The effect of different direct antivirals on hepatic steatosis in nondiabetic and naïve hepatitis C-infected Egyptian patients.

Background: Hepatitis C is associated with metabolic effects and fatty liver disease. The effect of different direct antivirals on the liver steatosis, and the metabolic profile, still needs to be established. The aim of this study is to determine the effect of achieving the sustained virological response after 12 weeks (SVR-12 weeks) with different combinations of direct antiviral drugs, on the hepatic steatosis, and fibrosis presented by laboratory and transient elastography parameters. Our study population is nondiabetic, chronically infected HCV Egyptian patients and naïve to any form of HCV treatment. Methods: This cohort study was carried on 100 nondiabetic HCV treatment-naïve patients attending the Hepatology Clinic, in the Gastroenterology and Hepatology Department, Ain Shams University, and Kobry El Koba Military Hospital. The patients were divided into four groups according to their treatment regimens as follows: group A: 25 patients who received sofosbuvir (400 mg) and daclatasvir (60 mg) daily for 12 weeks; group B: 25 patients who received sofosbuvir (400 mg) and ledipasvir (90 mg) daily for 12 weeks; group C: 25 patients who received ombitasvir (12.5 mg), paritaprevir (75 mg), and ritonavir (50 mg) daily for 12 weeks; and group D: 25 patients who received sofosbuvir (400 mg) and simeprevir (150 mg) daily for 12 weeks. All patients were subjected to the following investigations: HCV quantitative PCR before and after 12 weeks of treatment, clinical and laboratory metabolic evaluation including alfa-fetoprotein level, thyroid profile assessment, ferritin level, pelvi-abdominal ultrasound, and FibroScan examination. Results: All patients achieved SVR after 12 weeks. FibroScan median decreased ( Conclusions: DAAs affect the metabolic profile of the treated patients. There is a noticed improvement in the FibroScan, NAFLD score, and lipid profile after achieving the SVR-12 weeks. However, LDL is increased after viral cure, mostly due to viral-host molecular interaction.