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Hepatitis C and diabetes: the inevitable coincidence?

机译:丙型肝炎和糖尿病:不可避免的巧合?

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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.
机译:2型糖尿病(T2D)和HCV感染是常见疾病,全世界分别涉及至少170亿和1.3亿人。但是,此类病例的分布在不同地理区域的相同年龄组中并不重叠。在有关HCV阳性肝硬化中T2D患病率增加的开创性报道之后,人们对HCV和T2D之间关系的兴趣逐渐增加。 HCV能够直接诱导胰岛素抵抗(IR),而引起这种作用的特定病毒基因型的作用受到争议。一直以来,IR被发现与HCV感染中的纤维化密切相关,尽管在纤维化前阶段通常也与T2D相关。 HCV感染可能与代谢综合征的患病率降低有关,这是由于病毒引起的BMI降低(在人群中报告,但未在临床研究中报告)和低蛋白血症。与不同的对照组相比,糖尿病患者的HCV感染风险增加了三到十倍,荟萃分析显示,与HBV阳性患者相比,HCV阳性的T2D患病风险高1.8倍。此外,在接受肝或肾移植的患者中,HCV阳性与T2D风险增加有关。在慢性丙型肝炎中,T2D和IR是肝纤维化进展更快和抗病毒治疗反应减弱的独立预测因子。肝硬化和T2D患者对肝性脑病和肝细胞癌(HCC)的敏感性更高。但是,抗病毒治疗对IR和T2D的有益作用尚存争议。从理论上讲,控制慢性丙型肝炎,尤其是肝硬化患者的血糖,可以改善预后和对抗病毒药的反应,尽管对此的证据有限。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实体,在抗病毒治疗方案中添加“代谢”策略的潜在作用,IR对肝衰竭,门脉高压的影响以及HCC,尤其是在移植环境中进行治疗的患者。

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