肝源性糖尿病临床特征分析

The clinical features of hepatogenous diabetes

目的探讨肝源性糖尿病的临床特征及其可能机制,以提高对该病的认识和诊治水平。方法回顾性分析102例肝源性糖尿病患者,并与原发性2型糖尿病进行对比分析。结果102例肝源性糖尿病患者中17%有口干、多饮、多食、多尿等典型糖尿病症状;空腹血糖为(7.8±2.6)mmol/L,餐后2h血糖(12.7±3.0)mmol/L;口服葡萄糖耐量试验(OGTT)显示,肝源性糖尿病患者的空腹血糖水平显著低于原发性2型糖尿病(P<0.01),余各时段血糖两组差异无统计学意义;胰岛素+C肽释放试验显示,两组胰岛素分泌均呈高峰延迟型,但肝源性糖尿病患者各时段胰岛素及C肽分泌水平均高于原发性2型糖尿病(P<0.05)。经饮食控制、应用胰岛素或口服降糖药治疗后血糖大多能控制在正常或接近正常水平。102例肝源性糖尿病患者中仅5例伴糖尿病并发症,4例死亡病例死因均为慢性肝病并发症。结论肝源性糖尿病临床症状不典型,以餐后高血糖为特征,应用胰岛素治疗效果较好,短期不良预后主要与原发慢性肝病有关。胰岛素抵抗可能是其重要的发病机制。

Objective To investigate the clinical features and the possible etiology of hepatogenous diabetes. Methods One hundred and two cases with hepatogenous diabetes were retrospectively analyzed and compared with those of primary type 2 diabetes mellitus. Results Only 17% patients with hepatogenous diabetes showed the typical diabetic symptoms such as dry mouth, polydipsia, polyphagia, polyuria, et al. The patients with hepatogenous diabetes showed fasting plasma glucose （FPG） as （7.8 ±2.6） mmol/L and postprandial plasma glucose （PPG） as （ 12.7 ± 3.0）mmol/L. In OGTT, The patients with hepatogenous diabetes showed a much lower level of FPG than that of primary type 2 diabetes mellitus （P〈0. 01）. In insulin and C-peptide release test, both the two groups showed a delayed insulin peak, but the patients with hepatogenous diabetes showed higher insulin values at all the four period than those of primary type 2 diabetes mellitus （P〈.05）. After the treatment of diet control together with the using of insulin or other oral drugs, most patients showed normal or near normal levels of blood glucose. Only 5 cases had diabetic complications, and 4 cases died of complications of underlying chronic hepatic diseases. Conclusion The hepatogenous diabetes is clinically asymptomatic, and is characterized by higher PPG. The insulin treatment is effective for the patients with hepatogenous diabetes, and the short-time prognosis is more likely to be affected by the underlying hepatic disease. Insulin resistance may play a key rote in the etiology of the hepatogenous diabetes.