Hepatic Steatosis as a Predictor of Early Response to Pegylated Interferon and Ribavirin Therapy in Patients with Chronic Hepatitis C

Background and Aims: Hepatic steatosis seems to be a risk factor for poor response to interferon and ribavirin therapy in patients with chronic hepatitis C. The aim of this study was to determine presence of hepatic steatosis in chronic hepatitis C and its influence on early virological response in patients treated with combined antiviral therapy (pegylated interferon and ribavirin). Methods: We studied 96 patients treated at Gastroenterohepatology Department, in the period of four years (2005-2009). There were 71 males and 25 females enrolled in this study. 72 patients had genotype 1, 5 patients had genotype 2, 17 patients had genotype 3 and 2 patients had genotype 4. Liver histology was evaluated in order to establish presence of inflammation, fibrosis and steatosis. HCV RNA levels in sera were measured by real time PCR. Early virological response (EVR) was defined as negative serum HCV RNA at week 12. In order to measure the effect influence of steatosis on early response to therapy, as well as genotype and response to therapy, we calculated relative risk and the corresponding p-value after 12 and 48 weeks. Results: The overall rate of EVR was 70%. The rate was significantly lower in the group with steatosis, regardless of the presence of micro or macrosteatosis, amounting to 60%. Serum cholesterol level was significantly higher in females than in males (7.4±0.7 vs. 5.1±0.3 mg/mL). The values of relative risks (and p-values) for effect of steatosis on the response are RRS12=8.4615 (2.87E-05), and RRS48=0.9844 (0.7399), while the values for the effect of genotype to therapy were RRG12=1.3378 (0.7543), and RRG48=3.5862 (0.2709). Conclusions: Our findings suggested that hepatic steatosis may have a strong influence on interferon therapy response in the sence that it is eight times more probable to not respond in the presence of steatosis. The presence of steatosis was highly associated with progressive disease and failure to achieve the EVR; therefore it can be a predictor of poor response to antiviral therapy.