Literature DB >> 14992430

Hepatic steatosis in hepatitis C virus genotype 3 infection: does it correlate with body mass index, fibrosis, and HCV risk factors?

Pratima Sharma1, Vijayan Balan, Jose Hernandez, Marianne Rosati, James Williams, Hector Rodriguez-Luna, Joan Schwartz, Edwyn Harrison, Monte Anderson, Thomas Byrne, Hugo E Vargas, David D Douglas, Jorge Rakela.   

Abstract

Hepatic steatosis is a recognized feature of hepatitis C viral infection, particularly in genotype 3. The demographics and the associations contributing to moderate to severe steatosis in genotype 3 are not very well studied. The aim of this study is to determine the demographics and association of steatosis with fibrosis, obesity, diabetes, lipid levels, and risk factors among patients with hepatitis C virus (HCV) genotype 3. Two hundred ninety-three consecutive HCV patients (genotype 1, n = 218; genotype 2, n = 43; genotype 3, n = 32) at our institution were studied retrospectively. Demographic information such as height, weight, genotype, risk factors, serum cholesterol and triglyceride, and liver biopsy was collected. Steatosis was graded using the Brunt classification. HCV genotype 3-infected patients were younger (P < 0.04) and had lower serum cholesterol levels (P < 0.02) compared to nongenotype 3 patients. Moderate to severe steatosis was more prevalent in HCV genotype 3 patients (P < 0.001) with intravenous drug abuse as a risk factor (P = 0.04). Genotype 3 was the independent predictor of steatosis in all patients. There was no statistical association between grade of steatosis and body mass index, fibrosis, necroinflammation, or hyperlipidemia when only HCV genotype 3 patients were included in the multivariate logistic model. Hepatic steatosis is a feature of genotype 3. Patients with HCV genotype 3 are younger and have lower serum cholesterol levels. Genotype 3 is the independent predictor for steatosis in HCV patients. HCV genotype 3 patients with moderate to severe steatosis are more likely to have intravenous drug use as a risk factor.

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Year:  2004        PMID: 14992430     DOI: 10.1023/b:ddas.0000011597.92851.56

Source DB:  PubMed          Journal:  Dig Dis Sci        ISSN: 0163-2116            Impact factor:   3.199


  22 in total

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Journal:  J Hepatol       Date:  2001-03       Impact factor: 25.083

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Journal:  J Hepatol       Date:  1998-08       Impact factor: 25.083

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Journal:  J Hepatol       Date:  2002-12       Impact factor: 25.083

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Authors:  Alexander Monto; Judy Alonzo; Jessica J Watson; Carl Grunfeld; Teresa L Wright
Journal:  Hepatology       Date:  2002-09       Impact factor: 17.425

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3.  Hepatic steatosis as a possible risk factor for the development of hepatocellular carcinoma after eradication of hepatitis C virus with antiviral therapy in patients with chronic hepatitis C.

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Review 4.  Hepatitis C virus infection: Are there still specific problems with genotype 3?

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6.  Diabetes Mellitus Increases Risk of Hepatocellular Carcinoma in Chronic Hepatitis C Virus Patients: A Systematic Review.

Authors:  Harleen K Dyal; Maria Aguilar; Gabriella Bartos; Edward W Holt; Taft Bhuket; Benny Liu; Ramsey Cheung; Robert J Wong
Journal:  Dig Dis Sci       Date:  2015-12-24       Impact factor: 3.199

7.  Apolipoprotein epsilon3 allele is associated with persistent hepatitis C virus infection.

Authors:  D A Price; M F Bassendine; S M Norris; C Golding; G L Toms; M L Schmid; C M Morris; A D Burt; P T Donaldson
Journal:  Gut       Date:  2005-11-18       Impact factor: 23.059

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Authors:  Malgorzata Sidorkiewicz
Journal:  Metabolites       Date:  2021-04-27

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Review 10.  HCV Proteins Modulate the Host Cell miRNA Expression Contributing to Hepatitis C Pathogenesis and Hepatocellular Carcinoma Development.

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