In our series, ATT was a contributing factor in 58% of all cases of DILI (n = 313) and in 76.6% of patients with drug-induced ALF. Others who presented with ALF included users of phenytoin (n = 5), dapsone (n = 3), paracetamol (n = 1), complementary medicine (n = 1), amoxicillin-clavulanate (n = 1), hormones (n = 1), atorvastatin (n = 1), and chemotherapeutics (n Enzalutamide = 2). How can the differences be explained? Were patients with only select types

of ALF admitted while others sought admission elsewhere? Moreover, is it possible to determine the proportion of patients with ALF among all ATT-caused DILI patients because such patients are reported by the institute?8 Despite the increasing prevalence of tuberculosis and acquired immune deficiency syndrome in the last decade, we were surprised to read about the decreasing incidence of ALF due to ATT and the absence of human immunodeficiency virus infection; this is contrary to our experience. In summary, ATT-induced ALF is a major cause of drug-induced ALF in India, but it is PI3K Inhibitor Library high throughput not the only cause; phenytoin, dapsone, and others also contribute. Inappropriate medications contribute to a large number of ATT-caused cases

of DILI and ALF, which are potentially preventable. A high Model for End-Stage Liver Disease score or a combination of the bilirubin level, prothrombin time, and creatinine level is associated with mortality, and patients may be selected for early referral for transplantation. Harshad Devarbhavi M.D., D.M.* † ‡, Ross Dierkhising M.S.† Dichloromethane dehalogenase §, Walter K. Kremers Ph.D.§ §, * Department of Gastroenterology, St. John’s Medical College Hospital, Bangalore, India, † William J. Von Liebig Transplant Center, ‡ Division of Gastroenterology,

Department of Internal Medicine, § Department of Health Sciences Research, Mayo Clinic and Mayo Clinic College of Medicine, Rochester, MN. “
“Cholesterol is an essential molecule for the life cycle of the hepatitis C virus (HCV). This review focuses on the roles of cholesterol in HCV infection and introduces HCV events related to cholesterol metabolism and applications for cholesterol metabolism as a therapeutic target. HCV appears to alter host lipid metabolism into its preferable state, which is clinically recognized as steatosis and hypocholesterolemia. While hepatic fatty acid and triglyceride syntheses are upregulated in chronic hepatitis C patients, no direct evidence of increased hepatic de novo cholesterol biosynthesis has been obtained. Impaired VLDL secretion from hepatocytes is suggested to increase intracellular cholesterol concentrations, which may lead to hypocholesterolemia. Clinically, lower serum cholesterol levels are associated with lower rates of sustained virological responses (SVR) to pegylated-interferon plus ribavirin therapy, but the reason remains unclear.