摘要
目的研究艾拉莫德联合依那西普对难治性类风湿关节炎(resistant rheumatoid arthritis,RRA)患者CD4^+、CD8^+T细胞及免疫球蛋白的影响。方法将符合入组标准的60例RRA患者随机分为试验组和对照组,每组各30例,试验组口服艾拉莫德片,25 mg/次,每日2次,同时给予依那西普25 mg皮下注射,每周2次;对照组给予依那西普25 mg皮下注射,每周2次;疗程为12周。分别采用四色流式细胞术和免疫比浊法检测2组患者治疗前后CD4^+T、CD8^+T、CD4^+/CD8^+以及免疫球蛋白IgG、IgA、IgM指标,同时观察试验过程的不良反应。计算治疗前后类风湿关节炎疾病活动分数(DAS28),检测C反应蛋白(CPR)、类风湿因子(RF)。结果 12周后,试验组患者CD4^+、CD4^+/CD8^+值较对照组升高明显,差异具有统计学意义(P<0.05);试验组免疫球蛋白IgG、IgA、IgM水平较对照组下降明显,差异具有统计学意义(P<0.05);2组患者CD8^+T水平治疗前后差异无统计学意义(P<0.05)。2组患者治疗后DAS28、ESR、CPR、RF指标均低于治疗前,差异有统计学意义(P<0.05);试验组治疗后IgG、IgA、IgM指标低于对照组治疗后,差异有统计学意义(P<0.05)。结论艾拉莫德联合依那西普治疗RRA可能通过调节患者CD4^+/CD8^+T细胞免疫失衡、降低免疫球蛋白而发挥治疗作用。
Rheumatoid arthritis （RA） is a chronic autoimmune disease that destroys the cartilage and bone in the joint. The occurrence of this disease may be related to autoantibodies synovial membrane, and antigen antibody complexes infiltrating synovium, activation of tumor necrosis factor-alpha （TNF-alpha） and other inflammatory cytokines, resulting in destruction of articular cartilage and bone. This study was performed to evaluate the immune mechanism of action of Iguratimod combined with Etanercept in the treatment of refractory rheumatoid arthritis （RRA）. Total of 60 patients with RRA were randomly divided into experimental group and control group, with 30 patients in each group. The experimental group was gave Iguratimod orally （25 mg per time, twice daily） and Etanercept subcutaneously （25 mg per time, twice a week）, while control group was treated with Etanercept subcutaneously （25 mg per time, twice a week） for 12 weeks. And then, the levels of CD4＋T cells, CD8＋T cells and CD4＋/CD8＋ were detected by four-color flow eytometry, and the levels of immunolobulins were measured by immunoturbidimetry before and after treatment; the activity score of rheumatoid arthritis （RA） before and after treatment was calculated, and C reactive protein and rheumatoid factor were detected. Data showed that after 12 weeks demonstrated higher levels of CD4＋T ceils and CD4＋/CD8＋ （P〈0.05）, lower compared with control group. There was no differences in CD8＋T cells before treatment, the experimental group level of immuuoglobulin （P〈0.05）, as and after treatment in both groups （P〉 0.05）; no significant difference in adverse reaction was found between the two gToups （P〉0.05）. DAS28, ESR, CPR and RF indicators were decreased after treatment （P〈0.05） in the two groups of patients. After the treatment, IgG, IgA and IgM indicators of experimental group were lower than those in the control group （P〈0.05）. Taken together, the mechanism of Iguratimod combined Etanercept treatment against refractory rheumatoid may relates with adjusting the immune imbalance of CD4＋/CD8＋T cells and downregulating immunoglobulin.
出处
《免疫学杂志》
CAS
CSCD
北大核心
2018年第2期141-145,共5页
Immunological Journal
基金
重庆市万州区卫计委医学科研计划(20150319)
