肺结核合并糖尿病患者应用胸腺五肽辅助治疗效果观察

目的：评价胸腺五肽联合抗结核药物治疗肺结核合并糖尿病的临床疗效。方法对92例初治涂阳肺结核合并2型糖尿病患者随机分为观察组和对照组，每组46例。观察组在行常规一线抗结核和降糖治疗的同时加用胸腺五肽2 mg／d静脉滴注，共30 d，对照组仅给予降糖及常规一线抗结核治疗方案，比较2组在病变吸收、痰菌转阴情况的差异，测定治疗前及治疗1个月后外周血T淋巴细胞亚群： CD3+细胞、CD4+细胞、CD8+细胞及血清IFN-γ、IL-10变化并作比较。结果观察组痰菌阴转、病灶吸收情况、空洞闭合及缩小等方面，均优于对照组，同时伴CD3+细胞、CD4+细胞回升，CD8+细胞下降，CD4+／CD8+回升，IL-10降低和IFN-γ升高（ P <0|．05）。结论抗结核治疗的同时加用胸腺五肽，可提高初治涂阳肺结核合并糖尿病患者的痰菌阴转率、促进病变吸收、增强机体免疫力，并有利于外周血IFN-γ水平的提高，促进IL-10下降，使Th1／Th2恢复平衡。

Therapeutic effects of thymopetidum on pulmonary tuberculosis complicated by diabetes mellitus

Objective To observe and evaluate the therapeutic effects of thymopetidum on pulmonary tuberculosis ( TB ) complicated by diabetes mellitus .Methods Ninety -two patients with TB complicated by diabetes mellitus were randomly divided into two groups:observation group and control group ,with 46 patients in each group .The patients in control group were treated by conventional anti-TB therapeutic schedule and hypoglycemics , however , the patients in observation group,on the basis of control group ,were given thymopetidum (2mg/d) by intravenous drip ,with a treatment course of 30 days for both groups.The changes of T lymphocyte subsets (CD3+,CD4+,CD8+) and IFN-γ,IL-10 were detected before treatment and after 1-month treatment ,moreover , the therapeutic effects were observed and compared between two groups .Results The sputum negative conversion rate , remission of pulmonary lesion and diminution or closure of pulmonary cavities in observation group were superior to those in control group , meanwhile,the levels of T lymphocyte subsets (CD3+,CD4+,CD4+/CD8+) were obviously increased, however, the levels of CD8+,IL-10 were significantly decreased in observation group (P <0.05). Conclusion The conventional anti -TB therapeutic schedule combined with thymopetidum can increase sputum negative conversion rate, promote remission of pulmonary lesion , enhance immunity of organism , moreover, which can increase the levels of IFN-γin peripheral blood,decrease the levels of IL-10 to recover the balance of Th1/Th2.