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THU0191 Clinical Efficacy of Add-on Iguratimod Therapy in Patients with Active Rheumatoid Arthritis Despite of Methotrexate: 52-Week Results – a Multicenter Registry Study
  1. Y. Kanayama1,
  2. Y. Hirano2,
  3. A. Kaneko3,
  4. N. Takahashi4,
  5. Y. Yoshioka4,
  6. H. Kanda3,
  7. S. Hirabara2,
  8. T. Kojima4,
  9. N. Ishiguro4
  10. on behalf of Tsurumai Biologics Communication Registry (TBCR) plus
  1. 1Orthopedic Surgery And Rheumatology, Toyota Kosei Hospital, Toyota
  2. 2Rheumatology, Toyohashi Municipal Hospital, Toyohashi
  3. 3Orthopedic Surgery And Rheumatology, Nagoya Medical Center
  4. 4Orthopedic Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan

Abstract

Background Iguratimod (IGU) is a small-molecule antirheumatic drug that was approved in Japan in September 2012. IGU suppressed tumor necrosis factor-alpha-induced production of interleukin (IL)-6, IL-8, and monocyte chemoattractant protein 1 via inhibition of nuclear factor kappa B activation in cultured human synovial cells and human acute monocytic leukemia cells. IGU also reduced immunoglobulin production by acting directly on human B lymphocytes without affecting B lymphocyte proliferation. Recently, an increased release of extracellular adenosine and a decreased production of lymphotoxins such as ammonia and superoxide have been shown to be involved in the anti-inflammatory mechanisms of methotrexate. Thus, the combination of MTX and IGU may have synergic efficacy for rheumatoid arthritis (RA) treatment.

Objectives To evaluate the clinical efficacy of add-on IGU in patients with Japanese active RA who had shown inadequate responses to MTX therapy from initiation to 52-week.

Methods Patients with a diagnosis of RA according to the 2010 ACR/EULAR criteria who had been unresponsive to MTX therapy (DAS>3.2 or CDAI>10), and who had been prescribed add-on IGU from Tsurumai Biologics Communication Registry (TBCR)-plus between November 2012 and September 2013 were enrolled. The final study cohort of 41 patients received continuous IGU therapy more than 52 weeks. We reviewed the methods about the improvement of CRP, MMP3, DAS28-ESR and CDAI which was an index of disease activity of RA using Wilcoxon signed-rank test and the rate of remission patients at Week24, 52.

Results The group of patients included 6 males and 35 females. The mean age was 63.0±11.0 years old; the disease duration was 8.0±8.6 years and the methotrexate dose was 9.8±4.2 mg/week. Clinical findings related to RA were as follows: mean tender joint count, 5.2±5.6; swollen joint count, 4.4±4.4; patient's global assessment of disease activity, 39.1±20.5mm; Physician's global assessment of disease activity, 39.1±19.2mm; CRP, 2.0±2.4 mg/dL; ESR, 42.2±19.1 mm/h; MMP3, 258.2±314.2 ng/ml; DAS28 (ESR), 4.72±0.99; and CDAI, 17.5±9.8. There were no patients who had received Biologics treatment. The mean CRP improved to 1.8±2.3, 1.4±2.2, 1.2±2.1 and 1.1±1.9 at Week 4, 12, 24 and 52 (p=0.234, p=0.007, p<0.001, p<0.001), mean MMP3 improved to 231.2±291.8, 176.4±274.0, 149.4±271.2 and 147.8±267.3 at Week 4, 12, 24 and 52 (p=0.185, p=0.003, p<0.001, p<0.001), the mean DAS28 improved to 4.43±1.14, 3.59±1.10, 3.36±1.32 and 3.19±1.28 at Week 4, 12, 24 and 52 (p=0.004, p<0.001, p<0.001, p<0.001) and the mean CDAI improved to 13.7±8.9, 8.8±6.9, 8.4±7.8 and 7.6±7.2 at Week 4, 12 and 24 (p<0.001, p<0.001, p<0.001, p<0.001) significantly. At Week 24 and 52 the rate of patients who achieved remission were each 29.3%, 31.7% and 22.5%, 19.5% in DAS and CDAI criteria. At Week 24 and 52 the rate of patients who achieved LDA were each 51.2%, 58.5% and 75.0%, 78.0% in DAS and CDAI criteria.

Conclusions The study suggested that the new combination therapy of add-on IGU with MTX was effective in patients with active RA with inadequate response to MTX.

Disclosure of Interest Y. Kanayama: None declared, Y. Hirano Speakers bureau: Abbott Japan Co. Ltd.; Eisai Co. Ltd.; Mitsubishi Tanabe Pharma Corporation; Pfizer Co. Ltd.; Chugai Pharmaceutical Co. Ltd.; and Bristol-Myers Squibb Co. Ltd., A. Kaneko Speakers bureau: Abbott Japan Co. Ltd.; Eisai Co. Ltd.; Mitsubishi Tanabe Pharma Corporation; Pfizer Co. Ltd.; Chugai Pharmaceutical Co. Ltd.; and Bristol-Myers Squibb Co. Ltd., N. Takahashi Speakers bureau: Abbott Japan Co. Ltd.; Eisai Co. Ltd.; Mitsubishi Tanabe Pharma Corporation; Pfizer Co. Ltd.; Chugai Pharmaceutical Co. Ltd.; and Bristol-Myers Squibb Co. Ltd., Y. Yoshioka: None declared, H. Kanda: None declared, S. Hirabara: None declared, T. Kojima Speakers bureau: Abbott Japan Co. Ltd.; Eisai Co. Ltd.; Mitsubishi Tanabe Pharma Corporation; Pfizer Co. Ltd.; Chugai Pharmaceutical Co. Ltd.; and Bristol-Myers Squibb Co. Ltd., N. Ishiguro Speakers bureau: Abbott Japan Co. Ltd.; Eisai Co. Ltd.; Mitsubishi Tanabe Pharma Corporation; Pfizer Co. Ltd.; Chugai Pharmaceutical Co. Ltd.; and Bristol-Myers Squibb Co. Ltd.

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