Risk factors for cirrhosis in patients with chronic hepatitis C virus infection: Results of a case‐control study

Risk factors for cirrhosis in patients with chronic hepatitis C virus infection: Results of a case‐control study
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慢性丙型肝炎病毒感染患者发生肝硬化的危险因素:病例对照研究结果

DOI:
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发表时间:
1997
期刊:
影响因子:
13.5
通讯作者:
C. Petit
C. Petit
中科院分区:
医学1区
文献类型:
--
作者:
L. Serfaty;O. Chazouilleres;Armelle Poujol;Robert;L. Morand;Joubert;Catherine Dubois;Y. Chrétien;Jean;C. Petit

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病毒基因型,特别是基因型1b,在慢性丙型肝炎病毒(HCV)感染引起的肝损伤的严重程度中的作用尚不清楚,可能是因为混杂因素,如污染的日期和模式。宿主遗传或环境因素,如杂合子MZ α1-抗胰蛋白酶缺乏或酗酒,也可能是肝硬化发生的潜在风险因素。本研究的目的是比较慢性丙型肝炎患者和非慢性丙型肝炎患者的基因型、α1-抗胰蛋白酶表型、既往B型肝炎病毒感染和饮酒情况。我们进行了一项病例对照研究,比较了84例连续的慢性丙型肝炎患者(病例)和84例非慢性丙型肝炎患者(对照),这些患者选自同期住院的464例患者。对照组根据年龄、性别、危险因素和感染日期与病例配对。使用InnoLiPA技术(Innogenetics,Zwijnaarde,Belgium)确定HCV基因型,并根据Simmonds的方法进行分类。根据饮酒量将患者分为三组:<30 g/d(轻度),30 - 80 g/d(中度)和>80 g/d(重度)。肝硬化和非肝硬化患者在基因型分布方面没有显著差异(1a/1b/2a/3a/其他/未确定:10/48/7/17/0/2 vs 11/43/10/10/5/5),α1-抗胰蛋白酶表型分布(MM/MS/MZ:分别为84%/14%/2% vs. 87%/11%/2%),以及抗B肝炎核心抗原阳性抗体的患病率(29% vs. 23%)。病例组和对照组之间的饮酒量存在显著差异(L/M/H:分别为58%/27%/16% vs. 76%/15%/9%; P <0.05)。从本研究中可以得出两个关于慢性丙型肝炎病毒感染患者的结论:1)病毒基因型,尤其是1 B型,既往B型肝炎病毒感染和杂合型MZ α1-抗胰蛋白酶缺乏不是肝硬化的危险因素; 2)饮酒,即使是中度饮酒,也是肝硬化的危险因素。
The role of the viral genotype, especially genotype 1b, in the severity of liver injury induced by chronic hepatitis C virus (HCV) infection is unclear, probably because of confounding factors such as the date and mode of contamination. Host genetic or environmental factors such as heterozygous MZ α1‐antitrypsin deficiency or alcoholism, could also be potential risk factors for the development of cirrhosis. The aim of this study was to compare the prevalence of genotypes, α1‐antitrypsin phenotype, past hepatitis B virus infection, and alcohol consumption in cirrhotic and noncirrhotic patients with chronic hepatitis C. We conducted a case‐control study comparing 84 consecutive cirrhotic patients with chronic hepatitis C (cases) with 84 noncirrhotic patients with chronic hepatitis C (controls) selected from a cohort of 464 patients hospitalized during the same period. Controls were paired with cases according to age, sex, risk factors, and date of infection. HCV genotypes were determined using the InnoLiPA technique (Innogenetics, Zwijnaarde, Belgium) and classified according to the method of Simmonds. Patients were divided in three groups according to alcohol consumption: <30 g/d (light), 30 to 80 g/d (moderate), and >80 g/d (heavy). Cirrhotic and noncirrhotic patients were not significantly different in terms of genotype distribution (1a/1b/2a/3a/others/undetermined: 10/48/7/17/0/2 versus 11/43/10/10/5/5), α1‐antitrypsin phenotype distribution (MM/MS/MZ: 84%/14%/2% vs. 87%/11%/2%, respectively), and prevalence of antibody to hepatitis B core antigen positivity (29% vs. 23%). Alcohol consumption was significantly different between cases and controls (L/M/H: 58%/27%/16% vs. 76%/15%/9%, respectively; P < .05). Two conclusions regarding patients with chronic hepatitis C virus infection can be drawn from this study: 1) viral genotype, especially 1b, past hepatitis B virus infection, and heterozygous MZ α1‐antitrypsin deficiency are not risk factors for cirrhosis; and 2) alcohol consumption, even moderate, is a risk factor for cirrhosis.
DOI: --
发表时间: 1997
期刊: Forum (Genoa, Italy)
影响因子: --
作者:
Rizzetto,Mario;Starzl,ThomasE;Fassati,LuigiRainero;Colombo,Massimo
通讯作者: Colombo,Massimo