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Improvement of HbA1c during treatment with humanised anti-interleukin 6 receptor antibody, tocilizumab
  1. Atsushi Ogata,
  2. Atsuyoshi Morishima,
  3. Toru Hirano,
  4. Yoshihiro Hishitani,
  5. Keisuke Hagihara,
  6. Yoshihito Shima,
  7. Masashi Narazaki,
  8. Toshio Tanaka
  1. Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, Osaka, Japan
  1. Correspondence to Dr Atsushi Ogata, Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, 2–2 Yamadaoka, Suita, Osaka 565–0871, Japan; ogata{at}

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Type II diabetes mellitus (T2DM) and insulin resistance (IR) are associated with a systemic, chronic inflammatory response.1 Indeed, inflammatory markers such as interleukin 6 (IL-6) or C-reactive protein are independent risk factors for T2DM.2 Recent studies suggest that IL-6 is involved in the pathology of T2DM-related IR.3 Chronic exposure to IL-6 impairs insulin signalling in hepatocytes and adipocytes by stimulating the suppressor of cytokine signalling-1.3 4 Acute IL-6 infusion increases insulin sensitivity in muscle. The action of IL-6 on glucose homoeostasis is complex.

Although the influence of anti-tumour necrosis factor5 6 and anti-IL-1 treatments7 on glucose homoeostasis has been reported, no reports of the influence of anti-IL-6 treatment in humans have been published. We report that HbA1c decreased in diabetic patients with rheumatoid arthritis (RA) who were treated with a humanised anti-IL-6 antibody, tocilizumab (TCZ). …

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  • Funding This study was supported by the Program for Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation.

  • Competing interests AO has received consultant fees from Chugai Pharmaceutical, the manufacture of tocilizumab.

  • Patient consent Obtained.

  • Ethics approval This study was conducted with approval of the Human Research and Ethics Committees at Osaka University Hospital.

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