Szanto Paula, Grigorescu Mircea, Dumitru Iuliana, Serban Alexandru
3rd Medical Clinic, Iuliu Hatieganu University of Medicine and Pharmacy, Str. Croitorilor no. 19-21, 400162 Cluj-Napoca, Romania.
J Gastrointestin Liver Dis. 2006 Jun;15(2):117-24.
Steatosis is a frequent feature of hepatitis-C-virus (HCV) infection. Steatosis may be an important cofactor in both accelerating fibrosis and increasing liver necroinflammatory activity in chronic hepatitis C. Several studies suggested that steatosis induces resistance to interferon and ribavirin combination treatment.
to assess the prevalence of steatosis in chronic HCV-infection and the host factors associated with steatosis, to estimate the impact of steatosis on liver fibrosis, and to evaluate the response to antiviral therapy in patients with HCV-infection and steatosis.
A retrospective study was performed on 37 patients with chronic active HCV-infection treated with interferon and ribavirin: 21 women and 16 men, mean age 46.97 years. Presence of metabolic syndrome was assessed according to the ATPIII criteria. Cobas Amplicor HCV-Test was used to detect HCV-RNA. Steatosis was graded using the Brunt system.
Prior to the antiviral treatment, steatosis was present in 26 out of 37 patients (70%). Patients with steatosis were older, especially those with associated metabolic syndrome. Fibrosis stage was significantly advanced in patients with steatosis. Lower baseline viremia correlated with sustained response both in patients with and without steatosis. Absence of baseline steatosis was associated with higher biochemical and virological sustained response. None of the patients with metabolic syndrome had a sustained response to antiviral therapy. In all patients, the stage of fibrosis did not significantly improve 6 months after cessation of the antiviral treatment.
Steatosis is a frequently encountered histological feature in chronic HCV-infection. It is associated with older age, lower virologic response and worsening fibrosis irrespective of antiviral treatment.
脂肪变性是丙型肝炎病毒（HCV）感染的常见特征。脂肪变性可能是加速慢性丙型肝炎纤维化和增加肝脏坏死性炎症活动的重要辅助因素。多项研究表明，脂肪变性会导致对干扰素和利巴韦林联合治疗产生耐药性。
评估慢性HCV感染中脂肪变性的患病率以及与脂肪变性相关的宿主因素，估计脂肪变性对肝纤维化的影响，并评估HCV感染合并脂肪变性患者对抗病毒治疗的反应。
对37例接受干扰素和利巴韦林治疗的慢性活动性HCV感染患者进行了一项回顾性研究：21名女性和16名男性，平均年龄46.97岁。根据ATPIII标准评估代谢综合征的存在情况。使用Cobas Amplicor HCV检测法检测HCV-RNA。采用Brunt系统对脂肪变性进行分级。
在抗病毒治疗前，37例患者中有26例（70%）存在脂肪变性。有脂肪变性的患者年龄较大，尤其是那些合并代谢综合征的患者。脂肪变性患者的纤维化阶段明显更严重。无论有无脂肪变性，较低的基线病毒血症与持续应答相关。基线无脂肪变性与更高的生化和病毒学持续应答相关。代谢综合征患者对抗病毒治疗均无持续应答。在所有患者中，抗病毒治疗停止6个月后，纤维化阶段没有明显改善。
脂肪变性是慢性HCV感染中常见的组织学特征。无论是否进行抗病毒治疗，它都与年龄较大、病毒学应答较低和纤维化加重有关。
