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胰岛素抵抗和肝脂肪变性在丙型肝炎纤维化进展和治疗反应中的作用。

Role of insulin resistance and hepatic steatosis in the progression of fibrosis and response to treatment in hepatitis C.

机构信息

Department of Internal Medicine, Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University Medical Center, Richmond, VA 23298-0341, USA.

出版信息

Liver Int. 2011 Jan;31 Suppl 1:23-8. doi: 10.1111/j.1478-3231.2010.02397.x.

Abstract

Hepatitis C is a common cause of chronic viral infection of the liver. It is associated with insulin resistance and the development of type 2 diabetes mellitus. It is also associated with the development of hepatic steatosis. The presence of hepatic steatosis is associated with an increased risk of having hepatic fibrosis. This is also associated with the severity of insulin resistance. These findings are specifically germane for those with genotype1 infection. Genotype 3 infection independently causes steatosis and successful treatment of the virus is followed by resolution of steatosis. In genotype 1 infection, the presence of hepatic steatosis is also a risk factor for failure to respond to pegylated interferon and ribavirin therapy. Unfortunately efforts to treat insulin resistance prior to antiviral therapy have not been very successful. Newer efforts focused on the role of specific micro RNAs in mediating the metabolic effects of hepatitis C virus infection may provide to ameliorate the metabolic risks of HCV infection.

摘要

丙型肝炎是一种常见的肝脏慢性病毒感染。它与胰岛素抵抗和 2 型糖尿病的发生有关。它也与肝脂肪变性的发展有关。肝脂肪变性的存在与发生肝纤维化的风险增加有关。这也与胰岛素抵抗的严重程度有关。这些发现与基因型 1 感染的人特别相关。基因型 3 感染独立引起脂肪变性,成功治疗病毒后脂肪变性会得到解决。在基因型 1 感染中,肝脂肪变性的存在也是对聚乙二醇干扰素和利巴韦林治疗无反应的危险因素。不幸的是,在抗病毒治疗之前治疗胰岛素抵抗的努力并没有取得很大成功。新的努力集中在特定 microRNAs 在介导丙型肝炎病毒感染的代谢作用上,可能有助于减轻 HCV 感染的代谢风险。

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