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作 者:李静[1] 陈月英[1] 郭晓华[1] 罗巧云[1] 刘志红[1] 熊灵敏[1]
机构地区:[1]广州市解放军第458医院内分泌科,广东广州510602
出 处:《临床和实验医学杂志》2009年第6期16-17,19,共3页Journal of Clinical and Experimental Medicine
摘 要: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β细胞损害程度。方法检测以自发酮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。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.
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