Currently, there is no proven therapy for NASH. In this study, we assessed the efficacy of statin therapy in NASH patients with dyslipidemia. Methods:  Twenty patients with biopsy-proven NASH with dyslipidemia who agreed to participate in this multicentric prospective study were enrolled. The

patients were treated for 12 months with pitavastatin 2 mg/day. Clinical and histological alterations were comparatively evaluated before and after treatment. Standard weight loss counseling was continued during the treatment period. Follow-up liver biopsy was performed in 13 patients. Results:  Twenty-five percent of patients had hyperlipoproteinemia type IIa and 75% had hyperlipoproteinemia type IIb at baseline. The levels of alanine aminotransferase, γ-glutamyl transpeptidase and

lipid profiles were significantly improved by the treatment with pitavastatin for 12 months. Especially, these improvements were prominent in NASH SB203580 in vivo patients with hyperlipoproteinemia type IIb. While non-alcoholic fatty liver disease activity score and fibrosis stage did not change significantly in all patients, they did improve in 54% and 42% in individual patients, respectively. Conclusion:  NASH-related metabolic parameters improved with therapy including histology in some patients. However, three of 13 patients Daporinad mouse had progression of fibrosis during the treatment. Our pilot study demonstrated the efficacy of pitavastatin for the treatment of NASH with dyslipidemia, especially

with hyperlipoproteinemia type IIb and controlled trials are needed in the future. “
“Hepatitis C virus (HCV) infection is a leading cause of cirrhosis, hepatocellular carcinoma, and liver decompensation, and an indication of liver transplantation in many countries; it affects approximately 170 million people worldwide.1 Combination therapy Methane monooxygenase with pegylated interferon (PEG-IFN) plus ribavirin (RBV) can achieve an overall sustained virological response (SVR) rate of 54–63%.2–4 Furthermore, East Asian patients have higher SVR rates for HCV genotype 1 (HCV-1) infection than Western patients, and comparable rates for HCV-2 infection.5–9 Recently, adding direct acting antivirals (DAA) to PEG-IFN plus RBV has further increased SVR rates to 63–75% and 59–66% in untreated and treatment-experienced Western HCV-1 patients, respectively.10–13 Although prior studies showed that various pretreatment factors, such as age, sex, body mass index, insulin resistance, hepatic steatosis/fibrosis, ethnicity, HCV viral load, and HCV genotype, are all associated with SVR, the discovery of early HCV viral kinetics after IFN-based therapy has shed new light on the individualization of HCV therapy. Patients with a low baseline viral load and rapid virological response (RVR) can receive a truncated duration of therapy without compromising the SVR rates, while those with a high baseline viral load or without RVR should receive standard or even extended duration of therapy to secure SVR.