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Hepatitis C and steatosis: a reappraisal.
J Viral Hepat. 2006 Feb; 13(2):73-80.JV

Abstract

The overall prevalence of steatosis in patients with Hepatitis C virus (HCV) chronic infection is 55.5% (range 34.8-81.2%). This is a two to threefold increase compared with the prevalence of steatosis in chronic hepatitides because of other aetiologies and of the figures expected on the grounds of a steatosis-HCV chance association. HCV genotype 3 (HCV-3) has specific epidemiological features; furthermore, as compared with HCV-non-3 genotypes, it is associated with a higher prevalence (74.1%vs 47.9%, P < 0.01) and with more severe grades of steatosis (prevalence of grade 3 steatosis 29.6 vs 5.5 P < 0.01). Host and viral factors play a role, although to a variable extent, in the pathogenesis of HCV-3 and non-3 steatosis. HCV load and body mass index are associated with steatosis in HCV-3 and in HCV-non-3 patients respectively. Serum cholesterol levels and liver steatosis at baseline follow an inverse relationship in HCV infection. As hypocholesterolaemia corrects only in those sustained responders to antiviral treatment both in genotype 3 and in non-3 genotypes, the occurrence of a virally induced, acquired and reversible hypobetalipoproteinaemia seems plausible. Steatosis affects the natural course of HCV infection: it is associated with fibrosis, a possible mediator of increased risk to develop type 2 diabetes, it impairs the response to antiviral treatment in HCV-3 patients and might constitute a risk factor for the development of hepatocellular carcinoma. These observations indicate the need to evaluate the efficacy of combined antiviral and 'metabolic' approaches vs standard antiviral regimes in patients with steatosis and HCV chronic infection.

Authors+Show Affiliations

Unità Operativa di Medicina Interna e Gastroenterologia, Nuovo Ospedale Civile-Estense di Baggiovara, Modena, Italy. a.lonardo@libero.itNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

16436124

Citation

Lonardo, A, et al. "Hepatitis C and Steatosis: a Reappraisal." Journal of Viral Hepatitis, vol. 13, no. 2, 2006, pp. 73-80.
Lonardo A, Loria P, Adinolfi LE, et al. Hepatitis C and steatosis: a reappraisal. J Viral Hepat. 2006;13(2):73-80.
Lonardo, A., Loria, P., Adinolfi, L. E., Carulli, N., & Ruggiero, G. (2006). Hepatitis C and steatosis: a reappraisal. Journal of Viral Hepatitis, 13(2), 73-80.
Lonardo A, et al. Hepatitis C and Steatosis: a Reappraisal. J Viral Hepat. 2006;13(2):73-80. PubMed PMID: 16436124.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hepatitis C and steatosis: a reappraisal. AU - Lonardo,A, AU - Loria,P, AU - Adinolfi,L E, AU - Carulli,N, AU - Ruggiero,G, PY - 2006/1/27/pubmed PY - 2006/4/1/medline PY - 2006/1/27/entrez SP - 73 EP - 80 JF - Journal of viral hepatitis JO - J Viral Hepat VL - 13 IS - 2 N2 - The overall prevalence of steatosis in patients with Hepatitis C virus (HCV) chronic infection is 55.5% (range 34.8-81.2%). This is a two to threefold increase compared with the prevalence of steatosis in chronic hepatitides because of other aetiologies and of the figures expected on the grounds of a steatosis-HCV chance association. HCV genotype 3 (HCV-3) has specific epidemiological features; furthermore, as compared with HCV-non-3 genotypes, it is associated with a higher prevalence (74.1%vs 47.9%, P < 0.01) and with more severe grades of steatosis (prevalence of grade 3 steatosis 29.6 vs 5.5 P < 0.01). Host and viral factors play a role, although to a variable extent, in the pathogenesis of HCV-3 and non-3 steatosis. HCV load and body mass index are associated with steatosis in HCV-3 and in HCV-non-3 patients respectively. Serum cholesterol levels and liver steatosis at baseline follow an inverse relationship in HCV infection. As hypocholesterolaemia corrects only in those sustained responders to antiviral treatment both in genotype 3 and in non-3 genotypes, the occurrence of a virally induced, acquired and reversible hypobetalipoproteinaemia seems plausible. Steatosis affects the natural course of HCV infection: it is associated with fibrosis, a possible mediator of increased risk to develop type 2 diabetes, it impairs the response to antiviral treatment in HCV-3 patients and might constitute a risk factor for the development of hepatocellular carcinoma. These observations indicate the need to evaluate the efficacy of combined antiviral and 'metabolic' approaches vs standard antiviral regimes in patients with steatosis and HCV chronic infection. SN - 1352-0504 UR - https://www.unboundmedicine.com/medline/citation/16436124/Hepatitis_C_and_steatosis:_a_reappraisal_ L2 - https://doi.org/10.1111/j.1365-2893.2005.00669.x DB - PRIME DP - Unbound Medicine ER -