脓毒症病人糖耐量异常的相关因素及机制研究

Related factors and mechanism of impaired glucose tolerance in human with sepsis

目的 :探讨脓毒症 (sepsis)病人糖耐量异常 (IGT)的可能相关因素及其机制。 方法 :符合脓毒症诊断的 4 0例病人 ,根据静脉内葡萄糖耐量试验 (IVGTT)分为两组 :对照组 (IVGTT正常 ,n =1 6 )和IGT组 (IVGTT异常 ,n=2 4 )。比较两组病人基础血胰岛素、高血糖素、皮质醇、TNF α、IL 6和临床指标的差异 ,观察葡萄糖输注后激素和细胞因子的变化。 结果 :脓毒症病人的病情严重度 (APACHEⅡ评分和感染评分 )、混合感染和血培养阳性对IGT有显著影响。IGT组的平均住院日较对照组明显延长 (P <0 .0 1 )。IGT组血中胰岛素、高血糖素、皮质醇和IL 6、TNF α基础水平均较对照组明显升高。短时间输注高糖后 ,IGT组与对照组相比 ,血胰岛素升高幅度下降 (P<0 .0 5 ) ,高糖对高血糖素的抑制作用消失 (P <0 .0 1 )。 结论 :脓毒症病人的病情严重度、有无混合感染和菌血症是影响糖耐量异常的重要因素。血中激素和细胞因子水平的异常 ,以及胰岛素和高血糖素对高血糖反应的异常 。

Objectives: To study the related factors and mechanism of the impaired glucose tolerance(IGT) in human with sepsis. Methods: According to the results of intravenous glucose tolerance test, forty patients were classified into two groups: 16 control subjects and 24 IGT subjects. The counterregulatory hormone, the basal levels of plasma insulin, glucagons, cortisol, IL 6 and TNF α were compared in two groups, and the change of inflammatory cytokine and counterregulatory hormone after dextrose infusion were observed. Results: The severity of the disease (APACHEⅡscore, Sepsis score), mixed infection and bacteremia were significantly related to the results of glucose tolerance test( P <0.05). The basal levels of plasma insulin, glucagons, cortisol, IL 6 and TNF α were significantly higher in subjects with IGT compared with those of control subjects( P <0.05). After infusion of a 50% glucose solution, In IGT subjects , the ascend extent of circulation insulin levels were significantly less than that in control subjects ( P <0.05), and the depression of plasma glucagon levels were absented. Conclusions: The severity of the disease (APACHEⅡscore, Sepsis score), mixed infection and bacteremia are important factors that greatly influence on glucose tolerance in sepsis. The change of inflammatory cytokine and counterregulatory hormone, and the altered responses of plasma insulin and glucagon after dextrose infusion are important matters which bring on the impair of glucose tolerance in human with sepsis.