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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >Genotype-specific interactions of insulin resistance, steatosis, and fibrosis in chronic hepatitis C.
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Genotype-specific interactions of insulin resistance, steatosis, and fibrosis in chronic hepatitis C.

机译：慢性丙型肝炎的胰岛素抵抗，脂肪变性和纤维化的基因型特异性相互作用。

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摘要

The interaction between insulin resistance (IR), steatosis and genotype to fibrosis in chronic hepatitis C virus (HCV) infection has not been comprehensively assessed. We hypothesized that IR is a key mediator for the development of both steatosis and fibrosis in 346 untreated, nondiabetic patients solely infected with either genotype 1 or 3. We examined for genotype-specific interactions between IR, steatosis and fibrosis by performing subgroup analyses. Because cirrhosis is known to cause IR, we repeated the analysis in a cohort of 313 noncirrhotic HCV-infected patients. We confirmed the impact of IR on fibrosis by analysis of 153 lean subjects in whom any effect of steatosis would be minimized. In HCV genotype 3 patients, increased steatosis was linked to high viral load (P = 0.001), and was not associated with fibrosis (P = 0.1). In contrast, body mass index (P = 0.04) and homeostasis model assessment of insulin resistance (HOMA-IR) (P = 0.01) contributed directly to steatosis in HCV genotype 1. HOMA-IR rather than steatosis was independently associated with fibrosis for both HCV genotype 1 (OR, 3.22; P = 0.02) and genotype 3 (OR, 3.17; P = 0.04). Exclusion of cirrhotic subjects did not alter the findings with respect to the greater contribution of IR compared to hepatic steatosis, as a predictor of fibrosis (P = 0.02). Genotype-specific subgroup analyses did not alter this finding. The extent of HOMA-IR remained significantly associated with fibrosis in lean patients, independent of the confounding effect of body mass index on IR (OR, 8.02; P = 0.003). CONCLUSION: IR is a major independent determinant of fibrosis in chronic HCV infection, regardless of the genotype and the severity of liver damage.
机译：尚未对慢性丙型肝炎病毒（HCV）感染中胰岛素抵抗（IR），脂肪变性和纤维化基因型之间的相互作用进行全面评估。我们假设IR是346名仅感染基因型1或3的未经治疗的非糖尿病患者中脂肪变性和纤维化发展的关键介质。我们通过进行亚组分析检查了IR，脂肪变性和纤维化之间的基因型特异性相互作用。因为已知肝硬化会引起IR，所以我们在313名非肝硬化HCV感染患者中重复了该分析。我们通过分析153位瘦弱的受试者（其中脂肪变性的影响将降至最低）来确认IR对纤维化的影响。在HCV基因型3的患者中，脂肪变性增加与高病毒载量相关（P = 0.001），与纤维化无关（P = 0.1）。相比之下，体重指数（P = 0.04）和胰岛素抵抗的稳态模型评估（HOMA-IR）（P = 0.01）直接导致HCV基因型1的脂肪变性。HOMA-IR而非脂肪变性与两者的纤维化独立相关HCV基因型1（OR，3.22; P = 0.02）和基因型3（OR，3.17; P = 0.04）。与肝脂肪变性相比，肝硬化受试者的排除对IR的贡献更大，并没有改变这一发现，这是纤维化的预测指标（P = 0.02）。基因型特异性亚组分析并没有改变这一发现。瘦体重患者的HOMA-IR程度仍与纤维化密切相关，而与体重指数对IR的混杂影响无关（OR，8.02; P = 0.003）。结论：IR是慢性HCV感染中纤维化的主要独立决定因素，无论其基因型和肝损害的严重程度如何。

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