Christine M. Hunt, Julie I. Papay, Vid Stanulovic, Arie Regev – 13 March 2017 – Drug‐induced hepatocellular injury is identified internationally by alanine aminotransferase (ALT) levels equal to or exceeding 5× the upper limit of normal (ULN) appearing within 3 months of drug initiation, after alternative causes are excluded. Upon withdrawing the suspect drug, ALT generally decrease by 50% or more. With drug readministration, a positive rechallenge has recently been defined by an ALT level of 3‐5× ULN or greater.

Marie Sinclair, Anthony Schelleman, Daljean Sandhu, Peter W. Angus – 13 March 2017 – We report a case of dramatic systemic inflammatory symptoms and biochemical signs of inflammation related to multiple hepatic adenomas that completely resolved after cessation of the oral contraceptive pill (OCP) and associated adenoma regression. This represents a case of dramatic symptoms that resolved after estrogen withdrawal alone. (Hepatology 2017;66:989–991).

Christine M. Hunt, Julie I. Papay, Vid Stanulovic, Arie Regev – 13 March 2017 – Drug‐induced hepatocellular injury is identified internationally by alanine aminotransferase (ALT) levels equal to or exceeding 5× the upper limit of normal (ULN) appearing within 3 months of drug initiation, after alternative causes are excluded. Upon withdrawing the suspect drug, ALT generally decrease by 50% or more. With drug readministration, a positive rechallenge has recently been defined by an ALT level of 3‐5× ULN or greater.

Fernando Bril, Kenneth Cusi – 13 March 2017

Yong He, Dechun Feng, Man Li, Yanhang Gao, Teresa Ramirez, Haixia Cao, Seung‐Jin Kim, Yang Yang, Yan Cai, Cynthia Ju, Hua Wang, Jun Li, Bin Gao – 13 March 2017 – Acetaminophen (APAP) overdose is a leading cause of acute liver failure worldwide, in which mitochondrial DNA (mtDNA) released by damaged hepatocytes activates neutrophils through binding of Toll‐like receptor 9 (TLR9), further aggravating liver injury. Here, we demonstrated that mtDNA/TLR9 also activates a negative feedback pathway through induction of microRNA‐223 (miR‐223) to limit neutrophil overactivation and liver injury.

Yingyun Yang, Ye Zhou, Jin Hou, Chunmei Bai, Zhenyang Li, Jia Fan, Irene O.L. Ng, Weiping Zhou, Huichuan Sun, Qiongzhu Dong, Joyce M.F. Lee, Chung‐Mau Lo, Kwan Man, Yun Yang, Nan Li, Guoshan Ding, Yizhi Yu, Xuetao Cao – 13 March 2017 – Adjuvant interferon‐α (IFN‐α) therapy is used to control certain types of cancer in clinics. For hepatocellular carcinoma (HCC), IFN‐α therapy is effective in only a subgroup of patients; therefore, identifying biomarkers to predict the response to IFN‐α therapy is of high significance and clinical utility.

Anna D. Kosinska, Leila Pishraft‐Sabet, Weimin Wu, Zhong Fang, Marzena Lenart, Jieliang Chen, Kirsten K. Dietze, Cong Wang, Thekla Kemper, Yong Lin, Shiou‐Hwei Yeh, Jia Liu, Ulf Dittmer, Zhenghong Yuan, Michael Roggendorf, Mengji Lu – 13 March 2017 – Hepatitis B virus (HBV) infection shows significant gender‐related differences in pathogenesis, disease progression, and development of hepatocellular carcinoma. The gender‐associated differences in HBV replication and viral protein levels may be associated with distinct HBV‐specific immune responses in the host.

Femke Stelma, Meike H. van der Ree, Marjan J. Sinnige, Anthony Brown, Leo Swadling, J. Marleen L. de Vree, Sophie B. Willemse, Marc van der Valk, Paul Grint, Steven Neben, Paul Klenerman, Eleanor Barnes, Neeltje A. Kootstra, Hendrik W. Reesink – 11 March 2017 – MicroRNA‐122 is an important host factor for the hepatitis C virus (HCV). Treatment with RG‐101, an N‐acetylgalactosamine‐conjugated anti‐microRNA‐122 oligonucleotide, resulted in a significant viral load reduction in patients with chronic HCV infection. Here, we analyzed the effects of RG‐101 therapy on antiviral immunity.

Luigia Florimonte, Massimo Iavarone, Massimo Castellani, Mariagiulia Longo, Francesco Pallotti, Lorenzo Maffioli, Eva Orunesu, Riccardo Benti – 10 March 2017

Ryan J. Schulze, Karuna Rasineni, Shaun G. Weller, Micah B. Schott, Barbara Schroeder, Carol A. Casey, Mark A. McNiven – 10 March 2017 – Alcohol consumption is a well‐established risk factor for the onset and progression of fatty liver disease. An estimated 90% of heavy drinkers are thought to develop significant liver steatosis. For these reasons, an increased understanding of the molecular basis for alcohol‐induced hepatic steatosis is important.