Effect of the interaction between steatosis and alcohol intake on liver fibrosis progression in chronic hepatitis C
Effect of the interaction between steatosis and alcohol intake on liver fibrosis progression in chronic hepatitis C
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DOI：
10.1111/j.1572-0241.2002.05793.x
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发表时间：
2002-07-01
影响因子：
9.8
通讯作者：
Poupon, R
中科院分区：
文献类型：
--
作者：
Serfaty, L;Poujol-Robert, A;Poupon, R
目的：肝脂肪变性是丙型肝炎病毒感染患者常见的组织病理学表现。患有慢性丙型肝炎且同时存在脂肪变性和导致氧化应激的因素的患者，可能有更高的肝纤维化风险。在一部分明确感染日期的患者中，我们的研究旨在评估脂肪变性与可能诱导氧化应激的因素（即饮酒、铁过载和药物）之间潜在的协同作用。
方法：在700例抗丙型肝炎病毒阳性的筛查患者中，选取了142例未经治疗且进行了肝活检并具有一种已知危险因素的患者。根据克诺德尔评分对肝纤维化、炎症和坏死进行分级，若超过30%的肝细胞受到影响，则将脂肪变性判定为中度至重度。饮酒者定义为男性平均每日饮酒量超过30克，女性超过20克。
结果：在多变量分析中，有两个因素与广泛纤维化独立相关：碎屑样坏死的严重程度（比值比 = 3.27，置信区间 = 1.17 - 9.16）以及中度至重度脂肪变性与饮酒的组合（比值比 = 7.02，置信区间 = 1.12 - 44）。有脂肪变性的饮酒者的纤维化中位进展率约为无脂肪变性的饮酒者或有或无脂肪变性的非饮酒者的两倍（分别为0.25比0.1比0.13比0.08；p = 0.02）。与中度至重度脂肪变性显著相关的独立参数是体重指数（比值比 = 1.13，置信区间1.02 - 1.26）和感染基因型3（比值比 = 5.5，置信区间1.88 - 16），但与饮酒无关。
结论：除了碎屑样坏死严重程度的关键作用外，该研究强调了脂肪变性与即使少量饮酒之间的协同作用是广泛肝纤维化的一个促成因素。
OBJECTIVES: Liver steatosis is a common histopathological finding in patients infected with hepatitis C virus. Patients with chronic hepatitis C having both steatosis and factors causing oxidative stress may be at a higher risk of fibrogenesis. In a subset of patients with a definite date of contamination, our study aimed to assess the potential synergistic interaction between steatosis and factors likely to induce oxidative stress-namely, alcohol intake, iron overload, and drugs.METHODS: Out of 700 anti-HCV-positive screened patients, 142 untreated patients with liver biopsy and with one known risk factor were selected. Liver fibrosis, inflammation, and necrosis were graded according to the Knodell score, and steatosis as moderate to severe if more than 30% of hepatocytes were affected. Drinkers were defined as having daily mean alcohol intakes of more than 30 g in men and 20 g in women.RESULTS: In multivariate analysis, two factors were independently associated with extensive fibrosis: the degree of severity of piecemeal necrosis (OR = 3.27, CI = 1.17-9.16) and a combination of moderate to severe steatosis and alcohol intake (OR = 7.02, CI = 1.12-44). The median progression rate of fibrosis was about twice as high among drinkers with steatosis than among drinkers without steatosis or nondrinkers with or without steatosis (0.25 vs 0.1 vs 0.13 vs 0.08, respectively; p = 0.02). Independent parameters significantly associated with moderate to severe steatosis were body mass index (OR = 1.13, CI 1.02-1.26) and infection with genotype 3 (OR = 5.5, CI 1.88-16), but not alcohol consumption.CONCLUSIONS: As well as the key role of the severity of piecemeal necrosis, the study underlines the synergistic interaction between steatosis and even low alcohol consumption as a contributory factor in extensive liver fibrosis.