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Hepatitis C virus (HCV) infection is a major cause of chronic liver disease with approximately 180 million people infected worldwide.
Hepatic steatosis is a frequent histological finding in chronic hepatitis C infection, and is 2- to 3-fold more common than would be expected by chance alone.
A high body mass index with excess visceral fat distribution is associated with steatosis in patients infected with hepatitis C genotype 1 but not genotype 3.
Dr Phillip Harrison and colleagues from the United Kingdom assessed the effect host and viral factors play in steatosis development in patients with chronic hepatitis infection and its possible relationship with hepatocellular carcinoma.
This reinforces the concept that in patients with chronic hepatitis C, some have 'metabolic steatosis', predominantly hepatitis C genotype 1, and others "viral steatosis", mainly hepatitis C genotype 3.
The team found accumulating evidence that suggests steatosis may contribute to progression of fibrosis in chronic hepatitis C.
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| Steatosis may contribute to progression of fibrosis in hep C |
| Hepatology Research |
The team noted that hepatic insulin resistance appears to play a role through the pro-fibrogenic effects of compensatory hyperinsulinemia.
The research team examined the mechanisms by which chronic hepatitis C infection causes hepatic steatosis, the impact hepatic steatosis has on the natural history of the disease.
In addition, the team explored if treatments leading to a reduction in the amount of steatosis might lead to improved treatment outcomes.
Dr Harrison's team concludes, "We examined the basic medical science of steatosis in chronic hepatitis C, including proposed models of steatogenesis, the influence of viral and metabolic factors at the molecular level, and how these might impact on current and future therapies."
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