乙型肝炎病毒相关的肝源性糖尿病糖代谢异常的临床分析

惠威; 徐斌; 郭新会

乙型肝炎病毒相关的肝源性糖尿病糖代谢异常的临床分析

首都医科大学附属北京佑安医院肝病内分泌科

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中图分类号: R587.1
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出版历程
- 出版日期: 2012-07-20

Clinical study on glucose metabolic disorder in patients with diabetes and chronic hepatitis B virus infection

摘要

摘要:
目的探讨HBV相关的肝源性糖尿病糖代谢的临床特点及其发生机制。方法患者分为2型糖尿病组、慢性乙型肝炎合并肝源性糖尿病组（简称慢肝组）及乙型肝炎肝硬化合并肝源性糖尿病组（简称肝硬化组）,所有研究对象均行口服葡萄糖耐量试验（OGTT）联合胰岛素、C肽释放试验,并测定糖化血红蛋白（HbA1c）水平。结果肝硬化组空腹血糖、30 min、60 min血糖分别为（6.98±2.75）mmol/L、（11.93±2.98）mmol/L、（15.37±3.67）mmol/L,均明显低于慢肝组、糖尿病组（P<0.01）,后两组间差异无统计学意义;肝硬化组120 min血糖低于糖尿病组（P<0.01）。各时间点三组之间C-肽水平差异无统计学意义,峰值出现的时间基本一致（120 min）,均呈低峰延迟曲线。各时间点肝硬化组和慢肝组胰岛素水平的对数值均与糖尿病组存在统计学差异（P<0.01）,前两组水平高于糖尿病组,但两组间差异无统计学意义。峰值出现的时间基本一致（120 min）。三组之间HbA1c差异有统计学意义（P<0.05）,肝硬化组最低,糖尿病组最高。结论 HBV相关的肝硬化...
- 肝炎病毒,乙型 /
- 糖尿病 /
- 碳水化合物代谢
Abstract:
Objective To study the clinical features and mechanism of glucose metabolism in diabetic patients with chronic hepatitis B virus (HBV) infection.Methods Thirty-six patients with type 2 diabetes mellitus (T2DM) with chronic hepatitis (CH) and 50 T2DM patients with liver cirrhosis (LC) were recruited for study.Fifty-seven T2DM patients without liver diseases were recruited as controls.All study participants were given an oral glucose tolerance test (OGTT) with measurements of insulin and C-peptide release.In addition, the levels of glycated hemoglobin (HbA1c) were measured by biochemical analyzer.Results OGTT of the LC group indicated fasting blood glucose of (6.98±2.75) mmol/L, glucose at 30 min of (11.93±2.98) mmol/L, and glucose at 60 min of (15.37±3.67) mmol/L, all of which were significantly lower than the levels detected in either the CH group or the control group (all P<0.01) .Furthermore, the values for the CH group and the control group were not significantly different.The blood glucose levels at 120 min were significantly lower in the LC group than in the control group (P<0.01) .Among the three groups, there were no statistically significant differences in C-peptide levels at any time point.The peak time of C-peptide release occurred at 120 min, and a low peak latency curve was observed for all groups.At each time point, the logarithm of serum insulin levels in the LC and CH group were significantly higher than those in the control group (P<0.01) ;however, the levels were not significantly different between the LC and CH groups, and the peak serum insulin levels appeared at 120 min for both.The levels of HbA1c were significantly different between all three groups (P<0.05) , with the LC group having the lowest level and the control group having the highest.Conclusion Patients with chronic HBV infection and liver cirrhosis have impaired glucose metabolism and may be at higher risk of developing diabetes.Routine OGTT examination should be considered for this patient population.
- hepatitis B /
- diabetes mellitus /
- carbohydrate metabolism

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参考文献(19)

[1]Sibley SD, Palmer JP, Hirsch IB, et al.Visceral obesity he-patic lipase activity and dyslipidemia in type 1 diabetes[J].Clinic Endocrinal Metabolic, 2003, 88 (7) :3379.

[2]Kuriyama S, Miwa Y, Fukushima H, et al.Prevalence of diabe-tes and incidence of angiopathy in patients with chronic viral liv-er disease[J].J Clin Biochem Nutr, 2007, 40 (2) :116-122.

[3]Marchesini G, Ronchi M, Forlani G, et al.Cardiovascular dis-ease in Cirrhosis-a point-prevalence study in relation to glu-cose tolerance[J].Am J Gastroenterol, 1999, 94 (3) :655.

[4]Lu FM, Zhuang H.Management of hepatitis B in China[J].Chin Med J (Engl) , 2009, 122 (1) :3-4.

[5]Mehta SH, Brancati FL, Sulkowski MS, et al.Prevalence oftype 2 diabetes mellitus among persons with hepatitis C virusinfection in the United States[J].Ann Intern Med, 2000, 133 (8) :592-599.

[6]Hui JM, Sud A, Farrell GC, et al.Insulin resistance is asso-ciated with chronic hepatitis C virus infection and fibrosis pro-gression[corrected][J].Gastroenterology, 2003, 125 (6) :1695-1704.

[7]Kawaguchi T, Yoshida T, Harada M, et al.Hepatitis C virusdownregulates insulin receptor substrates 1 and 2 through up-regulation of suppressor of cytokine signaling El-Serag HB, Tran T, Everhart J E.Diabetes increases the riskof chron-ic liver disease and hepatocellular carcinoma[J].Gastroen-terology, 2004, 126:460-468.

[8]Knobler H, Schihmanter R, Zifroni A, et al.Increased risk oftype 2 diabetes in noncirrhotic patients with chronic hepatitis Cvirus infection[J].Mayo Clin Proc, 2000, 75 (4) :355-359.

[9]Kwon SY, Kim SS, Kwon OS, et al.Prognostic significanceof glycaemic control in patients with HBV and HCV-relatedcirrhosis and diabetes mellitus[J].Diabetic Medicine, 2005, 22 (11) :1530-1535.

[10]Report of the Expert Committee on the Diagnosis and Classi-fication of Diabetes Mellitus[J].Diabetes Care, 1997, 20 (7) :1183-1197.

[11]中华医学会传染病与寄生虫病学分会、肝病学分会.病毒性肝炎防治方案[J].中华肝脏病杂志, 2000, 8:324.

[12]Sibley SD, Palmer JP, Hirsch IB, et al.Visceral obesity, he-patic lipase activity, and dyslipidemia in type 1 diabetes[J].J Clin Endocrinol Metab, 2003, 88 (7) :3379.

[13]张霞, 沈薇, 沈鼎明.肝病伴糖代谢异常患者的临床分析[J].中华肝脏病杂志, 2006, 14 (4) :289.

[14]韩红梅, 朴云峰.肝源性糖尿病发病机制的研究现状[J].临床肝胆病杂志, 2006, 22 (2) :152-153.

[15]Yoshida T, Ninomiya K, Matsumoto F, et al.Glucag on andinsulin metabolism in cirrhotic patients[J].Hepatogastroen-terology, 1998, 45 (20) :468-471.

[16]Amerrican diabetes association.Clinical practice recommen-dation 2010[J].Diabetes Care, 2010, 33 (suppl 1) :S11-S61.

[17]Fujiwara F, Ishii M, Taneichi H, et al.Low incidence of vascularcomplications in patients with diabetes mellitus associated withliver cirrhosis as compared with type 2 diabetes mellitus[J].Tohoku J Exp Med, 2005, 205 (4) :1327-1334.

[18]Hno TI, Wu JC, Lee PC, et al.Diabetes mellitus as a risk factorof liver cirrhosis in patients with chronic hepatitis B virus infec-tion[J].J Clin Gastroenterol, 2000, 30 (3) :250-254.

[19]El-Serag HB, Tran T, Everhart JE.Diabetes increases theriskof chronic liver disease and hepatocellular carcinoma[J].Gastroenterology, 2004, 126 (2) :460-468.

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