BACKGROUND/AIMS: The prevalence and clinical implications of non-alcoholic fatty liver disease in patients with chronic hepatitis C remain unknown in Taiwan. METHODS: We addressed the relevant issues by analysing 95 naive Taiwanese patients infected with either hepatitis C virus (HCV) genotype 1 (n = 57) or 2 (n = 38), receiving interferon alone (n = 41) or in combination with ribavirin (n=54) therapy. A single pathologist scored steatosis and steatohepatitis at baseline and 24 weeks after antiviral treatment. RESULTS: At baseline, steatosis and steatohepatitis were present in 44 (46%) and four (4%) patients, respectively. Variables associated with steatosis in logistical regression were hyperglycaemia (P = 0.01), hypertriglyceridaemia (P = 004) and body mass index > or = 27 (P = 0.009), but not HCV genotype or viral load. The grade of steatosis correlated well with the number of metabolic syndrome parameters (P = 0.018). Interferon monotherapy, advanced age and HCV genotype 1, but not steatosis, correlated with lower sustained response rate. After treatment, steatosis improved in 19 and worsened in nine, which also did not correlate with HCV genotype (P = 0.850) or sustained response to antiviral therapy (P = 0.246). CONCLUSIONS: Hepatic steatosis in Taiwanese patients with chronic hepatitis C was associated with features of the metabolic syndrome, but did not correlate with HCV genotype, advanced fibrosis or the response to antiviral therapy.
BACKGROUND/AIMS: The prevalence and clinical implications of non-alcoholic fatty liver disease in patients with chronic hepatitis C remain unknown in Taiwan. METHODS: We addressed the relevant issues by analysing 95 naive Taiwanese patients infected with either hepatitis C virus (HCV) genotype 1 (n = 57) or 2 (n = 38), receiving interferon alone (n = 41) or in combination with ribavirin (n=54) therapy. A single pathologist scored steatosis and steatohepatitis at baseline and 24 weeks after antiviral treatment. RESULTS: At baseline, steatosis and steatohepatitis were present in 44 (46%) and four (4%) patients, respectively. Variables associated with steatosis in logistical regression were hyperglycaemia (P = 0.01), hypertriglyceridaemia (P = 004) and body mass index > or = 27 (P = 0.009), but not HCV genotype or viral load. The grade of steatosis correlated well with the number of metabolic syndrome parameters (P = 0.018). Interferon monotherapy, advanced age and HCV genotype 1, but not steatosis, correlated with lower sustained response rate. After treatment, steatosis improved in 19 and worsened in nine, which also did not correlate with HCV genotype (P = 0.850) or sustained response to antiviral therapy (P = 0.246). CONCLUSIONS:Hepatic steatosis in Taiwanese patients with chronic hepatitis C was associated with features of the metabolic syndrome, but did not correlate with HCV genotype, advanced fibrosis or the response to antiviral therapy.