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RECENT ADVANCES IN CLINICAL PRACTICE |
1 Service dHépatologie and INSERM CRB3, Hôpital Beaujon, Clichy, France
2 Service de Pathologie Clinique, Hôpital Universitaire, Genève, Switzerland
3 Services de Pathologie Clinique, de Gastroentérologie et dHépatologie, Hôpital Universitaire, Genève, Switzerland
Correspondence to:
Correspondence to:
Dr P Marcellin
Service dHépatologie and INSERM CRB3, Hôpital Beaujon, Clichy 92 110, France; patrick.marcellin@bjn.ap-hop-paris.fr
Keywords: fibrosis; insulin resistance; genotype; non-alcoholic steatohepatitis; treatment
| The first 150 words of the full text of this article appear below. |
SUMMARY
Hepatic steatosis is a common histological feature of chronic hepatitis C. Various factors are associated with hepatic steatosis, including obesity, high alcohol consumption, diabetes type II, and hyperlipidaemia. These factors may contribute to steatosis in patients with chronic hepatitis C. In humans, hepatitis C virus (HCV) genotype 3 is more commonly associated with steatosis. In vitro studies and the transgenic mouse model have suggested that the HCV core protein (genotype 1) can induce lipid accumulation within hepatocytes.
However, what is the relevance of steatosis in chronic hepatitis C? It seems that in certain populations, steatosis may be associated with fibrosis progression and this may be genotype specific. The mechanisms underlying this association are unknown; neither is it clear whether this holds true for all patients or only a subgroup. Indeed, after antiviral treatment, virus related steatosis disappears whereas the host associated steatosis remains unaffected.
This review describes and discusses the
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