Quality of life is significantly impaired in long‐term survivors of acute liver failure and particularly in acetaminophen‐overdose patients

Amol S. Rangnekar, Caitlyn Ellerbe, Valerie Durkalski, Brendan McGuire, William M. Lee, Robert J. Fontana – 18 June 2013 – Functional outcomes for long‐term survivors of acute liver failure (ALF) are not well characterized. The aim of this prospective study was to determine health‐related quality of life in long‐term adult ALF survivors. Acute Liver Failure Study Group registry participants completed the Centers for Disease Control and Prevention Health‐Related Quality of Life 14 and Short Form 36 (SF‐36) questionnaires at 1‐ and/or 2‐year follow‐up study visits.

Improved Waiting‐List Outcomes in Argentina After the Adoption of a Model for End‐Stage Liver Disease–Based Liver Allocation Policy

Nora Gabriela Cejas, Federico G. Villamil, Javier C. Lendoire, Viviana Tagliafichi, Arturo Lopez, Daniela Hansen Krogh, Carlos A. Soratti, Liliana Bisigniano – 15 June 2013 – In July 2005, Argentina became the first country after the United States to introduce the Model for End‐Stage Liver Disease (MELD) for organ allocation. In this study, we investigated waiting‐list (WL) outcomes (n = 3272) and post–liver transplantation (LT) survival in 2 consecutive periods of 5 years before and after the implementation of a MELD‐based allocation policy.

Calcineurin Inhibitor–Free Mycophenolate Mofetil/Sirolimus Maintenance in Liver Transplantation: The Randomized Spare‐the‐Nephron Trial

Lewis Teperman, Dilip Moonka, Anthony Sebastian, Linda Sher, Paul Marotta, Christopher Marsh, Baburao Koneru, John Goss, Dennis Preston, John P. Roberts, Spare‐the‐Nephron Trial Liver Transplantation Study Group – 15 June 2013 – Mycophenolate mofetil (MMF) and sirolimus (SRL) have been used for calcineurin inhibitor (CNI) minimization to reduce nephrotoxicity following liver transplantation.

Population‐based epidemiology, malignancy risk, and outcome of primary sclerosing cholangitis

Kirsten Boonstra, Rinse K. Weersma, Karel J. Erpecum, Erik A. Rauws, B.W. Marcel Spanier, Alexander C. Poen, Karin M. Nieuwkerk, Joost P. Drenth, Ben J. Witteman, Hans A. Tuynman, Anton H. Naber, Paul J. Kingma, Henk R. Buuren, Bart Hoek, Frank P. Vleggaar, Nan Geloven, Ulrich Beuers, Cyriel Y. Ponsioen, on behalf of the EpiPSCPBC Study Group – 14 June 2013 – Extensive population‐based studies are much needed to accurately establish epidemiology and disease course in patients with primary sclerosing cholangitis (PSC).

Hepatocyte nuclear factor‐4α reverses malignancy of hepatocellular carcinoma through regulating miR‐134 in the DLK1‐DIO3 region

Chuan Yin, Pei‐Qin Wang, Wen‐Ping Xu, Yuan Yang, Qing Zhang, Bei‐Fang Ning, Ping‐Ping Zhang, Wei‐Ping Zhou, Wei‐Fen Xie, Wan‐Sheng Chen, Xin Zhang – 14 June 2013 – Hepatocyte nuclear factor‐4α (HNF4α) is a dominant transcriptional regulator of hepatocyte differentiation and hepatocellular carcinogenesis. There is striking suppression of hepatocellular carcinoma (HCC) by HNF4α, although the mechanisms by which HNF4α reverses HCC malignancy are largely unknown.

Isolate‐dependent use of claudins for cell entry by hepatitis C virus

Sibylle Haid, Christina Grethe, Michael T. Dill, Markus Heim, Lars Kaderali, Thomas Pietschmann – 14 June 2013 – Hepatitis C Virus (HCV) entry involves at least four cellular factors, including CD81, the scavenger receptor class B type I (SCARB‐1), occludin (OCLN), and claudin‐1 (CLDN1). In addition, CLDN6 and CLDN9 have been shown to substitute for CLDN1 as HCV entry factors in human nonliver cells. We examined the role of different CLDN proteins during HCV entry by using cell lines expressing either predominantly CLDN1 (Huh‐7.5) or CLDN6 (HuH6).

Liver transplantation normalizes serum hepcidin level and cures iron metabolism alterations in HFE hemochromatosis

Edouard Bardou‐Jacquet, Julie Philip, Richard Lorho, Martine Ropert, Marianne Latournerie, Pauline Houssel‐Debry, Dominique Guyader, Olivier Loréal, Karim Boudjema, Pierre Brissot – 14 June 2013 – Defects in human hemochromatosis protein (HFE) cause iron overload due to reduced hepatic hepcidin secretion. Liver transplantation (LT) is a key treatment for potential complications from HFE‐related hereditary hemochromatosis (HH). This study evaluated hepcidin secretion and iron burden after LT to elucidate HH pathophysiology.

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