Hepatocellular fat accumulation and low serum cholesterol in patients infected with HCV-3a
Hepatocellular fat accumulation and low serum cholesterol in patients infected with HCV-3a
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DOI：
10.1111/j.1572-0241.2002.07056.x
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发表时间：
2002-11-01
影响因子：
9.8
通讯作者：
Ferenci, P
中科院分区：
文献类型：
--
作者：
Hofer, H;Bankl, HC;Ferenci, P
目的：本研究的目的是前瞻性地调查慢性丙型肝炎患者中肝脏脂肪变性的患病率，包括病毒基因型、肝脏铁浓度、全身铁、体重指数和血脂参数。此外，丙型肝炎病毒（HCV）根除抗病毒治疗对血清胆固醇水平的影响进行了study.METHODS：肝细胞脂肪和肝铁测定从137干扰素初治的慢性丙型肝炎患者（100名男性，37名女性，平均年龄40.8 +/- 10.7岁）参加了两个前瞻性临床试验的干扰素/利巴韦林治疗的肝活检。在基线、治疗期间和治疗后测定体重指数和空腹胆固醇水平。结果：在HCV-3a感染的患者中发现明显的脂肪变性（含脂肪肝细胞>20%），而在HCV-1和HCV-4感染的患者中分别为17.9%和21.7%（p < 0.01）。HCV-3a感染患者的脂肪变性与体重指数、肝脏铁含量、铁蛋白或转铁蛋白饱和度无关。基线时，HCV-3a感染患者的血清胆固醇（147 +/- 42 mg/dl; p < 0.01）低于HCV-1（188 +/- 36）或HCV-4（172 35）。与HCV-1或HCV-4感染患者相比，HCV-3a病毒学应答者在治疗结束时和治疗后6个月血清胆固醇升高（基线146 +/- 38，治疗结束166 +/- 29，p < 0.05，持续病毒学应答200 +/- 34，p < 0.01）。然而，血清胆固醇保持不变，在HCV-3a nonresponders.CONCLUSIONS：我们的数据表明，除了诱导脂肪变性，HCV-3a降低血清胆固醇。这种代谢效应在成功根除HCV-3a后是完全可逆的。这种独特的特性是其他HCV基因型所不具备的。(C)2002年，我胃肠病学。
OBJECTIVES: The aim of this study was to prospectively investigate the prevalence of hepatic steatosis in chronic hepatitis C patients with respect to viral genotype, hepatic iron concentration, total body iron, body mass index, and serum lipid parameters. Furthermore, the effect of hepatitis C virus (HCV) eradication by antiviral therapy on serum cholesterol levels was studied.METHODS: Hepatocellular fat and hepatic iron were determined in liver biopsies obtained from 137 interferon-naive patients with chronic hepatitis C (100 men, 37 women, mean age 40.8 +/- 10.7 yr) enrolled in two prospective clinical trials of interferon/ribavirin therapy. Body mass index and fasting cholesterol levels were determined at baseline, during, and after therapy.RESULTS: Marked steatosis (>20% of fat-containing hepatocytes) was found in 74.5% of patients infected with HCV-3a compared with 17.9% in HCV-1 and 21.7% in HCV-4-infected patients (p < 0.01). Steatosis in HCV-3a-infected patients did not correlate with the body mass index, hepatic iron content, ferritin, or transferrin saturation. At baseline, serum cholesterol was lower in patients infected with HCV-3a (147 +/- 42 mg/dl; p < 0.01) compared with HCV-1 (188 +/- 36) or HCV-4 (172 35). In contrast to HCV-1- or HCV-4-infected patients, serum cholesterol increased in HCV-3a virological responders at the end of treatment and 6 months after therapy (baseline 146 +/- 38, end of treatment 166 +/- 29, p < 0.05, sustained virological response 200 +/- 34, p < 0.01). However, serum cholesterol remained unchanged in HCV-3a nonresponders.CONCLUSIONS: Our data suggest that, in addition to inducing steatosis, HCV-3a lowers serum cholesterol. This metabolic effect is fully reversible after successful HCV-3a eradication. This unique property is not shared by other HCV genotypes. (C) 2002 by Am. Coll. of Gastroenterology.