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  • Response to: ‘Corresponence on ‘Shared epitope defines distinct associations of cigarette smoking with levels of anticitrullinated protein antibody and rheumatoid factor’ by Ishikawa et al’ by Regueiro and Gonzalez

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Correspondence response
Response to: ‘Corresponence on ‘Shared epitope defines distinct associations of cigarette smoking with levels of anticitrullinated protein antibody and rheumatoid factor’ by Ishikawa et al’ by Regueiro and Gonzalez
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  1. Yuki Ishikawa1,2,
  2. Katsunori Ikari3,4,
  3. Chikashi Terao1,5,6
  1. 1 Laboratory for Statistical and Translational Genetics, Center for Integrative Medical Sciences, RIKEN, Yokohama, 230-0045, Japan
  2. 2 Section for Immunobiology, Joslin Diabetes Center, Boston, Massachusetts, United States
  3. 3 Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), Tokyo, 102-0076, Japan
  4. 4 Department of Orthopaedic Surgery, Tokyo Women’s Medical University, Tokyo 162-0054, Japan
  5. 5 Clinical Research Center, Shizuoka General Hospital, Shizuoka, 420-0881, Japan
  6. 6 Department of Applied Genetics, The School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, 422-8526, Japan
  1. Correspondence to Dr Chikashi Terao, Laboratory for Statistical and Translational Genetics, Center for Integrative Medical Sciences, RIKEN, Yokohama 230-0045, Japan; chikashi.terao{at}riken.jp

https://doi.org/10.1136/annrheumdis-2019-216872

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    We are pleased to welcome the correspondence by Regueiro and Gonzalez1 on our work.2

    As they wondered if cigarette smoking (CS) introduced a differential association between the two subsets of patients with shared epitope (SE) and high anticitrullinated cyclic peptide/protein antibody (ACPA) described in figure 3B of the original manuscript, we add further explanation as follows; as shown in figure 3B of the original manuscript, smokers at the time of disease onset (SaO) with SE alleles have higher (OR 3.10, 95% CI 1.82 to 5.11, p=2.3×10−5) than never smokers with SE alleles (OR 2.24, 95% CI 1.56 to 3.24, p=1.5×10−5), while SaO without SE alleles does not have significant risk of high ACPA levels (OR 0.49, 95% CI 0.16 to 1.53, p=0.22). This indicates that CS does not independently affect ACPA production, but rather interacts with SE alleles and further increases the risk. Furthermore, we presented the linear association between SaO with SE alleles and ACPA levels (not presence of high ACPA level) in online …

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