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Response to: ‘HLA-A* 31:01 is not associated with the development of methotrexate pneumonitis in the UK population: results from a genome wide association study’ by Bluett et al
  1. Hiroshi Furukawa1,2,
  2. Shomi Oka1,2,
  3. Kota Shimada3,4,
  4. Naoyuki Tsuchiya1,
  5. Shigeto Tohma2
  6. on behalf of the Rheumatoid Arthritis associated Interstitial Lung Disease (RA-ILD) Study Consortium
  1. 1 Molecular and Genetic Epidemiology Laboratory, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan
  2. 2 Clinical Research Center for Allergy and Rheumatology, Sagamihara National Hospital, National Hospital Organization, Sagamihara, Japan
  3. 3 Department of Rheumatology, Sagamihara National Hospital, National Hospital Organization, Sagamihara, Japan
  4. 4 Department of Rheumatic Diseases, Tokyo Metropolitan Tama Medical Center, Fuchu, Japan
  1. Correspondence to Dr Hiroshi Furukawa, Molecular and Genetic Epidemiology Laboratory, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8575, Japan; furukawa-tky{at}umin.org

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We appreciate the comments by Bluett et al 1 on our report of an association of HLA-A*31:01 with methotrexate-induced interstitial lung disease (ILD) in patients with rheumatoid arthritis (RA).2 They have tried to reveal the genetic factors associated with methotrexate-induced ILD, but found no significant association except three suggestive loci in chromosome 1, 9 and 14. This study did not show the association of A*31:01 with methotrexate-induced ILD, though the p value of the analysis was still 0.21 in spite of the small sample size with 62 cases and 175 controls. The meta-analysis with our previous study2 or other forthcoming HLA association studies on methotrexate-induced ILD may reveal more conclusive results in the future.

Genetic factors would be involved in the pathogenesis of methotrexate-induced ILD, because the susceptibility of methotrexate-induced ILD in Japanese patients with RA are thought to be higher than other ethnic groups or patients with other autoimmune diseases.3 4 However, there are few reports of genome-wide association study of drug-induced ILD.5 Since the prevalence of drug-induced ILD is low and the clinical conditions of the patients with drug-induced ILD are various,6 genetic analyses …

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