{"title":"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","authors":"K. Ishikawa, J. Ishikawa","doi":"10.18314/jbo.v4i1.1378","DOIUrl":null,"url":null,"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.","PeriodicalId":249116,"journal":{"name":"Journal of Bone Biology and Osteoporosis","volume":"23 2","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2018-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"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\",\"authors\":\"K. Ishikawa, J. Ishikawa\",\"doi\":\"10.18314/jbo.v4i1.1378\",\"DOIUrl\":null,\"url\":null,\"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.\",\"PeriodicalId\":249116,\"journal\":{\"name\":\"Journal of Bone Biology and Osteoporosis\",\"volume\":\"23 2\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-12-18\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Bone Biology and Osteoporosis\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.18314/jbo.v4i1.1378\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Bone Biology and Osteoporosis","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.18314/jbo.v4i1.1378","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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
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.