摘要目的 探讨镓铝砷激光联合药物治疗类风湿关节炎(RA)的机制.方法 将22例RA患者分为观察组和对照组,每组11例.观察组采用镓铝砷激光+甲氨蝶呤治疗,对照组仅采用甲氨蝶呤治疗.采用流式细胞双抗染色法分别测定患者治疗前、后外周血和膝关节滑液中CD4+CD25+treg(调节性T细胞)的数量,采用酶联免疫吸附法测定治疗前、后患者膝关节滑液中前列腺素E2(PGE2)的含量.同时检测10名健康人(正常对照组)外周血CD4+CD25+treg细胞数量.结果 观察组膝关节局部症状改善优于对照组;2组治疗后膝关节滑液中PGE2含量分别为(3.82±1.34)和(1.69±0.98),均较治疗前下降,其中观察组下降幅度明显高于对照组,差异具有统计学意义(P＜0.05);患者外周血CD4+CD25+treg细胞数量为(3.84±3.20)%,明显低于正常对照组,差异存在统计学意义(P＜0.05).滑液中CD4+CD25+treg远多于外周血.观察组治疗后关节滑液中CD4+CD25+treg的数量为(9.78±10.28)%,与治疗前比较差异存在统计学意义(P＜0.05).结论 镓铝砷激光联合甲氨蝶呤治疗类风湿关节炎临床疗效优于单纯应用甲氨蝶呤,联合治疗的机制可能在于明显减少靶器官局部炎性介质和CD4+CD25+treg细胞数量.

abstractsObjective To explore the mechanism of combined treatment with methotrexate (MTX) and Ga-Al-As laser irradiation for rheumatoid arthritis (RA) and to assess the effectiveness of Ga-Al-As laser therapy for RA. Methods Twenty-two patients with RA were randomly and evenly divided into two groups: the treatment group treated with Ga-Al-As laser irradiation combined with MTX and the control group treated with MTX only. Ten age-matched normal subjects were observed as normal controls. The amount of CD4 + CD25 + regulatory T cells in peripheral blood (PB) of the normal controls and that in the PB and synovial fluid (SF) of the 22 patients before and after therapy were counted by flow cytometry. Meanwhile, the amount of prostaglandin E2 (PGE2) in synovial fluid of the patients was measured before and after treatment by enzyme-linked immunosorbent assay(ELISA). Results After combined treatment the clinical symptoms of the patients were improved significantly, and the amount of PGE2in SF decreased significantly. The count of CD4 + CD25 + regulatory T cells in PB of RA patients was ( 3.84 ±3.20) % , compared to ( 10.05 ± 7.04) % in healthy individuals. The count of CD4 + CD25 + regulatory T cells in SF of RA patients was ( 14.89 ± 12.30) % , much higher than that in PB. The count of CD4 + CD25 + regulatory T cells in SF decreased significantly in treatment group compared to control group (P ＜0.05). Conclusion Ga-Al-As laser irradiation eombined with MTX can effectively improve the clinical symptoms of RA patients. It may be related to the decrease of amount of PGE2 and count of CD4 + CD25 + regulatory T cell in PB and SF.