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脂肪变性在慢性丙型肝炎感染及其管理中的重要性:综述。

The importance of steatosis in chronic hepatitis C infection and its management: A review.

机构信息

Hepatology Department, Derriford Hospital, Derriford Road, Plymouth, Devon.

出版信息

Hepatol Res. 2010 Mar;40(3):237-47. doi: 10.1111/j.1872-034X.2010.00626.x.

Abstract

Hepatitis C virus (HCV) infection is a major cause of chronic liver disease with approximately 180 million people infected worldwide. Hepatic steatosis is a frequent histological finding in chronic hepatitis C (CHC) infection and is 2- to 3-fold more common than would be expected by chance alone. A high body mass index with excess visceral fat distribution is associated with steatosis in patients infected with HCV genotype 1 but not genotype 3, re-enforcing the concept that in patients with CHC, some have "metabolic steatosis", predominantly HCV genotype 1, and others "viral steatosis", mainly HCV genotype 3. Accumulating evidence suggests that steatosis may contribute to progression of fibrosis in CHC. Hepatic insulin resistance appears to play a role through the pro-fibrogenic effects of compensatory hyperinsulinemia. The aim of this review was to assess the effect host and viral factors play in steatosis development in patients with CHC infection and its possible relationship with hepatocellular carcinoma. The review examines the mechanisms by which CHC infection causes hepatic steatosis, the impact hepatic steatosis has on the natural history of the disease and finally, explores if treatments leading to a reduction in the amount of steatosis might lead to improved treatment outcomes. The basic medical science of steatosis in CHC will be discussed including proposed models of steatogenesis and the influence of viral and metabolic factors at the molecular level and how these might impact on current and future therapies.

摘要

丙型肝炎病毒 (HCV) 感染是导致慢性肝病的主要原因,全球约有 1.8 亿人感染。肝脂肪变性是慢性丙型肝炎 (CHC) 感染的常见组织学发现,比单纯偶然发生的情况常见 2-3 倍。高体重指数伴内脏脂肪分布过多与 HCV 基因型 1 感染患者的脂肪变性有关,但与 HCV 基因型 3 无关,这再次证实了在 CHC 患者中,一些人存在“代谢性脂肪变性”,主要是 HCV 基因型 1,而另一些人存在“病毒性脂肪变性”,主要是 HCV 基因型 3。越来越多的证据表明,脂肪变性可能导致 CHC 纤维化的进展。肝胰岛素抵抗似乎通过代偿性高胰岛素血症的促纤维化作用发挥作用。本综述的目的是评估宿主和病毒因素在 CHC 感染患者脂肪变性发展中的作用及其与肝细胞癌的可能关系。该综述检查了 CHC 感染导致肝脂肪变性的机制,脂肪变性对疾病自然史的影响,最后探讨了减少脂肪变性量的治疗方法是否可能导致改善治疗结果。将讨论 CHC 中脂肪变性的基础医学科学,包括脂肪生成的拟议模型以及病毒和代谢因素在分子水平上的影响,以及这些因素如何影响当前和未来的治疗方法。

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