首页> 外文期刊>Antiviral therapy >HIV coinfection and antiretroviral therapy enhances liver steatosis in patients with hepatitis C, but only in those infected by HCV genotype other than 3.
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HIV coinfection and antiretroviral therapy enhances liver steatosis in patients with hepatitis C, but only in those infected by HCV genotype other than 3.

机译:HIV合并感染和抗逆转录病毒疗法可增强丙型肝炎患者的肝脂肪变性,但仅适用于感染了3型HCV基因型的患者。

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BACKGROUND: Liver steatosis is a common finding in hepatitis C virus (HCV) infection and is associated with an increased progression of the disease. However, HCV genotype 3 steatosis presents a peculiar and virus-induced pathogenesis. We analysed the effect of HIV coinfection and antiretroviral therapy on hepatic steatosis and the effect of the steatosis on fibrosis in patients with or without HCV genotype 3 infection. METHODS: All consecutive HIV-infected and uninfected patients who had undergone a liver biopsy for evaluation of HCV infection at the Infectious Diseases Clinic (Modena, Italy) were included in this study. Primary outcomes were the presence or absence of steatosis or the presence of moderate or advanced fibrosis. RESULTS: A total of 284 patients were enrolled: 187 infected by HCV and 97 coinfected with HIV and HCV. In HCV genotype 3 patients, only HCV-related variables, such as plasma HCV RNA levels (odds ratio [OR] per log10 1.68, P < 0.001) and estimated duration of HCV infection (OR per year 1.17, P = 0.004) were associated with steatosis. In patients infected with other HCV genotypes, steatosis was associated with older age (OR per 5 years 1.47, P < 0.001), with exposure to d-drugs in HIV-HCV-coinfected patients (OR 2.60, P = 0.04) and specifically exposure to stavudine (OR 2.76 HIV-HCV-coinfected versus not HIV-infected patients, P = 0.04). Steatosis was independently associated with bridging fibrosis only in patients infected by HCV genotype other than 3 (OR 4.03, P = 0.01). CONCLUSIONS: Hepatic steatosis, in both HCV-monoinfected and in HIV-HCV-coinfected patients, is strongly correlated with HCV genotype 3, probably through interactions between HCV virus and liver cells. HIV-related increase of steatosis in patients with HCV is probably related to antiretroviral drugs, especially stavudine, in patients infected by HCV genotype other than 3.
机译:背景:肝脂肪变性是丙型肝炎病毒(HCV)感染的常见发现,并且与疾病进展的增加有关。但是,HCV基因型3脂肪变性表现出特殊的和病毒诱导的发病机理。我们分析了HIV合并感染和抗逆转录病毒疗法对肝脂肪变性的影响以及脂肪肝对有或没有HCV基因型3感染的患者的纤维化的影响。方法:本研究包括所有连续的HIV感染和未感染患者,这些患者均在传染病诊所(意大利摩德纳)进行了肝活检以评估HCV感染。主要结局是存在或不存在脂肪变性或存在中度或晚期纤维化。结果:总共284例患者入组:187例HCV感染和97例同时感染HIV和HCV。在HCV基因型3的患者中,仅与HCV相关的变量相关,例如血浆HCV RNA水平(每log10的比值比[OR] 1.68,P <0.001)和HCV感染的估计持续时间(每年OR的1.17,P = 0.004)有脂肪变性。在感染其他HCV基因型的患者中,脂肪变性与年龄较大(每5年OR为1.47,P <0.001),HIV-HCV合并感染的患者接触d药物(OR 2.60,P = 0.04)有关,特别是司他夫定(OR 2.76 HIV-HCV合并感染患者与未感染HIV的患者,P = 0.04)。仅在感染HCV基因型为3以外的患者中,脂肪变性与桥接纤维化独立相关(OR 4.03,P = 0.01)。结论:HCV单感染的和HIV-HCV合并感染的患者的肝脂肪变性与HCV基因型3密切相关,可能是通过HCV病毒和肝细胞之间的相互作用引起的。 HCV患者中与HIV相关的脂肪变性增加可能与抗HCV基因型3以外的患者的抗逆转录病毒药物尤其是司他夫定有关。

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