Filipe S. Cardoso, Michelle Gottfried, Shannan Tujios, Jody C. Olson, Constantine J. Karvellas, For the US Acute Liver Failure Study Group – 6 November 2017

Elena Khanova, Raymond Wu, Wen Wang, Rui Yan, Yibu Chen, Samuel W. French, Cristina Llorente, Stephanie Q. Pan, Qihong Yang, Yuchang Li, Raul Lazaro, Charles Ansong, Richard D. Smith, Ramon Bataller, Timothy Morgan, Bernd Schnabl, Hidekazu Tsukamoto – 6 November 2017 – Alcoholic hepatitis (AH) continues to be a disease with high mortality and no efficacious medical treatment. Although severe AH is presented as acute on chronic liver failure, what underlies this transition from chronic alcoholic steatohepatitis (ASH) to AH is largely unknown.

Aditi Varshney, Jiban J. Panda, Avishek K. Singh, Nitin Yadav, Chhagan Bihari, Subhrajit Biswas, Shiv K. Sarin, Virander S. Chauhan – 6 November 2017 – Hepatocellular carcinoma (HCC) is an aggressive tumor with limited systemic and locoregional modalities of treatment. Although microRNA (miRNA) based therapies have significant potential, their targeted delivery remains a major challenge. miR‐199a‐3p functions as an important tumor suppressor in HCC, which regulates various cellular processes.

Chetan Kalal, Akash Shukla, Ravi Mohanka, Samir Shah – 6 November 2017

Kenneth E. Sherman, Marion G. Peters, David Thomas – 6 November 2017 – Among persons living with human immunodeficiency virus (HIV) infection, liver disease remains a major cause of morbidity and mortality. While the etiologies are varied and often overlapping in the individual patient, the underlying mechanisms, including oxidative stress, direct activation of stellate cells, HIV interaction with hepatocytes, and bacterial translocation with systemic immune activation, seem to be unifying characteristics.

Cameron Sikavi, Phillip H. Chen, Alex D. Lee, Elena G. Saab, Gina Choi, Sammy Saab – 6 November 2017 – The treatment of chronic hepatitis C (HCV) in human immunodeficiency virus 1 (HIV)–infected individuals has been historically marked by low sustained virologic response (SVR) rates in comparison to those without HIV infection, resulting in the Food and Drug Administration labeling those coinfected as a “special population with an unmet medical need.” We systematically reviewed the treatment of chronic HCV infection in those infected with HIV.

Cyrielle Caussy, Mosab H. Alquiraish, Phirum Nguyen, Carolyn Hernandez, Sandra Cepin, Lynda E. Fortney, Veeral Ajmera, Ricki Bettencourt, Summer Collier, Jonathan Hooker, Ethan Sy, Emily Rizo, Lisa Richards, Claude B. Sirlin, Rohit Loomba – 6 November 2017 – The optimal threshold of controlled attenuation parameter (CAP) for the detection of hepatic steatosis using both M and XL probe is unknown in nonalcoholic fatty liver disease (NAFLD).

Dar‐In Tai, Wen‐Juei Jeng, Chun‐Yen Lin – 6 November 2017 – Genome‐wide association studies have indicated that human leukocyte antigen (HLA)‐DP and HLA‐DQ play roles in persistent hepatitis B virus (HBV) infection in Asia. To understand the evolution of HBV‐related single nucleotide polymorphisms (SNPs) and to correlate these SNPs with chronic HBV infection among different populations, we conducted a global perspective study on hepatitis‐related SNPs. We selected 12 HBV‐related SNPs on the HLA locus and two HBV and three hepatitis C virus immune‐related SNPs for analysis.

Olympia E. Anastasiou, Foteini Almpani, Anke Herrmann, Guido Gerken, Markus Ditschkowski, Sandra Ciesek – 6 November 2017 – Hepatitis B virus (HBV) reactivation (HBVr) in recipients of allogeneic hematopoetic stem cells (aHSCs) appears heterogeneously with respect to its frequency, manifestation, and outcome. The aim of this study was to present data from a large German cohort of recipients of aHSC transplantation (aHSCT), focusing on the incidence of HBVr in antibody to hepatitis B core antigen (anti‐HBc)‐positive aHSCT recipients, its clinical outcome, and the role of mutations in HBV.

Wen‐Juei Jeng, Yi‐Cheng Chen, Rong‐Nan Chien, I‐Shyan Sheen, Yun‐Fan Liaw – 6 November 2017 – Hepatitis B surface antigen (HBsAg) loss is a rare event during nucleos(t)ide analogue (Nuc) therapy. Limited data suggest that stopping Nuc therapy may increase HBsAg loss rate in hepatitis B e antigen–negative patients. A large study was conducted to investigate this issue in more detail. Of the 1,075 hepatitis B e antigen–negative patients treated with Nuc for a median of 156 (61‐430) weeks, 5 showed HBsAg seroclearance during treatment at an estimated annual incidence of 0.15%.