论文部分内容阅读
目的探讨TNF-α、IFN-γ和IL-6促进Ⅰ型糖尿病发生的机制。方法采用酶联免疫吸附法对新发病患者组(A组)19例、Ⅰ型糖尿病并发酮症酸中毒组(B组)14例、Ⅰ型糖尿病合并有慢性并发症组(C组)12例和正常对照组22例的血清IL-6、TNF-α和IFN-γ的水平进行测定。结果 (1)A组、B组和C组治疗前的TNF-α、IFN-γ水平显著高于正常对照组(P<0.01);C组IFN-γ、TNF-α和IL-6水平高于A组、C组,差异有统计学意义(P<0.05);(2)A组给予胰岛素治疗血糖稳定3个月后TNF-α、IFN-γ下降,但仍高于对照组(P<0.05);C组高于A组、B组;(3)B组给予胰岛素治疗,血糖稳定2周后TNF-α、IFN-γ稍有下降,但较对照组仍高(P<0.01),C组给予胰岛素治疗1月后有下降,但仍显著高于正常对照组(P<0.01);(4)C组IL-6水平明显升高,在治疗后下降并接近正常对照组(P<0.05)。结论 (1)TNF-α、IFN-γ水平的升高可能是Ⅰ型糖尿病的发病机制之一;(2)TNF-α、IFN-γ水平与Ⅰ型糖尿病患者的病程有关,并可作为评价Ⅰ型糖尿病的疗效指标之一;(3)在TIDM合并有慢性并发症患者中不仅存在TNF-α、IFN-γ水平的异常,同时也存在IL-6水平的异常,IL-6水平的升高有可能是TIDM发生慢性并发症的机制之一。
Objective To investigate the mechanism of TNF-α, IFN-γ and IL-6 in promoting type 1 diabetes mellitus. Methods Nineteen patients with newly diagnosed disease (group A), 14 with type I diabetes complicated with ketoacidosis (group B) and 12 with type I diabetes (group C) with chronic complication And normal control group of 22 cases of serum IL-6, TNF-α and IFN-γ levels were measured. Results (1) The levels of TNF-α and IFN-γ in group A, B and C before treatment were significantly higher than those in normal control group (P <0.01). The levels of IFN-γ, TNF-α and IL- (P <0.05). (2) The levels of TNF-α and IFN-γ in group A were significantly lower than those in control group (P < (P <0.05); C group was higher than A group and B group; (3) Insulin treatment was given to B group. After stable blood glucose for 2 weeks, TNF-αand IFN-γwere slightly decreased (P <0.01) (P <0.01). (4) The level of IL-6 in group C was significantly higher than that in normal control group (P < 0.05). Conclusions (1) Elevated levels of TNF-α and IFN-γ may be one of the pathogenesis of type 1 diabetes. (2) The levels of TNF-α and IFN-γ are related to the course of type 1 diabetes mellitus, (3) Not only abnormalities of TNF-α and IFN-γ in patients with chronic complications of TIDM, but also abnormal levels of IL-6 and IL-6 High likely to be one of the mechanisms of chronic complications of TIDM.