INTRODUCTION: Hepatic steatosis is common in patients with chronic hepatitis C virus (HCV) infection, and its occurrence may be related to both host and viral factors. Relationship between improvement in steatosis and response to anti-viral treatment remains unclear. This study assessed the factors associated with steatosis in patients infected with genotype 4 HCV, and to correlate degree of changes in steatosis with host factors and response to treatment. METHODS: Records of 175 patients with chronic genotype 4 HCV infection, who had received interferon and ribavirin combination therapy, were reviewed retrospectively to extract data on body mass index (BMI), presence of diabetes mellitus, and liver histology findings. Paired BMI data and liver biopsies (pre- and 24-weeks post-treatment) were available in 86 patients. Baseline steatosis and its changes (before and after treatment) were the dependent variables in a univariate and multivariate analyses. RESULTS: Steatosis was found in 88/175 (50.3%) of baseline biopsies. Its presence was related to baseline BMI (r=0.33, P<0.01), but not with viral load, or grade of liver inflammation or fibrosis. On follow up, improvement in steatosis was significantly associated with degree of weight loss but not with response to anti-viral treatment. CONCLUSION: Steatosis is common in genotype 4 HCV infection, and its presence appears to be related to high BMI, but not to viral load or degree of liver injury.
INTRODUCTION:Hepatic steatosis is common in patients with chronic hepatitis C virus (HCV) infection, and its occurrence may be related to both host and viral factors. Relationship between improvement in steatosis and response to anti-viral treatment remains unclear. This study assessed the factors associated with steatosis in patients infected with genotype 4 HCV, and to correlate degree of changes in steatosis with host factors and response to treatment. METHODS: Records of 175 patients with chronic genotype 4 HCV infection, who had received interferon and ribavirin combination therapy, were reviewed retrospectively to extract data on body mass index (BMI), presence of diabetes mellitus, and liver histology findings. Paired BMI data and liver biopsies (pre- and 24-weeks post-treatment) were available in 86 patients. Baseline steatosis and its changes (before and after treatment) were the dependent variables in a univariate and multivariate analyses. RESULTS:Steatosis was found in 88/175 (50.3%) of baseline biopsies. Its presence was related to baseline BMI (r=0.33, P<0.01), but not with viral load, or grade of liver inflammation or fibrosis. On follow up, improvement in steatosis was significantly associated with degree of weight loss but not with response to anti-viral treatment. CONCLUSION:Steatosis is common in genotype 4 HCV infection, and its presence appears to be related to high BMI, but not to viral load or degree of liver injury.
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