高敏C-反应蛋白在酮症或酮症酸中毒起病的2型糖尿病患者的检测意义

目的了解自发酮症或酮症酸中毒起病的2型糖尿病患者的免疫炎性反应和胰岛8细胞损害程度。方法检测以自发酾症或酮症酸中毒起病的2型糖尿病患者血清高敏c-反应蛋白（hs—CRP）、抗谷氨酸脱羧酶（GAD）抗体的水平，及空腹胰岛素、c-肽及餐后2h胰岛素、c-肽水平。用酶联免疫吸附试验（ELISA）法测定hs—CRP的水平，胰岛素（Ins）、C-肽、GAD抗体用化学发光法检测。结果①自发酮症或酮症酸中毒起病的2型糖尿病患者患者血清hs—cRP与对照组（32382．11±1685．68ng／ml比10775．25±1615．77ng／ml）相比明显增高，差异有统计学意义（P〈0．05）。（2）以酮症酸中毒起病的2型糖尿病患者外周血GAD抗体阳性率（14．0％），与对照组（13．3％）比较，差异无统计学意义（P〉0．05）。③自发酮症或酮症酸中毒起病的2型糖尿病患者外周血空腹胰岛素、c-肽、餐后2h胰岛素、餐后2hc-肽水平明显低于对照组差异有统计学意义（P〈0．05）。结论机体免疫炎症反应是促使2型糖尿病患者自发酮症或酮症酸中毒的重要机制，是导致2型糖尿病患者急性胰岛β细胞损伤的主要原因。

Significance of the detection of high-sensitivity C-reactive protein (hs-CRP) in type 2 diabetes patients with onset of ketoacidosis or ketosis

Objective To detect high - sensitivity C - reactive protein （ hs - CRP）, anti - glutamic acid decarboxylase （GAD） antibody level, and fasting insulin, C - peptide and 2 h postprandial insulin and C - peptide levels and understand immune inflammatory response and the extent of islet beta - ceU impairment occurred in type 2 diabetes patients with onset of spontaneous ketosis or ketoacidesis. Methods The level of hs- CRP was determined by enzyme- linked immunesorbent assay （ELISA）. Insulin, C -poptide and GAD antibody were analyzed with chemi- luminescence detection. Results （1）Serum hs -CRP（32 382.11 ±1 685.68 ng/ml） was significantly increased in type 2 diabetes patients with onset of spontaneous ketosis or ketoacidosis compared with that in control group （ 10 775.25 ± 1 615.77 ng/ml） （ P 〈0.05）. （2）GAD antibody - positive rate of peripheral blood（ 14.0% ） was no significant in type 2 diabetes patients with onset of spontaneous ketosis or ketoacidesis compared with that in control group（ 13.3% ） （ P 〉 0.05 ）. （3）Fasting insulin, C - peptide and 2 h postprandial insulin and C - peptide levels levels in type 2 diabetes patients with onset of spontaneous ketosis or ketoacidesis were significantly lower than those in control group （ P 〈0.05 ）. Conclusion Immune inflammatory response is an important mechanism for type 2 diabetes patients with onset of spontaneous ketosis or ketoacidesis and is also a critical factor for acute pancreatic islet beta - cell impairment in type 2 diabetes patients.