We read with great interest the review by Asselah et al (Gut 2006;55:123–30) on the relevance of steatosis in chronic hepatitis C. They correctly reported that steatosis occurs more frequently in patients with chronic hepatitis C (55%) than in the general population (20–30%) of adults in the Western world,1 and that it is associated with various factors, including obesity, high alcohol consumption, diabetes mellitus, and hyperlipidaemia. They also discuss experimental models demonstrating that hepatitis C virus (HCV) proteins derived from genotype 1 isolates can induce steatosis.2,3,4,5 Among the conclusions, they claim the need for larger studies which take into account confounding factors for steatosis.
We have recently published our experience in assessing the impact of steatosis on antiviral treatment in a group of 102 naive patients with chronic hepatitis C of different genotypes.6 We excluded subjects with at least one of the following features: present or past alcohol consumption, body mass index of 30 or more (indicating obesity), hyperglycaemia, hypercholesterolaemia, and hypertriglyceridaemia. This was done to rule out possible concomitant metabolic disorders—namely, alcoholic hepatitis and non‐alcoholic fatty liver disease. However, we observed that hepatic steatosis was present histologically in 51% of cases; we then hypothesised a potential direct pathogenic role of the virus in induction of liver steatosis, not limited to HCV genotype 3.
We also observed significantly higher necroinflammatory activity and a greater prevalence of the advanced stage of fibrosis in HCV patients with steatosis.
Interestingly, the presence of steatosis was not associated with a lower sustained virological response. To our knowledge, no previous work has reported on a selected population such as ours, and we obviously agree on the need for larger trials which could explain the mechanisms that promote the occurrence of steatosis in chronic hepatitis C.
Footnotes
Conflict of interest: None declared.
References
- 1.Clark J M, Brancati F L, Diehl A M. Nonalcoholic fatty liver disease. Gastroenterology 20021221649–1657. [DOI] [PubMed] [Google Scholar]
- 2.Barba G, Harper F, Harada T.et al Hepatitis C virus core protein shows a cytoplasmic localization and associates to cellular lipid storage droplets. Proc Natl Acad Sci U S A 1997941200–1205. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Shi S T, Polyak S J, Tu H.et al Hepatitis C virus NS5A colocalizes with the core protein on lipid droplets and interacts with apolipoproteins. Virology 2002292198–210. [DOI] [PubMed] [Google Scholar]
- 4.Perlemuter G, Sabile A, Letteron P.et al Hepatitis C virus core protein inhibits microsomal triglyceride transfer protein activity and very low density lipoprotein secretion: a model of viral‐related steatosis. FASEB J 200216185–194. [DOI] [PubMed] [Google Scholar]
- 5.Okuda M, Li K, Beard M R.et al Mitochondrial injury, oxidative stress, and antioxidant gene expression are induced by hepatitis C virus core protein. Gastroenterology 2002122366–375. [DOI] [PubMed] [Google Scholar]
- 6.Guidi M, Muratori P, Granito A.et al Hepatic steatosis in chronic hepatitis C: impact on response to anti‐viral treatment with peg‐interferon and ribavirin. Aliment Pharmacol Ther 200522943–949. [DOI] [PubMed] [Google Scholar]