Insulin resistance is associated with steatosis in nondiabetic patients with genotype 1 chronic hepatitis C
Insulin resistance is associated with steatosis in nondiabetic patients with genotype 1 chronic hepatitis C
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DOI：
10.1002/hep.20983
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发表时间：
2006-01-01
期刊：
影响因子：
13.5
通讯作者：
Craxì, A
中科院分区：
文献类型：
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作者：
Cammà, C;Bruno, S;Craxì, A
关于丙型肝炎病毒基因型 I 与肝脂肪变性之间的关系以及后者在纤维化进展和治疗反应中的作用，存在相互矛盾的数据。我们评估了基因 1 型慢性丙型肝炎中与肝脂肪变性相关的因素以及肝脂肪对纤维化发展和干扰素反应性的影响。对 291 名患有基因型 I 慢性丙型肝炎的非糖尿病患者进行了检查，了解脂肪变性的存在及其与临床、病毒学和生化数据（包括胰岛素抵抗（IR））的相关性，并通过稳态模型评估（HOMA）评分进行评估。脂肪变性分为轻度（1%-20%的肝细胞受累）、中度（21%-40%的肝细胞受累）和重度（>40%的肝细胞受累）。 291 名受试者中有 110 名（37.8%）患有轻度脂肪变性，291 名受试者中有 55 名（18.9%）患有中度/重度脂肪变性。通过逻辑回归，中度/重度脂肪变性与女性（比值比 [OR] 2.74；95% CI 1.40-5.35）、高 γ-谷氨酰转移酶水平（OR 1.52；95% CI 1.22-1.91）和 HOMA 评分（OR 1.076；95% CI 1.001-1.26）独立相关。通过逻辑回归，中度/重度脂肪变性（OR 2.78；95% CI 1.21-6.4）和血小板计数（OR 0.97；95% CI 0.96-0.98）是晚期纤维化的独立预测因子。与轻度/无脂肪变性患者相比，中度/重度脂肪变性患者持续病毒学应答的 OR 为 0.52（95% CI 0.30-0.90）。总之，在代谢综合征低风险的基因 1 型丙型肝炎非糖尿病欧洲患者中，脂肪变性的患病率接近 60%。 IR 是中度/重度脂肪变性的危险因素，尤其是男性。中度/重度脂肪变性具有临床意义，与晚期纤维化和抗病毒治疗反应低下有关。
Conflicting data exist regarding the relationship between hepatitis C virus genotype I and hepatic steatosis as well as the latter's role in the progression of fibrosis and treatment response. We assessed factors associated with hepatic steatosis in genotype 1 chronic hepatitis C and the impact of hepatic fat on fibrosis development and interferon responsiveness. Two hundred ninety-one non-diabetic patients with genotype I chronic hepatitis C were examined for the presence of steatosis and its correlation with clinical, virological, and biochemical data, including insulin resistance (IR), evaluated by the homeostasis model assessment (HOMA) score. Steatosis was graded as mild (1%-20% of hepatocytes involved), moderate (21%-40% of hepatocytes involved), and severe (>40% of hepatocytes involved). Steatosis was mild in 110 of 291 (37.8%) and moderate/severe in 55 of 291 (18.9%) subjects. By logistic regression, moderate/severe steatosis was independently associated with the female sex (odds ratio [OR] 2.74; 95% Cl 1.40-5.35), high gamma-glutamyltransferase levels (OR 1.52; 95% Cl 1.22-1.91), and HOMA-score (OR 1.076; 95% CI 1.001-1.26). By logistic regression, moderate/severe steatosis (OR 2.78; 95% CI 1.21-6.4), and platelet counts (OR 0.97; 95% CI 0.96-0.98) were independent predictors of advanced fibrosis. Patients with moderate/severe steatosis had an OR of 0.52 (95% CI 0.30-0.90) for sustained virological response compared with patients with mild/absent steatosis. In conclusion, in nondiabetic European patients with genotype 1 hepatitis C at low risk for the metabolic syndrome, the prevalence of steatosis was nearly 60%. IR is a risk factor for moderate/severe steatosis, especially in men. Moderate/severe steatosis has clinical relevance, being associated with advanced fibrosis and hyporesponsiveness to antiviral therapy.