FIB‐4 stage of liver fibrosis predicts incident heart failure among HIV‐infected and uninfected patients

Kaku A. So‐Armah, Joseph K. Lim, Vincent Lo Re, Janet P. Tate, Chung‐Chou H. Chang, Adeel A. Butt, Cynthia L. Gibert, David Rimland, Vincent C. Marconi, Matthew B. Goetz, Maria C. Rodriguez‐Barradas, Matthew J. Budoff, Hilary A. Tindle, Jeffrey H. Samet, Amy C. Justice, Matthew S. Freiberg, for the Veterans Aging Cohort Study Project Team – 24 May 2017 – Liver fibrosis is common, particularly in individuals who are infected with human immunodeficiency virus (HIV). HIV‐infected individuals have excess congestive heart failure (CHF) risk compared with uninfected people.

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Omair Atiq, Jasmin Tiro, Adam C. Yopp, Adam Muffler, Jorge A. Marrero, Neehar D. Parikh, Caitlin Murphy, Katharine McCallister, Amit G. Singal – 24 May 2017

Death and liver transplantation within 2 years of onset of drug‐induced liver injury

Paul H. Hayashi, Don C. Rockey, Robert J. Fontana, Hans L. Tillmann, Neil Kaplowitz, Huiman X. Barnhart, Jiezhan Gu, Naga P. Chalasani, K. Rajender Reddy, Averell H. Sherker, Jay H. Hoofnagle, for the Drug‐Induced Liver Injury Network (DILIN) Investigators – 23 May 2017 – Drug‐induced liver injury (DILI) is an important cause of death and indication for liver transplantation (fatality). The role of DILI in these fatalities is poorly characterized, particularly when fatalities occur >26 weeks after DILI onset.

Prevalence and economic burden of extrahepatic manifestations of hepatitis C virus are underestimated but can be improved with therapy

Nancy Reau, Francis Vekeman, Eric Wu, Yanjun Bao, Yuri Sanchez Gonzalez – 23 May 2017 – Despite guideline recommendations, access to hepatitis C virus (HCV) treatment is frequently restricted, with some payers approving therapy for only those with advanced disease or cirrhosis. However, delaying potentially curative treatment until the development of advanced liver disease may have costly consequences in terms of both hepatic complications and extrahepatic manifestations (EHMs) of HCV.

TGR5 contributes to hepatic cystogenesis in rodents with polycystic liver diseases through cyclic adenosine monophosphate/Gαs signaling

Tatyana V. Masyuk, Anatoliy I. Masyuk, Maria Lorenzo Pisarello, Brynn N. Howard, Bing Q. Huang, Pui‐Yuen Lee, Xavier Fung, Eduard Sergienko, Robert J. Ardecky, Thomas D.Y. Chung, Anthony B. Pinkerton, Nicholas F. LaRusso – 23 May 2017 – Hepatic cystogenesis in polycystic liver disease is associated with increased levels of cyclic adenosine monophosphate (cAMP) in cholangiocytes lining liver cysts. Takeda G protein receptor 5 (TGR5), a G protein–coupled bile acid receptor, is linked to cAMP and expressed in cholangiocytes.

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