Anty Rodolphe, Gelsi Eve, Giudicelli Jean, Mariné-Barjoan Eugenia, Gual Philippe, Benzaken Sylvia, Saint-Paul Marie-Christine, Sadoul Jean Louis, Huet Pierre Michel, Tran Albert
Centre Hospitalier de Nice, Pôle digestif, Nice, France.
Eur J Gastroenterol Hepatol. 2007 Aug;19(8):671-7. doi: 10.1097/MEG.0b013e3281532b9a.
Steatosis and metabolic abnormalities seem to be frequent and deleterious in chronic hepatitis C. Changes in glucose homeostasis and in adiponectin levels, an adipokine with anti-inflammatory and insulin-sensitive properties, were evaluated in patients with chronic hepatitis C according to steatosis, liver fibrosis and body mass index.
Seventy-three patients with chronic hepatitis C (40 men, 33 women) infected with genotypes non-3 and 22 healthy controls (11 men and 11 women) were included in the study and all had a biochemical evaluation, including metabolic parameters, adiponectin measurement, and a liver biopsy. Insulin sensitivity was assessed with the HOMA 1-IR insulin resistance model.
Steatosis was found in 65.7% of the patients and significant fibrosis (METAVIR F2-F4) was present in 28.7%. The presence of steatosis could only be predicted by fibrosis, whereas significant fibrosis could be predicted by steatosis and age. Adiponectin levels were significantly decreased (-32%) with the severity of the steatosis. Although overweight chronic hepatitis C patients (body mass index>or=25 kg/m2) had insulin resistance and hypoadiponectinemia, lean chronic hepatitis C patients (body mass index<25 kg/m2) had already significantly higher glycemia and lower adiponectin levels than in controls.
This study confirms the high incidence of steatosis in patients infected by hepatitis C virus genotypes non-3, well linked to the development of fibrosis and metabolic abnormalities. Importantly, the present findings put emphasis on the early development of these metabolic abnormalities as they were already found in lean patients with chronic hepatitis C. The direct implication of hepatitis C virus is thus further stressed in the development of steatosis and insulin resistance, with or without involvement of host factors.
脂肪变性和代谢异常在慢性丙型肝炎中似乎很常见且有害。根据脂肪变性、肝纤维化和体重指数,对慢性丙型肝炎患者的葡萄糖稳态变化和脂联素水平(一种具有抗炎和胰岛素敏感性特性的脂肪因子)进行了评估。
本研究纳入了73例感染非3型基因型的慢性丙型肝炎患者(40例男性,33例女性)和22名健康对照者(11例男性和11例女性),所有患者均进行了生化评估,包括代谢参数、脂联素测量和肝活检。采用HOMA 1-IR胰岛素抵抗模型评估胰岛素敏感性。
65.7%的患者存在脂肪变性,28.7%的患者存在显著纤维化(METAVIR F2-F4)。脂肪变性的存在仅可通过纤维化预测,而显著纤维化可通过脂肪变性和年龄预测。脂联素水平随脂肪变性严重程度显著降低(-32%)。尽管超重的慢性丙型肝炎患者(体重指数≥25 kg/m²)存在胰岛素抵抗和低脂联素血症,但瘦的慢性丙型肝炎患者(体重指数<25 kg/m²)的血糖已经显著高于对照组,脂联素水平则低于对照组。
本研究证实了非3型丙型肝炎病毒感染患者中脂肪变性的高发生率,这与纤维化和代谢异常的发展密切相关。重要的是,目前的研究结果强调了这些代谢异常的早期发展,因为在瘦的慢性丙型肝炎患者中已经发现了这些异常。因此,在脂肪变性和胰岛素抵抗的发展中,无论是否涉及宿主因素,丙型肝炎病毒的直接影响都进一步得到强调。