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目的观察还原型谷胱甘肽、甲钴胺、α-硫辛酸联合治疗2型糖尿病周围神经病变的影响。方法选择2014年1月~2015年6月,成都市新都区人民医院收治的2型糖尿病周围神经病变患者90例,随机分为观察组(45例)和对照组(45例)。对照组患者给予甲钴胺和α-硫辛酸治疗,观察组在对照组的基础上再静脉滴注还原型谷胱甘肽,均治疗4周。结果观察组治疗后腓总神经和正中神经的感觉神经传导速度(SCV)及运动神经传导速度(MCV)高于对照组,差异有统计学意义(t=4.994、5.144、5.553、4.446,均P<0.01);观察组治疗后丙二醛(MDA)低于对照组,差异有统计学意义(t=4.426,P<0.01),超氧化物歧化酶(SOD)活性、血清总抗氧化能力(TAOC)高于对照组,差异有统计学意义(t=5.237、4.364,均P<0.01)。观察组和对照组的临床总有效率分别为91.11%(44/45)和71.11%(32/45),差异有统计学意义(χ~2=6.954,P<0.05)。结论还原型谷胱甘肽联合甲钴胺、α-硫辛酸治疗2型糖尿病周围神经病变,有效提高神经传导速度,其机制与减轻氧化应激有关。
Objective To observe the effects of glutathione, mecobalamin and α-lipoic acid on the peripheral neuropathy in type 2 diabetic patients. Methods From January 2014 to June 2015, 90 patients with type 2 diabetic peripheral neuropathy admitted to Xindu District People’s Hospital of Chengdu were randomly divided into observation group (45 cases) and control group (45 cases). Patients in the control group were treated with methylcobalamin and α-lipoic acid, and the observation group was treated with reduced glutathione by intravenous drip for 4 weeks on the basis of the control group. Results The sensory nerve conduction velocity (SCV) and motor nerve conduction velocity (MCV) of the common peroneal nerve and the median nerve in the observation group were significantly higher than those in the control group (t = 4.994, 5.144, 5.553, 4.446, P <0.01). The MDA level in the observation group was lower than that in the control group (t = 4.426, P <0.01), the activity of superoxide dismutase (SOD) and the total antioxidant capacity TAOC) than the control group, the difference was statistically significant (t = 5.237,4.364, all P <0.01). The total effective rate of the observation group and the control group were 91.11% (44/45) and 71.11% (32/45), respectively. The difference was statistically significant (χ ~ 2 = 6.954, P <0.05). Conclusions Reduced glutathione combined with mecobalamin and α-lipoic acid can effectively improve the nerve conduction velocity in type 2 diabetic peripheral neuropathy. Its mechanism is related to the reduction of oxidative stress.