Borghi Vanni, Puoti Massimo, Mussini Cristina, Bellelli Stefania, Angeletti Claudio, Sabbatini Francesca, Prati Francesca, Cossarizza Andrea, Esposito Roberto
Clinic of Infectious and Tropical Diseases, University of Modena and Reggio Emilia, Modena, Italy.
Antivir Ther. 2008;13(8):1057-65.
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.
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.
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).
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.
肝脂肪变性是丙型肝炎病毒（HCV）感染中的常见表现，且与疾病进展加快相关。然而，HCV基因3型脂肪变性呈现出一种独特的、由病毒诱导的发病机制。我们分析了合并感染HIV及抗逆转录病毒治疗对肝脂肪变性的影响，以及脂肪变性对合并或未合并HCV基因3型感染患者纤维化的影响。
本研究纳入了在意大利摩德纳传染病诊所因评估HCV感染而接受肝活检的所有连续的HIV感染和未感染患者。主要结局为是否存在脂肪变性或是否存在中度或重度纤维化。
共纳入284例患者：187例为HCV感染，97例为HIV和HCV合并感染。在HCV基因3型患者中，仅血浆HCV RNA水平（每log10的比值比[OR]为1.68，P<0.001）和HCV感染估计持续时间（每年OR为1.17，P = 0.004）等与HCV相关的变量与脂肪变性有关。在感染其他HCV基因型的患者中，脂肪变性与年龄较大（每5岁OR为1.47，P<0.001）、HIV-HCV合并感染患者接触d类药物（OR为2.60，P = 0.04）以及特别是接触司他夫定（HIV-HCV合并感染患者与未感染HIV患者相比OR为2.76，P = 0.04）有关。仅在感染非3型HCV基因型的患者中，脂肪变性与桥接纤维化独立相关（OR为4.03，P = 0.01）。
在HCV单感染和HIV-HCV合并感染患者中，肝脂肪变性与HCV基因3型密切相关，可能是通过HCV病毒与肝细胞之间的相互作用。在感染非3型HCV基因型的患者中，HCV患者中与HIV相关的脂肪变性增加可能与抗逆转录病毒药物尤其是司他夫定有关。
