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Inhibition of plasma IL-6 in addition to maintenance of an efficacious trough level of infliximab associated with clinical remission in patients with rheumatoid arthritis: analysis of the RISING Study
  1. Tsutomu Takeuchi1,
  2. Nobuyuki Miyasaka2,
  3. Yoshihiko Tatsuki3,
  4. Toshiro Yano3,
  5. Toru Yoshinari3,
  6. Tohru Abe4,
  7. Takao Koike5
  1. 1Division of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, Shinjuku-ku, Tokyo, Japan
  2. 2Department of Medicine and Rheumatology, Graduate School of Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan
  3. 3Mitsubishi Tanabe Pharma Corporation, Osaka, Japan
  4. 4Saitama Medical Center, Saitama Medical University, Kawagoe, Japan
  5. 5Sapporo Medical Center NTT EC, Chuo-ku, Sapporo, Japan
  1. Correspondence to Tsutomu Takeuchi; Division of Rheumatology, Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan; tsutake{at}z5.keio.jp

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Many clinical studies have reported the excellent clinical efficacy of infliximab (IFX), an antitumour necrosis factor α (anti-TNFα) monoclonal antibody, in the treatment of rheumatoid arthritis (RA).1 IFX is also reported to induce a rapid and marked reduction in circulating interleukin 6 (IL-6) levels, suggesting that its efficacy may result from the suppression of IL-6 as well as TNF.2,,5 In the RISING Study (NCT00691028),6 7 we observed patients who showed no response to IFX therapy, despite maintaining a serum IFX level higher than the threshold level for clinical response. Here, we examined data on clinical response to better understand the mechanism of action of IFX.

In this study, patients with methotrexate-refractory RA treated with 3 mg/kg of IFX at weeks 0, 2 and 6 were randomly assigned to receive 3, 6 or 10 mg/kg of IFX every 8 weeks from week 14 to 46 in combination …

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