Lonardo Amedeo, Adinolfi Luigi Elio, Petta Salvatore, Craxì Antonio, Loria Paola
Department of Internal Medicine, University of Modena and Reggio Emilia, Modena, Italy.
Expert Rev Anti Infect Ther. 2009 Apr;7(3):293-308. doi: 10.1586/eri.09.3.
Type 2 diabetes (T2D) and HCV infection are common conditions involving, respectively, at least 170 and 130 million people worldwide. However, the distribution of such cases does not overlap in the same age groups in different geographic areas. Following pioneering reports of increased prevalence of T2D in HCV-positive cirrhosis, interest concerning the relationship between HCV and T2D has escalated. HCV is able to induce insulin resistance (IR) directly and the role of specific viral genotypes responsible for such effect is disputed. IR has consistently been found to be closely linked to fibrosis in HCV infection, although also typically associated with T2D in prefibrotic stages. HCV infection could be associated with a reduced prevalence of metabolic syndrome owing to virus-associated reduction in BMI (reported in population but not clinical studies) and hypobetaliproteinemia. A three- to ten-fold increased risk of HCV infection was reported among diabetic patients in comparison with different control groups and a meta-analysis showed a 1.8-fold excess risk of T2D among HCV-positive compared with HBV-positive patients. Moreover, HCV positivity is associated with an increased risk of T2D in patients receiving liver or kidney transplantations. T2D and IR are independent predictors of a more rapid progression of liver fibrosis and impaired response to antiviral treatment in chronic hepatitis C. Patients with cirrhosis and T2D have an increased susceptibility to hepatic encephalopathy and hepatocellular carcinoma (HCC). However, the beneficial effects of antiviral treatment on IR and T2D are controversial. Theoretically, glycemic control in chronic hepatitis C, and particularly in cirrhotic patients, could improve the prognosis and the response to antivirals, although the evidence for this is limited. Future studies should elucidate the relationship between insulin signaling, HCV and interferon signaling, entity of cardiovascular risk in patients with HCV infection, the potential role of 'metabolic' strategies added to antiviral treatment schedules, the impact of IR on liver failure, portal hypertension and HCC, particularly in patients managed in a transplant setting.
2型糖尿病（T2D）和丙型肝炎病毒（HCV）感染是常见病症，在全球范围内分别涉及至少1.7亿和1.3亿人。然而，这些病例在不同地理区域的同一年龄组中的分布并不重叠。在关于HCV阳性肝硬化中T2D患病率增加的开创性报告之后，人们对HCV与T2D之间关系的兴趣不断升级。HCV能够直接诱导胰岛素抵抗（IR），而负责这种效应的特定病毒基因型的作用存在争议。一直发现IR与HCV感染中的纤维化密切相关，尽管在纤维化前期阶段通常也与T2D相关。由于病毒相关的体重指数降低（在人群研究而非临床研究中报道）和低β脂蛋白血症，HCV感染可能与代谢综合征患病率降低有关。与不同对照组相比，糖尿病患者中HCV感染风险增加了三至十倍，一项荟萃分析显示，与HBV阳性患者相比，HCV阳性患者患T2D的风险高出1.8倍。此外，HCV阳性与接受肝或肾移植的患者患T2D的风险增加有关。T2D和IR是慢性丙型肝炎中肝纤维化进展更快和对抗病毒治疗反应受损的独立预测因素。肝硬化和T2D患者对肝性脑病和肝细胞癌（HCC）的易感性增加。然而，抗病毒治疗对IR和T2D的有益作用存在争议。从理论上讲，慢性丙型肝炎，特别是肝硬化患者的血糖控制可以改善预后和对抗病毒药物的反应，尽管这方面的证据有限。未来的研究应阐明胰岛素信号传导、HCV和干扰素信号传导之间的关系、HCV感染患者心血管风险的情况、添加到抗病毒治疗方案中的“代谢”策略的潜在作用、IR对肝衰竭、门静脉高压和HCC的影响，特别是在移植环境中管理的患者中。
