中国医师进修杂志
中國醫師進脩雜誌
중국의사진수잡지
CHINESE JOURNAL OF POSTGRADUATES OF MEDICINE
2008年
34期
10-12
,共3页
肝源性糖尿病%胰岛素抵抗%谷氨酸脱羧酶抗体
肝源性糖尿病%胰島素牴抗%穀氨痠脫羧酶抗體
간원성당뇨병%이도소저항%곡안산탈최매항체
Hepatogenic diabetics%Insulin resistance%Glutamate decarboxylase antibody
目的 探讨肝源性糖尿病的发病机制.方法 对135例肝硬化患者分别进行空腹血糖、餐后2h血糖、血清空腹胰岛素、谷氨酸脱羧酶抗体、胰岛素释放指数及胰岛素敏感指数测定,并进行比较分析.结果 肝硬化肝源性糖尿病的发生率为39.3%(53/135),其中,丙型肝炎后肝硬化肝源性糖尿病发生率53.3%(16/30),较乙型肝炎后肝硬化(37.1%,26/70)和酒精性肝硬化(31.4%,11/35)明显升高,差异有统计学意义(P＜0.01).肝源性糖尿病患者空腹胰岛素、胰岛素释放指数、谷氨酸脱羧酶抗体阳性率均显著高于健康体检者(P＜0.01),而胰岛索敏感指数显著低于健康体检者(P＜0.01).结论 肝源性糖尿病的发生与肝硬化病因有关.除肝功能损害、胰岛素抵抗、病毒感染、免疫功能紊乱等导致胰岛β细胞功能的损伤外,胰岛素分泌相对或绝对缺乏亦是肝源性糖尿病发生的重要影响因素.
目的 探討肝源性糖尿病的髮病機製.方法 對135例肝硬化患者分彆進行空腹血糖、餐後2h血糖、血清空腹胰島素、穀氨痠脫羧酶抗體、胰島素釋放指數及胰島素敏感指數測定,併進行比較分析.結果 肝硬化肝源性糖尿病的髮生率為39.3%(53/135),其中,丙型肝炎後肝硬化肝源性糖尿病髮生率53.3%(16/30),較乙型肝炎後肝硬化(37.1%,26/70)和酒精性肝硬化(31.4%,11/35)明顯升高,差異有統計學意義(P＜0.01).肝源性糖尿病患者空腹胰島素、胰島素釋放指數、穀氨痠脫羧酶抗體暘性率均顯著高于健康體檢者(P＜0.01),而胰島索敏感指數顯著低于健康體檢者(P＜0.01).結論 肝源性糖尿病的髮生與肝硬化病因有關.除肝功能損害、胰島素牴抗、病毒感染、免疫功能紊亂等導緻胰島β細胞功能的損傷外,胰島素分泌相對或絕對缺乏亦是肝源性糖尿病髮生的重要影響因素.
목적 탐토간원성당뇨병적발병궤제.방법 대135례간경화환자분별진행공복혈당、찬후2h혈당、혈청공복이도소、곡안산탈최매항체、이도소석방지수급이도소민감지수측정,병진행비교분석.결과 간경화간원성당뇨병적발생솔위39.3%(53/135),기중,병형간염후간경화간원성당뇨병발생솔53.3%(16/30),교을형간염후간경화(37.1%,26/70)화주정성간경화(31.4%,11/35)명현승고,차이유통계학의의(P＜0.01).간원성당뇨병환자공복이도소、이도소석방지수、곡안산탈최매항체양성솔균현저고우건강체검자(P＜0.01),이이도색민감지수현저저우건강체검자(P＜0.01).결론 간원성당뇨병적발생여간경화병인유관.제간공능손해、이도소저항、병독감염、면역공능문란등도치이도β세포공능적손상외,이도소분비상대혹절대결핍역시간원성당뇨병발생적중요영향인소.
Objective To investigate the pathogenesis of hepatogenic diabetes.Methods The fasting and 2-hour postprandial plasma glucose,fasting sertum insulin,glutamate decarboxylase antibody,insulin release index (IRI)and insulin sensitivity index(ISI)Was determined and analyzed in 135 liver cirrhosis patients.Results The incidence of hepatogenic diabetes wag 39.3%(53/135)in liver cirrhosis patients.The incidence of hepatogenic diabetes in post hepatitis C liver cirrhosis patients(53.3%.16/30)was muchh igher than that in post hepatitis B liver cirrhosis patients(37.1%,26/70)and alcohofic liver cirrhosis patients(31.4%.11/35)(P＜0.01).The fasting serum insulin,IRI and the positivity rate of glutamate decarboxylase antibody was much higher in hepatogenic diabetes than that in controls(P＜0.01),and ISl was much lower than that in controls(P＜0.01).Conclusions The development of hepatogenic diabetics is relsted with the etiological factor of liver cirrhosis.Besides impairment of the hepatocellular function and insulin resistance,viral infection and immunologic derangement and so on results in impairment of beta cell of islet function.Relative or absolute deficiency of insulin secretion is an important influential factor in the development of hepatogenic diabetics.
