【摘要】 目的 :探讨肝硬化门脉高压患者糖代谢异常的病因和机理。方法 :对 30例肝硬化门脉高压患者 ,32例Ⅱ型糖尿病患者和 15例正常人进行了空腹和餐后血糖、糖化血红蛋白、空腹胰岛素、C肽、胰高血糖素试验 ,计算胰岛素释放指数和胰岛素敏感性指数 ,对各组检查结果进行比较分析。结果 :肝硬化组存在着糖耐量异常 ,餐后血糖、糖化血红蛋白、血清胰岛素、C肽和胰高血糖素多种指标显著高于正常对照组 (P <0 0 1)。胰岛素敏感指数显著低于正常对照组 (P<0 0 1)。肝硬化Child分级比较 ,随着病情加重 ,糖代谢紊乱逐渐突出。肝硬化者胰岛素、C肽和胰岛素释放指数显著高于Ⅱ型糖尿病患者 (P <0 0 1) ,但胰岛素敏感指数和胰高血糖素比较两组之间无明显差异 (P >0 0 5 )。结论 :肝硬化门脉高压患者存在着糖代谢异常 ,这种代谢异常主要是由于肝功能损害、胰岛素抵抗和胰高血糖素升高所致。更多还原

【Abstract】 Purpose: To investigate the pathogeny and mechanism of abnormal glucose metabolism on the liver cirrhosis patients with portal hypertension. Methods: Tests for fasting plasma glucose, postprandial glucose, HbA 1C , fasting plasma insulin, c-peptide and glucagon were performed in 30 liver cirrhosis, 32 type Ⅱ diabetes patients and 15 controls. Insulin release index(IRI) and insulin sensitivity index(ISI) were calculated. Results: Cirrhosis existed hepatogenous glucose tolerance impairment, HbA 1C , insulin, c-peptide and glucagon index were significantly higher than that in controls(P<0.01), ISI was markedly lower than controls(P<0.01). Child-pugh liver function classifications were compared in cirrhosis. With disease aggravated, the changes of glucose metabolism became heavier. Insulin, c-peptide and IRI in cirrhosis were higher than type Ⅱ diabetes(P<0.01), ISI and glucagon were not difference in two groups(P>0.05). Conclusion: There is abnormal glucose metabolism on the liver cirrhosis patients with portal hypertension. Insulin resistance, hyperglucagon and hepatonic dysfunction may play important roles in occurrence and development of hepatic abnormal glucose metabolism.更多还原