Cross-sectional studies suggest that hepatic steatosis is a cytopathic effect of hepatitis C virus (HCV) genotype 3, but not genotype 1, infections.
In this study, a research team from Australia assessed whether antiviral treatment altered hepatic steatosis in chronic hepatitis C.
The team evaluated 28 patients with genotype 1 and 34 with genotype 3 HCV.
|No change in steatosis among patients without a sustained viral response.|
They determined the severity of steatosis in both pre- and post-treatment liver biopsies using computer-assisted morphometric image analysis, and conventional semiquantitative scoring.
The researchers found that before treatment hepatic steatosis was present in 57% of patients infected with HCV genotype 1 and in 62% of those with genotype 3.
The team also found that sustained viral response (SVR) was achieved in 32% of patients with genotype 1 and in 65% with genotype 3.
In neither group were there significant changes in body weight or alcohol consumption between pre- and post-treatment biopsies.
The team determined that in patients with HCV genotype 1, there was no change in hepatic steatosis after treatment, irrespective of the treatment response.
However, among those infected with genotype 3, SVR significantly reduced steatosis, but there was no change in steatosis among those without a SVR.
Logistic regression analysis, showed SVR to be the only variable predictive of improvement in hepatic steatosis (OR = 36).
Dr Dinesh Kumar’s team concluded, “These data provide strong support for a direct causal association between HCV genotype 3 infection and hepatic steatosis”.
In a related editorial Dr Francesco Negro, from Geneva, Switzerland, discusses the mechanisms by which HCV causes chronic, progressive liver damage.
He concludes, “Although steatosis of the liver is a frequent occurrence in chronic hepatitis C, it is not always due to HCV, and therefore may be resistant to antiviral treatment”.