Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis
Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis
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DOI：
10.1002/hep.21429
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发表时间：
2006-12-01
期刊：
影响因子：
13.5
通讯作者：
George, Jacob
中科院分区：
文献类型：
--
作者：
Bugianesi, Elisabetta;Marchesini, Gulio;George, Jacob
肝脂肪变性与纤维化有关，但后者是否独立于脂肪浸润的病因尚不清楚。我们分析了132例由基因型3型慢性丙型肝炎（CHC-3）引起的“病毒性”脂肪变性患者和132例由非酒精性脂肪肝病（NARD）引起的“代谢性”脂肪变性患者的临床特征、胰岛素抵抗（HOMA-R）和组织学参数之间的关系，这些患者的年龄、BMI和肝脏脂肪堆积程度相匹配。两个研究人群的肝功能检查结果具有可比性。NAFLD中胰岛素抵抗特征的患病率较高，HOMA-R也是如此（P = 0.008）。Logistic回归分析证实CHC-3组脂肪变性与高病毒载量和低血清胆固醇相关，NAFLD组与高转氨酶、高血糖、高铁蛋白和高甘油三酯血症相关。在单变量分析中，晚期纤维化与NAFLD的脂肪变性相关，但与CHC-3无关。与纤维化严重程度相关的其他参数为CHC-3中的HOMA-R和低血小板计数，以及NAFLD中的高转氨酶、HOMA-R、铁蛋白和低HDL-胆固醇。在多变量分析中，只有低血小板计数（OR = 0.78; 95%CI，0.67-0.92）和HOMA-R（OR = 2.98; 1.13-7.89）是CHC-3中晚期纤维化的独立预测因子。在NAFLD中，通过脂肪分级（OR = 3.03; 1.41-6.53）、铁蛋白（OR = 1.13; 1.03-1.25）和HOMA-R（OR = 1.16; 1.02-1-31）预测严重纤维化。总之，胰岛素抵抗是NAFLD和CHC-3中晚期纤维化的独立预测因子，但脂肪变性的程度仅在NAFLD中有助于晚期疾病。在CHC-3中观察到的病毒诱导的肝脂肪变性对肝纤维化没有显著贡献。
Hepatic steatosis has been associated with fibrosis, but it is unknown whether the latter is independent of the etiology of fat infiltration. We analyzed the relationship between clinical characteristics, insulin resistance (HOMA-R) and histological parameters in 132 patients with "viral" steatosis caused by genotype 3 chronic hepatitis C (CHC-3) and 132 patients with "metabolic" steatosis caused by nonalcoholic fatty liver disease (NARD), matched by age, BMI, and degree of liver fat accumulation. Tests of fiver function were comparable in the two study populations. The prevalence of features of insulin resistance was higher in NAFLD, as was HOMA-R (P = .008). Logistic regression analysis confirmed that steatosis was associated with a high viral load and low serum cholesterol in CHC-3, and with high aminotransferase, glucose, ferritin and hypertriglyc-eridemia in NAFLD. At univariate analysis, advanced fibrosis was associated with steatosis in NAFLD, but not in CHC-3. Other parameters related to fibrosis severity were HOMA-R and a low platelet count in CHC-3, and high aminotransferases, HOMA-R, ferritin and low HDL-cholesterol in NAFLD. On multivariate analysis, only low platelet count (OR = 0.78; 95% CI, 0.67-0.92) and HOMA-R (OR = 2.98; 1.13-7.89) were independent predictors of advanced fibrosis in CHC-3. In NAFLD, severe fibrosis was predicted by fat grading (OR = 3.03; 1.41-6.53), ferritin (OR = 1.13; 1.03-1.25) and HOMA-R (OR = 1.16; 1.02-1-31). In conclusion insulin resistance is an independent predictor of advanced fibrosis in both NAFLD and CHC-3, but the extent ofsteatosis contributes to advanced disease only in NAFLD. Virus-induced hepatic steatosis as seen in CHC-3 does not contribute significantly to liver fibrosis.