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作 者:周文煜[1] 陈文莉[1] 黄小妹[1] 余立凯[2] 李永吉[2] 黄安斌[2]
机构地区:[1]武汉市中心医院肾病风湿科,430022 [2]华中科技大学同济医学院附属协和医院风湿免疫科,430022
出 处:《中华风湿病学杂志》2012年第4期267-270,共4页Chinese Journal of Rheumatology
摘 要:目的观察重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白(rhTNFR:Fc,商品名益赛普)对类风湿关节炎(RA)患者IgM-类风湿因子(RF),IgG-RF,IgA.RF的影响,探讨rhTNFR:Fc治疗RA的免疫学机制。方法选择华中科技大学同济医学院附属协和医院及武汉市中心医院2007-2008年110例RA患者,采用随机数字表法随机分为rhTNFR:Fc组和甲氨蝶呤组。rhTNFR:Fc组55例,每周2次皮下注射rhTNFR:Fc(25mg/次),24周。甲氨蝶呤组55例,每周1次口服甲氨蝶呤片,7.5m∥次起,8周内逐步加到15mg/次,24周。观察药物对IgM.RF、IgG-RF、IgA-RF的影响,临床疗效评价采用28个关节疾病活动度(DAS28)疗效评定标准。组内治疗前后的差异采用配对t检验分析,组间治疗前后的差异采用两样本t检验分析。结果①2组患者病情均明显改善,rhTNFR:Fc的IgM-RF降低时间早于甲氨蝶呤组(P〈0.05)。②rhTNFR:Fc组血清IgM.RF(29±16)U/ml明显降低(P〈O.05),IgG-RF(145±20)u,ml和IgA.RF(153±34)U/ml明显升高(R0.05)。③甲氨蝶呤组IgM-RF(44±14)U/ml,IgG-RF(62±14)U/ml和IgA-RF.RF(66±19)u/ml均明显降低(P=0.05)。④对临床指标的分析表明rhTNFR:Fc治疗RA疗效确切。结论rhTNFR:Fc与甲氨蝶呤均能有效缓解RA的病情。rhTNFR:Fc能显著降低RA患者血清中IgM-RF的水平,而对IgG-RF,IgA.RF水平有升高作用,可能与其治疗RA的免疫学机制有关。Objective To observe the effect of recombinant human tumor necrosis factor receptor Fc fusion Protein (rhTNFR:Fc) treatment on IgM-RF, IgG-RF, IgA-RF of patients with rheumatoid arthritis. Methods A randomized, activecomparator controUed, parallel group study were conducted. 110 patients were enrolled and were randomly divided to the treatment group, in which patients were treated with twice weekly subcutaneous injection of rhTNFR:Fe (25 mg) (rhTNFR:Fc treatment group, n=55), and the MTX froup, in which MTX (the mean dosage was 15 mg/week) (MTX group, n=55) for 24 weeks. Blood routine, IgM-RF, IgG-RF, IgA-RF, and disease activity score 28 (DAS28) were monitored. Student's ttest was used for statistical analysis. Results The level of IgM-RF decreased significantly in the rhTNFR:Fc treatment group 24 week (29±16) U/ml later. However, the level of IgG-RF (145 ±20) U/ml, IgA-RF (153±34) U/ml increased significantly in the rhTNFR:Fc group, and the level of IgG-RF (62±14) U/ml, IgA-RF (66~19) U/ml decreased significantly in the MTX group. Conclusion Although rhTNFR:Fc, is effective in treating the clinical symptoms of RA, it seems to affect RF Droducinz-B cells either directly or indirectly.
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