Iguratimod, A Synthetic Disease Modifying Anti- Rheumatic Drug (Sdmard), and Various Dmards Suppress Joint Destruction. The Pathophysiological Mechanisms of the Inhibition of Bone/Cartilage Destruction

K. Ishikawa, J. Ishikawa
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Abstract

Objective: To elucidate the radiographic outcomes for rheumatoid arthritis (RA) patients using the synthetic disease-modifying antirheumatic drug (sDMARD) Iguratimod (IGU) and other DMARDs including injectable sodium aurothiomalate, bucillamine, salazosulphapyridine, infliximab, etanercept, tocilizumab and/or abatacept.Patients and Methods: 213 patients were enrolled in this study. Total Genant-modified Sharp scores (GSS) of hands/wrists and feet at baseline and at week 104 were calculated in 31 RA patients treated with a daily dose of 25 mg or 50 mg for 104 weeks.Results: Total GSS of 31 patients at week 104 showed no progression (total GSS  <= 0.84: the smallest detectable change) in 16 (52%) patients with a mean score reduction (95% CI) of-4.3 (-8.1 ~ -0.5) (p < 0.05).Conclusion: Treatment with the sDMARD, IGU showed no radiographic progression in 16 (52%) RA patients at week 104. Concerning the suppression mechanism of joint destruction by IGU and other DMARDs, we speculate that DMARDs prevent bone/cartilage destruction by inhibiting the receptor activator of nuclear factor-kappa B (NF- kB) lig and (RANKL) and through other antirheumatic actions.
Iguratimod,一种合成的疾病修饰抗风湿药物(Sdmard)和多种药物抑制关节破坏。抑制骨/软骨破坏的病理生理机制
目的:探讨类风湿关节炎(RA)患者使用合成疾病改善抗风湿药物(sDMARD) Iguratimod (IGU)和其他dmard(包括可注射的金硫硫酸钠、buillamine、salazosulphapyridine、英夫利昔单抗、依那西普、tocilizumab和/或abatacept)的影像学结果。患者和方法:213例患者入组。在基线和104周时计算31例RA患者的手/手腕和脚的Genant-modified Sharp评分(GSS),这些患者每天服用25mg或50mg,持续104周。结果:在第104周,31例患者的总GSS无进展(总GSS <= 0.84:可检测到的最小变化),16例(52%)患者的平均评分降低(95% CI) -4.3 (-8.1 ~ -0.5) (p < 0.05)。结论:经sDMARD治疗,16例(52%)RA患者在第104周时IGU未见影像学进展。关于IGU和其他DMARDs对关节破坏的抑制机制,我们推测DMARDs通过抑制核因子κ B受体激活因子(NF- kB)和RANKL以及其他抗风湿作用来防止骨/软骨破坏。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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