The core domain of hepatitis C virus glycoprotein E2 generates potent cross‐neutralizing antibodies in guinea pigs

Patricia T. Vietheer, Irene Boo, Jun Gu, Kathleen McCaffrey, Stirling Edwards, Catherine Owczarek, Matthew P. Hardy, Louis Fabri, Rob J. Center, Pantelis Poumbourios, Heidi E. Drummer – 20 December 2016 – A vaccine that prevents hepatitis C virus (HCV) infection is urgently needed to support an emerging global elimination program. However, vaccine development has been confounded because of HCV's high degree of antigenic variability and the preferential induction of type‐specific immune responses with limited potency against heterologous viral strains and genotypes.

New therapeutic concepts in bile acid transport and signaling for management of cholestasis

Michael Trauner, Claudia Daniela Fuchs, Emina Halilbasic, Gustav Paumgartner – 20 December 2016 – The identification of the key regulators of bile acid (BA) synthesis and transport within the enterohepatic circulation has revealed potential targets for pharmacological therapies of cholestatic liver diseases.

New therapeutic concepts in bile acid transport and signaling for management of cholestasis

Michael Trauner, Claudia Daniela Fuchs, Emina Halilbasic, Gustav Paumgartner – 20 December 2016 – The identification of the key regulators of bile acid (BA) synthesis and transport within the enterohepatic circulation has revealed potential targets for pharmacological therapies of cholestatic liver diseases.

Screening for hepatocellular carcinoma: What is missing?

Neil J. Mehta, Aygul Dogan Celik, Marion G. Peters – 19 December 2016 – While there are guidelines from all major liver societies for the screening and management of hepatocellular carcinoma (HCC), many issues remain surrounding the actual practice of screening. This review discusses how to diagnose and screen HCC and more importantly, how well we diagnose and screen for HCC. Improved survival and outcomes after HCC diagnosis depend upon accurate diagnosis of cirrhosis and the timeliness of screening.

Human immunodeficiency virus–infected and uninfected adults with non–genotype 3 hepatitis C virus have less hepatic steatosis than adults with neither infection

Jennifer C. Price, Yifei Ma, Rebecca Scherzer, Natalie Korn, Kyle Tillinghast, Marion G. Peters, Susan M. Noworolski, Phyllis C. Tien – 16 December 2016 – Hepatic steatosis (HS) is common in individuals with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections, but the independent contributions of HCV and HIV to HS are unclear.

Metabolic and histological implications of intrahepatic triglyceride content in nonalcoholic fatty liver disease

Fernando Bril, Diana Barb, Paola Portillo‐Sanchez, Diane Biernacki, Romina Lomonaco, Amitabh Suman, Michelle H. Weber, Jeffrey T. Budd, Maria E. Lupi, Kenneth Cusi – 16 December 2016 – The cut‐off point of intrahepatic triglyceride (IHTG) content to define nonalcoholic fatty liver disease (NAFLD) by proton magnetic resonance spectroscopy (1H‐MRS) was established based on the 95th percentile in a group of healthy individuals (i.e., ≥5.56%).

Anti‐TNF‐α for necrotizing sarcoid granulomatosis of the liver

Marcial Sebode, Sören Weidemann, Malte Wehmeyer, Ansgar W. Lohse, Christoph Schramm – 16 December 2016 – We present a case of hepatosplenic necrotizing sarcoid granulomatosis, a variant form of “classical” sarcoidosis, that became clinically apparent in the form of multiple hepatic and splenic masses mimicking malignancy. Flow cytometry of intrahepatic T cells isolated from liver biopsy led to the targeted treatment with anti‐tumor necrosis factor‐alpha, which was highly effective in inducing remission. (Hepatology 2017;65:1410‐1412)

The ascending pathophysiology of cholestatic liver disease

Peter L.M. Jansen, Ahmed Ghallab, Nachiket Vartak, Raymond Reif, Frank G. Schaap, Jochen Hampe, Jan G. Hengstler – 16 December 2016 – In this review we develop the argument that cholestatic liver diseases, particularly primary biliary cholangitis and primary sclerosing cholangitis (PSC), evolve over time with anatomically an ascending course of the disease process. The first and early lesions are in “downstream” bile ducts. This eventually leads to cholestasis, and this causes bile salt (BS)–mediated toxic injury of the “upstream” liver parenchyma. BS are toxic in high concentration.

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