchyma,2–4 with a reported prevalence of 1% of the Caucasian RA population prescribed MTX.5

To investigate this association further, we conducted a genome-wide association study. Rheumatologists working within the National Health Service in the UK identified Caucasian patients …

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Footnotes

  • Contributors JB recruited patients, NHS sites, co-conducted the GWAS and analysis.

    S-AO applied to the ethics committee, recruited patients and NHS sites.

    JM co-conducted the GWAS and analysis.

    AA co-genotyped the HLA 31:01.

    MP co-wrote the article.

    SMMV is PI of the control cohort.

    AB is the PI of the cases cohort.

  • Competing interests None declared.

  • Ethics approval National Research Ethics Service, NRES Comittee North West, Greater Manchester Central.

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

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