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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.2–5 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 …
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