首都医科大学学报 ›› 2011, Vol. 32 ›› Issue (5): 602-604.doi: 10.3969/j.issn.1006-7795.2011.05.003

• 糖尿病基础研究与临床实践 • 上一篇    下一篇

2型糖尿病合并乙型肝炎病毒携带患者的临床分析

胡虹英1,2, 刘颖1, 杨金奎1   

  1. 1. 首都医科大学附属北京同仁医院内分泌科,北京 100730;2. 首都医科大学附属北京地坛医院内分泌科,北京 100015
  • 收稿日期:2011-07-21 修回日期:1900-01-01 出版日期:2011-10-21 发布日期:2011-10-21
  • 通讯作者: 杨金奎

Clinical analysis of hepatitis B virus asymptomatic carriers with type 2 diabetes

HU Hong-ying1,2, LIU Ying1, YANG Jin-kui1   

  1. 1. Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China;2. Department of Endocrinology, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China
  • Received:2011-07-21 Revised:1900-01-01 Online:2011-10-21 Published:2011-10-21

摘要: 目的 探讨2型糖尿病合并乙型肝炎病毒携带患者的临床特点。方法 分别对71例2型糖尿病患者(对照组)及50例2型糖尿病合并乙型肝炎病毒携带(感染组)且肝功能正常的患者的临床资料进行回顾性分析。结果 感染组男性32人、女性18人,平均年龄(56.3±11.5)岁,对照组男性40人、女性31人,平均年龄(55.9±11.6)岁,感染组和对照组在糖尿病病程、脂肪肝患病率、糖尿病阳性家族史、体质量指数和腰臀比方面,差异无统计学意义。感染组的丙氨酸氨基转移酶〔(20.69±7.78)U/L〕及门冬氨酸氨基转移酶〔(25.11±7.48)U/L〕均明显高于对照组,差异有统计学意义(P<0.05)。感染组的空腹血糖〔(7.07±2.16)mmol/L〕和糖化血红蛋白〔(8.62±2.44)%〕均明显低于对照组〔(8.70±2.84)mmol/L,(9.66±2.74)%〕,差异有统计学意义;餐后2 h血糖感染组〔(11.28±1.96)mmol/L〕高于对照组〔(10.54±2.13)mmol/L〕,差异无统计学意义;血糖波动幅度(餐后2 h血糖/空腹血糖)感染组〔(1.61±0.59)mmol/L〕大于对照组〔(1.41±0.39)mmol/L〕,差异有统计学意义。2组的C肽释放试验呈现高峰后移至餐后2 h,差异无统计学意义。结论 2型糖尿病合并乙型肝炎病毒感染,病毒持续对肝脏造成损害,影响肝糖原的合成、分解以及糖异生作用,导致空腹血糖偏低,而餐后血糖较高,血糖波动大;肝炎病毒对胰腺B细胞分泌胰岛素的功能无明显破坏。

关键词: 2型糖尿病, 乙型肝炎, 胰岛素抵抗

Abstract: Objective To study the clinical feature of type 2 diabetes(T2D) patients who were hepatitis B virus(HBV) asymptomatic carriers(HBAC). Methods We collected data from 71 T2D patients with normal liver function(control group) and 50 T2D patients with HBAC(infected group), and compared the clinical data. Results The infected group consists of 32 males and 18 females. Their average age was(56.33±11.54) years. The control group consisted of 40 males and 31 females. Their average age was(55.86±11.56) years. There was no statistically significant difference between the control group and the HBV-infected group in terms of their courses of T2D, prevalence of fatty liver disease(FLD), family history of the diabetes, body mass index(BMI) and waist/hip ratio(WHR). The alanine aminotransferase(ALT) of the HBV-infected group〔(20.69±7.78)U/L〕 and aspartate aminotransferase(AST) of the HBV-infected group〔(25.11±7.48)U/L〕 were significantly higher than those of the control group(P<0.05). The fasting plasma glucose〔FPG,(7.07±2.16)mmol/L〕 and HbA1c (8.62±2.44 %) of the HBV-infected group were significantly lower than those of the control group(8.70±2.84 and 9.66±2.74%, respectively). The postprandial blood glucose(PBG) of the HBV-infected group〔(11.28±1.96)mmol/L〕 and the control group〔(10.54±2.13)mmol/L〕 had no significant difference. The blood glucose fluctuation(PBG/FPG) of the HBV-infected group(1.61±0.59) was significantly higher than that of control group(1.41±0.39). The release of C-peptide in the HBV-infected group and control group had no significant difference. Conclusion Liver function of patients with HBAC and T2D may be impaired. Synthesis, decomposition and gluconeogenesis of hepatic glycogen might be damaged, which may lead to a low FPG but high PBG and significant blood glucose fluctuation. The hepatitis B virus may not obviously impair release of insulin.

Key words: type 2 diabetes, hepatitis B, insulin resistance

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