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Mise à jour le : 27-02-2017

Les derniers abstracts de la revue Journal of Hepatology :

    Date de mise en ligne : Dimanche 26 février 2017
    Nikolaj Worm Ørntoft, Ole Lajord Munk, Kim Frisch, Peter Ott, Susanne Keiding, Michael Sørensen
    Hepatobiliary transport kinetics of the conjugated bile acid tracer 11C-CSar quantified in healthy humans and patients by Positrion Emission Tomography (PET)
    Bile acids are important for intestinal uptake of lipophilic compounds and regulation of metabolism [1–5]. Since the major pool of bile acids undergoes enterohepatic circulation and de novo synthesis only plays a minor role, efficient hepatocellular uptake from blood and subsequent secretion into bile is essential to prevent hepatic and systemic accumulation of these potentially cytotoxic compounds [3,4]. This becomes particularly evident in liver diseases associated with varying degrees of cholestasis.

    Date de mise en ligne : Vendredi 24 février 2017
    Elisabeth Krones, Kathrin Eller, Marion J. Pollheimer, Silvia Racedo, Alexander H. Kirsch, Bianca Frauscher, Annika Wahlström, Marcus Ståhlman, Michael Trauner, Florian Grahammer, Tobias B. Huber, Karin Wagner, Alexander R. Rosenkranz, Hanns-Ulrich Marschall, Peter Fickert
    NorUrsodeoxycholic Acid Ameliorates Cholemic Nephropathy in Bile Duct Ligated Mice
    Impairment of renal function in liver disease represents a severe life-threatening event and may be related to numerous causes including hepatorenal syndrome (HRS) [1–4]. Especially cirrhotic patients with concomitant infections and those deeply jaundiced represent a high-risk group with dismal prognosis [5–8]. Notably, infection and cholestasis commonly coexist as inflammation-induced cholestasis [9], and infection also represents a major trigger for acute on chronic liver failure (ACLF) [10].

    Date de mise en ligne : Vendredi 24 février 2017
    Atsushi Oba, Shu Shimada, Yoshimitsu Akiyama, Taketo Nishikawaji, Kaoru Mogushi, Hiromitsu Ito, Satoshi Matsumura, Arihiro Aihara, Yusuke Mitsunori, Daisuke Ban, Takanori Ochiai, Atsushi Kudo, Hiroshi Asahara, Atsushi Kaida, Masahiko Miura, Minoru Tanabe, Shinji Tanaka
    ARID2 modulates DNA damage response in human hepatocellular carcinoma cells
    Hepatocellular carcinoma (HCC) is the sixth most common cancer and the third most leading cause of cancer-related death [1]. Chronic hepatitis and cirrhosis due to hepatitis B virus, hepatitis C virus infection, alcohol use, and metabolic diseases are the most prevalent risk factors for HCC, but the molecular mechanisms underlying hepatocarcinogenesis are complicated and remain unclear [1]. Recent genome-wide sequencing has identified recurrent mutations of chromatin-remodeling factors (25–60%) as well as TP53 (25–40%) and CTNNB1 (25–40%) mutations in HCC.

    Date de mise en ligne : Jeudi 23 février 2017
    Christine Bernsmeier, Emanuele Albano
    Liver dendritic cells and NAFLD evolution: a remaining open issue
    Due to the growing diffusion of metabolic syndrome Non-Alcoholic Fatty Liver Disease (NAFLD), is expected to become a major cause of cirrhosis and HCC worldwide within the next decade. However, the mechanisms responsible for NAFLD progression to nonalcoholic steatohepatitis (NASH) and fibrosis/cirrhosis are still largely unclear and this hampers the development of diagnostic tools to identify NAFLD patient at risk of progressive disease [1]. In the attempt of unravelling the complex network responsible to sustain lobular inflammation in NASH, growing attention has been given to liver myeloid cells including hepatic dendritic cells (HDCs), addressed by Heier et al.

    Date de mise en ligne : Jeudi 23 février 2017
    M. Merino-Azpitarte, E. Lozano, M.J. Perugorria, A. Esparza-Baquer, O. Erice, A. Santos-Laso, C.J. O'Rourke, J.B. Andersen, R. Jiménez-Agüero, A. Lacasta, M. D'Amato, O. Briz, N. Jalan-Sakrikar, R.C. Huebert, K.M. Thelen, S.A. Gradilone, A.M. Aransay, J.L. Lavín, M.G. Fernández-Barrena, A. Matheu, M. Marzioni, G.J. Gores, L. Bujanda, J.J.G. Marin, J.M. Banales
    SOX17 Regulates Cholangiocyte Differentiation and Acts as a Tumor Suppressor in Cholangiocarcinoma
    Cholangiocarcinoma (CCA) is a heterogeneous group of biliary malignancies with poor prognosis [1]. The etiopathogenesis remains largely unknown [1]. Incidence is rising worldwide and CCA already represents the second most common primary liver tumor and ∼3% of all gastrointestinal cancers [1]. CCA is generally asymptomatic in early stages and is commonly diagnosed at advanced phases, when symptoms associated with biliary obstruction arise; this circumstance compromises the potential therapeutic options [1].

    Date de mise en ligne : Mardi 21 février 2017
    Panu K. Luukkonen, You Zhou, P.A. Nidhina Haridas, Om P. Dwivedi, Tuulia Hyötyläinen, Ashfaq Ali, Anne Juuti, Marja Leivonen, Taru Tukiainen, Linda Ahonen, Emma Scott, Jeremy M. Palmer, Johanna Arola, Marju Orho-Melander, Petter Vikman, Quentin M. Anstee, Vesa M. Olkkonen, Matej Orešič, Leif Groop, Hannele Yki-Järvinen
    Impaired hepatic lipid synthesis from polyunsaturated fatty acids in TM6SF2 E167K variant carriers with NAFLD
    Common non-alcoholic fatty liver disease (NAFLD) is associated with features of the metabolic syndrome, such as hypertriglyceridemia, and increased risk of cardiovascular disease (CVD) [1]. In 2014, a nonsynonymous adenine-to-guanine substitution (rs58542926) replacing glutamate at residue 167 with lysine (E167K) in transmembrane 6 superfamily member 2 (TM6SF2) was shown to increase liver fat content [2,3] and the risk of liver fibrosis [4]. In these and several subsequent studies, variant allele carriers (TM6SF2EK/KK) were found to be neither more obese nor more insulin-resistant than non-carriers (TM6SF2EE) [2,5–12].

    Date de mise en ligne : Mardi 21 février 2017
    Lionel Piroth, Linda Wittkop, Karine Lacombe, Eric Rosenthal, Camille Gilbert, Patrick Miailhes, Patrizia Carrieri, Julie Chas, Isabelle Poizot-Martin, Anne Gervais, Stéphanie Dominguez, Didier Neau, David Zucman, Eric Billaud, Philippe Morlat, Hugues Aumaitre, Caroline Lascoux-Combe, Anne Simon, Olivier Bouchaud, Elina Teicher, Firouzé Bani-Sadr, Laurent Alric, Daniel Vittecoq, François Boué, Claudine Duvivier, Marc-Antoine Valantin, Laure Esterle, François Dabis, Philippe Sogni, Dominique Salmon, ANRS CO13 HEPAVIH study group
    Efficacy and safety of direct-acting antiviral regimens in HIV/HCV-coinfected patients - French ANRS CO13 HEPAVIH cohort
    Hepatitis C virus (HCV) coinfection is frequent among people living with HIV, with a reported prevalence of 15% to 30% [1–3] and up to 82% among injecting drug users [4]. HCV coinfection has become a major cause of illness and death in the era of combination antiretroviral therapy (cART) [5]. Sustained virological responses (SVR) to interferon-based anti-HCV therapy used to be less frequent in case of HIV coinfection [6–8]. Since 2011, the treatment of chronic hepatitis C has improved dramatically with the advent of direct-acting antiviral (DAA) drugs [9].

    Date de mise en ligne : Vendredi 17 février 2017
    Leon A. Adams, Richard K. Sterling
    Developing a new algorithm to diagnose advanced liver fibrosis: A lift or a nudge in the right direction?
    Accurate identification of liver disease severity and fibrosis stage is paramount in the management of those with chronic liver disease. In the past, this was often done by liver biopsy. However, due to it’s invasiveness and risks of bleeding, pain, and sampling error, non-invasive assessment of liver disease has gained increasing attention over the last decade. Non-invasive tests can be divided into serum tests and imaging tests. Although standard “liver function” tests, such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are inaccurate when used alone, several models have been developed that use them in combination with other markers of advanced liver disease, such as platelet count.

    Date de mise en ligne : Vendredi 17 février 2017
    Manuel Ramos-Casals, Anna Linda Zignego, Clodoveo Ferri, Pilar Brito-Zerón, Soledad Retamozo, Milvia Casato, Peter Lamprecht, Alessandra Mangia, David Saadoun, Athanasios G Tzioufas, Zobair M Younossi, Patrice Cacoub, the International Study Group of Extrahepatic Manifestations related to HCV (ISG-EHCV) (See Appendix 1)
    Evidence-based recommendations on the management of extrahepatic manifestations of chronic hepatitis C virus infection
    The hepatitis C virus (HCV), a linear, single-stranded RNA virus identified in 1989, is a hepatotropic virus that causes liver cirrhosis and hepatocellular cancer and is a global health problem. It is recognized as one of the hepatic viruses most often associated with the development of extrahepatic manifestations, which can be classified according to the principal underlying etiopathogenic process (autoimmune, inflammatory, metabolic or neoplastic) [1]. HCV infected patients with extrahepatic involvement require a multidisciplinary approach and a complex therapeutic management.

    Date de mise en ligne : Jeudi 16 février 2017
    Camille Blériot, Marc Lecuit
    RIPK1, a key survival factor for hepatocytes
    “A living cell is a cell that has succeeded day after day in suppressing, for a time yet, its self-destruction” [1]. Staying alive is a continuing struggle, at the cellular and multicellular level. During development and upon various stimuli, cell death can be essential for survival of multicellular organisms. Hundreds of millions of years of evolution have let to the selection of regulated cell death (RCD) mechanisms. The most famous RCD process, referred to as apoptosis, has been described during the early 70’s [2], and has been since shown to be involved in many developmental and physiological processes [3].

    Date de mise en ligne : Jeudi 16 février 2017
    Søren S Olesen, Clive D Jackson, Marsha Y Morgan
    Tools and tactics for improving diagnosis of hepatic encephalopathy
    We read with interest the paper from Montagenese et al. (2016) on the possible use of two novel approaches to determine 'neuropsychiatric normality' in the context of a diagnosis of hepatic encephalopathy (HE) [1]. The authors challenge the conventional use of psychometric and neurophysiological testing based on reference to normative data and suggest that there may be advantages in defining ‘normality’ in terms of single patients’ lifelong performance and/or in terms of risk. Three cases serve as examples for the relevance of the suggested approaches.

    Date de mise en ligne : Jeudi 16 février 2017
    Sara Montagnese, Michele De Rui, Paolo Angeli, Piero Amodio
    Reply to: Tools and tactics for improving diagnosis of hepatic encephalopathy
    We have read with interest the letter by Olesen and colleagues [1], and we are grateful to them for acknowledging that our two new proposals [2] have “merit”.

    Date de mise en ligne : Mardi 14 février 2017
    Rohit Sinha, Khalida A. Lockman, Nethmee Mallawaarachchi, Marcus Robertson, John N. Plevris, Peter C. Hayes
    Carvedilol use is associated with improved survival in patients with liver cirrhosis and ascites
    Liver cirrhosis remains a leading cause of death worldwide. In the United Kingdom alone mortality from liver cirrhosis has risen dramatically in the last decade tandem with the rise in alcohol consumption and the epidemic of obesity [1]. Portal hypertension underlies many of its fatal complications. For this reason, non-selective beta-blocker (NSBB) was proposed to be beneficial in the management of patients with varices. Its unselective beta-blockade reduces cardiac output and splanchnic blood flow while the unopposed effect of alpha 1 receptors leads to splanchnic vasoconstriction thus reducing portal pressure and its attendant complications [2,3].

    Date de mise en ligne : Mardi 14 février 2017
    Zhipeng Yan, Jing Zeng, Youjun Yu, Kunlun Xiang, Hui Hu, Xue Zhou, Lili Gu, Li Wang, Jie Zhao, John A.T. Young, Lu Gao
    HBVcircle: a Novel Tool to Investigate Hepatitis B Virus Covalently Closed Circular DNA
    Hepatitis B virus (HBV) is one of the most dangerous human pathogens. A safe and effective vaccine has been available for longer than two decades; however, approximately 2 billion people worldwide have been infected with HBV and more than 350 million people are chronically infected [1]. Chronic Hepatitis B (CHB) infection predisposes its host to severe liver disease, including liver cirrhosis and hepatocellular carcinoma. HBV infection is ranked among the top health priorities worldwide. The currently approved drugs have contributed to substantial progress in CHB treatment; however, the cure rate remains less than 10% [2].

    Date de mise en ligne : Mardi 14 février 2017
    Roger Williams, Vicente Arroyo
    The Legacy of Juan Rodés (1938–2017), a European Leader in Hepatology and Clinical Research
    Hepatologists throughout the world, as well as, the scientific community of Spain and many others including the patients who owe so much to the work of the Liver Unit of the Hospital Clinic of Barcelona (Barcelona Liver Unit, BLU), will be mourning the passing of Juan Rodés. His inspirational lead to the Founding of the BLU and its seminal work represented the very best of clinical scientific enquiry.

    Date de mise en ligne : Mardi 14 février 2017
    Antonella Mosca, Valerio Nobili, Rita De Vito, Annalisa Crudele, Eleonora Scorletti, Alberto Villani, Anna Alisi, Christopher D. Byrne
    Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents
    Non-alcoholic fatty liver disease (NAFLD) is now largely regarded as the hepatic manifestation of metabolic syndrome (MetS) and NAFLD represents the most frequent chronic liver disease in children in Western countries [1]. NAFLD begins with the development of liver lipid accumulation and the condition progresses over time with the development of liver inflammation and fibrosis (non-alcoholic steatohepatitis or NASH). Although it was initially thought that NAFLD was a relatively harmless condition in children and adolescents, recent evidence shows that NASH occurs in this young population [2].

    Date de mise en ligne : Lundi 13 février 2017
    Thomas Vanwolleghem, Andre Boonstra
    Focus on the liver: host–virus interactions in HBV
    The hepatitis B virus (HBV) is a hepatotropic virus, yet most of the knowledge on its biology and the immune response induced by HBV are not obtained from liver studies, but rather from studies with blood. Since the cellular make-up of the liver is entirely different from blood, and since HBV exclusively replicates in the liver, the most relevant site to address the interaction of HBV with the host is the intrahepatic compartment.

    Date de mise en ligne : Lundi 13 février 2017
    Annalisa Berzigotti
    Non invasive evaluation of portal hypertension using ultrasound elastography
    Portal hypertension (PH) leads to serious complications such as bleeding from gastro-esophageal varices, ascites and porto-systemic encephalopathy in patients with chronic liver disease (CLD). Since the gold-standard methods for assessing PH and its complications (measurement of hepatic venous pressure gradient, HVPG; endoscopy), are invasive expensive and not available at all centers, non-invasive methods have been increasingly investigated in the last 20 years. The present review focuses on the role of ultrasound elastography, a novel group of non-invasive techniques able to measure stiffness in target organs, to identify the presence, severity and risk of complications of PH.

    Date de mise en ligne : Vendredi 10 février 2017
    Giuseppe Cabibbo, Salvatore Petta, Marco Barbara, Simona Attardo, Laura Bucci, Fabio Farinati, Edoardo G. Giannini, Giulia Negrini, Francesca Ciccarese, Gian Lodovico Rapaccini, Maria Di Marco, Eugenio Caturelli, Marco Zoli, Franco Borzio, Rodolfo Sacco, Roberto Virdone, Fabio Andrea Marra Mega, Filomena Morisco, Luisa Benvegnù, Antonio Gasbarrini, Gianluca Svegliati-Baroni, Francesco Giuseppe Foschi, Andrea Olivani, Alberto Masotto, Gerardo Nardone, Antonio Colecchia, Marcello Persico, Antonio Craxì, Franco Trevisani, Calogero Cammà, for the Italian Liver Cancer (ITA.LI.CA) group
    Hepatic Decompensation is the Major Driver of Death In HCV-infected cirrhotic patients with successfully treated early hepatocellular carcinoma
    The prognosis of patients with cirrhosis due to hepatitis C virus (HCV) is finally decided by the progression towards hepatic decompensation and hepatocellular carcinoma (HCC), the latter being the leading cause of mortality in patients with compensated cirrhosis. [1,2] HCV cirrhotic patients, regardless of HCV clearance, deserve surveillance for HCC to allow diagnosis of early disease stage (Barcelona Clinic Liver Cancer Stage [BCLC] 0 or A) passible of potentially curative treatments, such as like liver transplantation or, in most cases surgical resection or local ablation.

    Date de mise en ligne : Vendredi 10 février 2017
    Barbara Oliviero, Stefania Mantovani, Stefania Varchetta, Dalila Mele, Giulia Grossi, Serena Ludovisi, Elisa Nuti, Armando Rossello, Mario U. Mondelli
    Hepatitis C virus-Induced NK Cell Activation Causes Metzincin-Mediated CD16 Cleavage and Impaired Antibody-Dependent Cytotoxicity
    Natural killer (NK) cells are a major component of innate immunity, representing the first line of defense against pathogens and malignant cells. The activity of NK cells is finely tuned by several membrane receptors able to switch the NK function towards activation or inhibition after ligand recognition and interaction [1]. NK cells can recognize tumor or virus-infected cells without prior sensitization [2] and directly kill them by release of cytoplasmic granules containing cytolytic molecules such as granzyme and perforin [3].

    Date de mise en ligne : Vendredi 10 février 2017
    Suguru Yamashita, Junichi Shindoh, Takashi Mizuno, Yun Shin Chun, Claudius Conrad, Thomas A. Aloia, Jean-Nicolas Vauthey
    Hepatic Atrophy Following Preoperative Chemotherapy Predicts Hepatic Insufficiency after Resection of Colorectal Liver Metastases
    For patients with colorectal liver metastases (CLM), the introduction of effective systemic therapy and an increase in the utilization of extensive hepatectomy have led to significant improvements in long-term survivals during past decades [1]. However, while the perioperative mortality rate for hepatic resection is well below 5%, extensive preoperative chemotherapy remains a leading cause of morbidity and mortality [2–9].

    Date de mise en ligne : Vendredi 10 février 2017
    Hua Wu, Su Yao, Shen Zhang, Jing-Ru Wang, Peng-Da Guo, Xiu-Ming Li, Wen-Juan Gan, Lin Mei, Tian-Ming Gao, Jian-Ming Li
    Elevated expression of Erbin destabilizes ERα protein and promotes tumorigenesis in hepatocellular carcinoma
    Hepatocellular carcinoma (HCC) is one of the most prevalent cancers in the world. Epidemiologically, the incidence of HCC in males is 2- to 11-fold higher than in females [1], and the male patients with HCC usually have a poorer prognosis than female patients with HCC [2], suggesting the roles of sex hormones and their receptors in HCC.

    Date de mise en ligne : Vendredi 10 février 2017
    Ryo Nakagawa, Ryosuke Muroyama, Chisato Saeki, Kaku Goto, Yoshimi Kaise, Kazuhiko Koike, Masanori Nakano, Yasuo Matsubara, Keiko Takano, Sayaka Ito, Masayuki Saruta, Naoya Kato, Mikio Zeniya
    miR-425 regulates inflammatory cytokine production in CD4+ T cells via N-Ras upregulation in primary biliary cholangitis
    Primary biliary cholangitis (PBC), formally known as primary biliary cirrhosis, is a progressive autoimmune liver disease of unknown pathogenesis that predominantly affects middle-aged females [1–3]. Ursodeoxycholic acid (UDCA) treatment slows the disease progression in most patients; nevertheless, 10 years after diagnosis, approximately 32% of PBC patients in a late histologic stage and approximately 6% of patients in an early histologic stage progress to liver transplantation or death due to liver failure [4].

    Date de mise en ligne : Vendredi 10 février 2017
    Hannah K. Drescher, Angela Schippers, Thomas Clahsen, Hacer Sahin, Heidi Noels, Mathias Hornef, Norbert Wagner, Christian Trautwein, Konrad L. Streetz, Daniela C. Kroy
    β7-Integrin and MAdCAM-1 play opposing roles during the development of non-alcoholic steatohepatitis
    Currently, non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease in western countries. It is associated with human morbidity and mortality [1–3]. NAFLD in general encompasses a spectrum of hepatic alterations that begins with steatosis and can easily progress to more advanced degrees such as NASH (Non-alcoholic steatohepatitis), cirrhosis and hepatocellular carcinoma (HCC) [4,5]. The growing medical need for therapy becomes clear if one considers that more than 20% of the general population have fatty livers and are thus at risk to develop NASH [6].

    Date de mise en ligne : Mercredi 08 février 2017
    Manuel Romero-Gómez, Helena Cortez-Pinto
    Detecting liver fat from viscoelasticity: How good is CAP in clinical practice? The need for universal cut-offs
    To detect and quantify hepatic steatosis has been a challenge in the last years. Hepatocyte steatosis is the hallmark of NAFLD but also could play a prognostic role in several liver diseases like viral hepatitis, hemochromatosis, Wilson disease or even autoimmune hepatitis. Presence of steatosis has been associated to faster fibrosis progression [1]. Thus, further development of non-invasive methods to detect and quantify hepatic steatosis is an unmet need, and a challenge. Serum-based methods have been reported to be able to detect hepatic steatosis, combining biochemical and anthropometric parameters like Hepatic Steatosis Index (HIS) or Fatty Liver Index (FLI).

    Date de mise en ligne : Mercredi 08 février 2017
    Jose Luis Calleja, Javier Crespo, Diego Rincón, Belén Ruiz-Antorán, Inmaculada Fernandez, Christie Perelló, Francisco Gea, Sabela Lens, Javier García-Samaniego, Begoña Sacristán, María García-Eliz, Susana Llerena, Juan Manuel Pascasio, Juan Turnes, Xavier Torras, Rosa Maria Morillas, Jordi Llaneras, Miguel A. Serra, Moises Diago, Conrado Fernández Rodriguez, Javier Ampuero, Francisco Jorquera, Miguel A. Simon, Juan Arenas, Carmen Alvarez Navascues, Rafael Bañares, Raquel Muñoz, Agustin Albillos, Zoe Mariño, for the Spanish Group for the Study of the Use of Direct-acting Drugs Hepatitis C Collaborating Group
    Effectiveness, safety and clinical outcomes of direct-acting antiviral therapy in HCV genotype 1 infection: results from a Spanish real world cohort
    An estimated 130–170 million people globally are chronically infected with the hepatitis C virus (HCV), and are at significant risk of liver disease, cirrhosis and hepatocellular carcinoma (HCC).[1] Successful treatment leading to a sustained virologic response (SVR) effectively cures HCV infection, significantly reducing the risk of HCV-related complications, liver transplantation, and death.[2,3] Interferon (IFN)-based therapies were associated with treatment-limiting side effects and resulted in SVR rates of 40–50% in patients with HCV genotype 1 infection,[4] the most prevalent genotype worldwide.

    Date de mise en ligne : Mercredi 08 février 2017
    Mei Zhou, Jian Luo, Michael Chen, Hong Yang, R. Marc Learned, Alex M. DePaoli, Hui Tian, Lei Ling
    Mice species-specific control of hepatocarcinogenesis and metabolism by FGF19/FGF15
    A cartoon summarizing species-specific control of hepatocarcinogenesis and metabolism by FGF19 and FGF15.

    Date de mise en ligne : Mercredi 08 février 2017
    Kapish Gupta, Qiushi Li, Jun Jun Fan, Eliza Li Shan Fong, Ziwei Song, Shupei Mo, Haoyu Tang, Inn Chuan Ng, Chan Way Ng, Pornteera Pawijit, Shuangmu Zhuo, Chen-Yuan Dong, Boon Chuan Low, Aileen Wee, Yock Young Dan, Pakorn Kanchanawong, Peter So, Virgile Viasnoff, Hanry Yu
    Actomyosin Contractility Drives Bile Regurgitation as an Early Response During Obstructive Cholestasis
    The biliary function of the liver is critical for survival, serving to eliminate toxic endo- and xenobiotics, cholesterol, and inflammatory mediators.[1] The apical membranes of adjacent hepatocytes form the bile canalicular lumen, an intercellular structure surrounded by a dynamic pericanalicular actin cortex (PAC), which actively contracts to propel secreted biliary fluid towards the bile ducts.[2,3] A variety of liver diseases result in impaired bile flow, or obstructive cholestasis.[4–7] These include extrahepatic etiologies such as biliary strictures, stones and biliary atresia in infants; as well as intrahepatic causes that include primary biliary cirrhosis, vanishing duct syndrome and, alcoholic and viral hepatitis.

    Date de mise en ligne : Mercredi 08 février 2017
    Qing-Lei Zeng, Guang-Hua Xu, Ji-Yuan Zhang, Wei Li, Da-Wei Zhang, Zhi-Qin Li, Hong-Xia Liang, Chun-Xia Li, Zu-Jiang Yu
    Generic ledipasvir-sofosbuvir for patients with chronic hepatitis C: a real-life observational study
    Chronic hepatitis C virus (HCV) infection is a major global health problem that affects 130-170 million people worldwide and represents a major cause of liver cirrhosis and hepatocellular carcinoma (HCC) [1–3]. In China, the overall prevalence of HCV infection is estimated to be 2.2% [1], and there is a prevalence of 9.6% in Henan province because of the higher prevalence of blood transmission routes [1,2,4]. Genotype 1 is the most common in China, and it accounts for 58.4% of all HCV-infected persons, and thereinto genotype 1b is predominant [1,2].

    Date de mise en ligne : Mercredi 08 février 2017
    Ruth Zimmermann, Christian Kollan, Patrick Ingiliz, Stefan Mauss, Daniel Schmidt, Viviane Bremer
    Real-world treatment for chronic hepatitis C infection in Germany. Analyses from drug prescription data, 2010 - 2015
    Hepatitis C virus (HCV) infection is widely spread across the world with chronic HCV infection being one of the leading causes of chronic liver disease, cirrhosis, and hepatocellular carcinoma [1–3]. A rising burden of HCV-related morbidity and mortality has been reported from industrial countries due to the accumulation of patients living with HCV infection long term [4,5].

    Date de mise en ligne : Mercredi 08 février 2017
    Carlo Ferrari, Carolina Boni, Marzia Rossi, Andrea Vecchi, Valeria Barili, Diletta Laccabue, Paola Fisicaro, Gabriele Missale
    T cell regulation in HBV-related chronic liver disease
    HBV-specific T cell dysfunction is believed to play a central role in the pathogenesis of chronic HBV persistence [1,2]. HBV-specific T cells are more dysfunctional within the liver than in the periphery [3] as a result of the inhibitory effect of different mechanisms. They are likely to be active simultaneously within the inflamed liver together contributing to T cell functional impairment [4,5]. Some of them have been directly characterized in HBV infection, while others are assumed to be relevant because of their general importance within the liver.

    Date de mise en ligne : Lundi 06 février 2017
    Srinivasan Dasarathy, Manuela Merli
    Reply to: Myokines: a promising therapeutic target for hepatic encephalopathy
    We read with great interest the letter by Yang and Luo on our work on hyperammonemia-mediated regulation of skeletal muscle mass and function[1]. We have previously reported that hyperammonemia transcriptionally upregulates myostatin in the skeletal muscle that results in impaired protein synthesis[2]. Even though myostatin is believed to be a myokine, and circulating myostatin levels are elevated in cirrhosis[2,3], there is currently no evidence to support a direct cerebral effect of myostatin beyond that related to its effects on the skeletal muscle.

    Date de mise en ligne : Vendredi 03 février 2017
    Chun Yang, Ai-Lin Luo
    Myokines: A promising therapeutic target for hepatic encephalopathy
    Recently, we read with great interest the review by Dasarathy and Merli [1] and the editorial by Rombouts et al. [2] regarding the effects of hyperammonemia on muscle activity and mass. These authors suggested a beneficial role of muscle in the prevention and treatment of hepatic encephalopathy (HE) by inhibiting wasting of muscle mass and facilitating muscle protein synthesis. We agree with their conclusion, and that this possibility provides a novel alternative for clinical treatment of HE.

    Date de mise en ligne : Vendredi 03 février 2017
    Auvro R. Mridha, Alexander Wree, Avril A.B. Robertson, Matthew M. Yeh, Casey D. Johnson, Derrick M. Van Rooyen, Fahrettin Haczeyni, Narci C.-H. Teoh, Christopher Savard, George N. Ioannou, Seth L. Masters, Kate Schroder, Matthew A. Cooper, Ariel E. Feldstein, Geoffrey C. Farrell
    NLRP3 inflammasome blockade reduces liver inflammation and fibrosis in experimental NASH in mice
    Non-alcoholic fatty liver disease (NAFLD) increases standardised mortality from cardiovascular events, common cancers, cirrhosis and hepatocellular carcinoma [1,2]. Adverse liver outcomes are confined to the 10–25% of NAFLD patients with liver fibrosis, particularly with the pathology of steatohepatitis (NASH) [3,4]. NASH occurs when overnutrition is complicated by insulin resistance and metabolic syndrome [2,5,6], particularly with a personal or family history of type 2 diabetes. Despite these connections, detailed mechanisms linking metabolic obesity to liver pathology are unclear.

    Date de mise en ligne : Vendredi 03 février 2017
    EASL Recommendations for Treatment of Hepatitis C 2016 Panel
    Reply to: Contradictory advice for people who inject drugs in the 2016 EASL Recommendations on Treatment of Hepatitis C
    The EASL Recommendations for Treatment of Hepatitis C 2016 Panel read with interest the letter by Grebely et al. pointing to supposedly contradictory advice on HCV therapy in people who inject drugs (PWIDs). The panel does not see any contradiction in the recommendations. EASL recommends that “All treatment-naïve and treatment-experienced patients with compensated or decompensated chronic liver disease related to HCV, who are willing to be treated and who have no contraindications to treatment, must be considered for therapy”.

    Date de mise en ligne : Vendredi 03 février 2017
    Jason Grebely, Tracy Swan, Matthew Hickman, Julie Bruneau, Philip Bruggmann, Olav Dalgard, Alain Litwin, Markus Backmund, Gregory J. Dore, International Network for Hepatitis in Substance Users
    Contradictory advice for people who inject drugs in the 2016 EASL Recommendations on Treatment of Hepatitis C
    The 2016 EASL Recommendations on Treatment of Hepatitis C provide important international guidance for the clinical management of HCV infection. The guidance is crucial in the environment of rapidly changing direct-acting antiviral (DAA) therapeutics. However, there are inherent contradictions within the EASL Recommendations for people who inject drugs (PWID). The EASL Recommendations state that “Treatment should be considered without delay in individuals at risk of transmitting HCV (e.g., active injection drug users)”, given the potential for preventing HCV transmission and reductions in HCV prevalence at a population-level.

    Date de mise en ligne : Mercredi 01 février 2017
    Stacey Prenner, Lisa B. VanWagner, Steven L. Flamm, Riad Salem, Robert J. Lewandowski, Laura Kulik
    Hepatocellular Carcinoma Decreases the Chance of Successful Hepatitis C Virus Therapy with Direct-Acting Antivirals
    Hepatitis C virus (HCV) has been the leading cause of cirrhosis in the United States for several decades [1]. Until recently, the standard of care for HCV treatment was interferon based therapy (IFN), which was wrought with intolerable side effects, long treatment duration, and suboptimal sustained virologic response (SVR) rates of approximately 40% for patients with genotype 1 [2,3]. SVR rates were lower in patients with advanced fibrosis [4]. The approval of direct acting antiviral agents (DAA) has subsequently revolutionized therapy for HCV.

    Date de mise en ligne : Mercredi 01 février 2017
    Mette Vesterhus, Anders Holm, Johannes Roksund Hov, Ståle Nygård, Erik Schrumpf, Espen Melum, Liv Wenche Thorbjørnsen, Vemund Paulsen, Knut Lundin, Inge Dale, Odd Helge Gilja, Serge J.L.B. Zweers, Morten Vatn, Frank G. Schaap, Peter L.M. Jansen, Thor Ueland, Helge Røsjø, Bjørn Moum, Cyriel Y. Ponsioen, Kirsten Muri Boberg, Martti Färkkilä, Tom H. Karlsen, Fridtjof Lund-Johansen
    Novel serum and bile protein markers predict primary sclerosing cholangitis disease severity and prognosis
    Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease characterized by progressing inflammation and fibrosis of the intra- and extrahepatic bile ducts, leading to cirrhosis in the majority of patients. PSC is frequently associated with inflammatory bowel disease (IBD) and other immunologic diseases. To date, liver transplantation is the only curative treatment in PSC, as there is no medical therapy of proven benefit to halt disease progression. The disease course is highly variable between PSC patients, with transplant-free survival ranging from 12-21 years in different cohorts [1,2].

    Date de mise en ligne : Mercredi 01 février 2017
    Stephen R. Atkinson, Michael J. Way, Andrew McQuillin, Marsha Y. Morgan, Mark R. Thursz
    Homozygosity for rs738409:G in PNPLA3 is associated with increased mortality following an episode of severe alcoholic hepatitis
    Cirrhosis is a major cause of global mortality accounting for around one million deaths per annum [1]. Alcohol misuse is the leading cause of cirrhosis in the Western world and is responsible for nearly half of cirrhosis-related deaths [2].

    Date de mise en ligne : Vendredi 27 janvier 2017
    Craig McClain, Shirish Barve
    A tale of two institutions
    Over the past five years, major concerns have been raised regarding reproducibility in science [1–4]. Journal articles documented inability to reproduce published scientific findings, and industry reported that drug targets selected for development based on scientific publications were not able to be validated. Some of the factors thought to contribute to these reproducibility problems range from selective reporting, to inclusion of only one sex, to poor documentation of techniques/methodology, to unrecognized experimental variables, to inappropriate statistical analysis, all the way to fabricated information.

    Date de mise en ligne : Mercredi 25 janvier 2017
    Len Verbeke, Frederik Nevens, Wim Laleman
    Steroidal or non-steroidal FXR agonists – Is that the question?
    Soon after its discovery in 2005, the Farnesoid X receptor (FXR) has been identified as a master regulator of bile acid homeostasis, with endogenous bile acids serving as its natural ligand [1]. As such, a systemic overload of bile acids instigates a negative feedback signal on both the liver and gut through FXR signaling, to prevent the novel synthesis and reabsorption of bile acids as a protective mechanism in conditions of cholestasis [2]. The chemical modification of bile acids such as chenodeoxycholic acid has led to the development of highly potent and selective steroidal FXR agonists, amongst which obeticholic acid (OCA) has received the most preclinical and clinical attention [3].

    Date de mise en ligne : Mercredi 25 janvier 2017
    Riccardo Lencioni, Robert Montal, Ferran Torres, Joong-Won Park, Thomas Decaens, Jean-Luc Raoul, Masatoshi Kudo, Charissa Chang, José Ríos, Valerie Boige, Eric Assenat, Yoon-Koo Kang, Ho-Yeong Lim, Ian Walters, Josep M. Llovet
    Objective response by mRECIST as a predictor and potential surrogate end-point of overall survival in advanced HCC
    In 60% of cases, patients with hepatocellular carcinoma (HCC) are diagnosed when tumors are no longer eligible for potentially curative therapies [1]. In this setting, only two treatments have been included in guidelines after demonstrating survival advantages in randomized controlled trials. Patients at an intermediate stage benefit from chemoembolization and have an estimated median overall survival (OS) of 26months [2], while at advanced stages, sorafenib extends survival from 8 to almost 11months [3].

    Date de mise en ligne : Lundi 23 janvier 2017
    Agrin Moeini, Daniela Sia, Zhongyang Zhang, Genis Camprecios, Ashley Stueck, Hui Dong, Robert Montal, Laura Torrens, Iris Martinez-Quetglas, M. Isabel Fiel, Ke Hao, Augusto Villanueva, Swan N. Thung, Myron E. Schwartz, Josep M. Llovet
    Mixed hepatocellular cholangiocarcinoma tumors: Cholangiolocellular carcinoma is a distinct molecular entity
    Liver cancer is the second leading cause of cancer-related deaths, with more than 850,000 new cases annually worldwide [1]. Mixed hepatocellular cholangiocarcinoma (HCC-CCA) is a rare type of primary liver cancer accounting for less than 1% of all primary liver malignancies [2,3]. Diagnosis is based on histological examination and requires the intimate mix of both hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA) elements [2]. Due to its low incidence and the lack of an established pathological diagnosis, the features and clinical behavior of these tumors remain ill-defined.

    Date de mise en ligne : Lundi 23 janvier 2017
    Michelle J. Farquhar, Isla S. Humphreys, Simon A. Rudge, Garrick K. Wilson, Bishnupriya Bhattacharya, Maria Ciaccia, Ke Hu, Qifeng Zhang, Laurent Mailly, Gary M. Reynolds, Margaret Aschcroft, Peter Balfe, Thomas F. Baumert, Stephanie Roessler, Michael J.O. Wakelam, Jane A. McKeating
    Autotaxin-lysophosphatidic acid receptor signalling regulates hepatitis C virus replication
    Chronic viral hepatitis is a global health problem with at least 170 million hepatitis C virus (HCV) infected individuals at risk of developing liver disease that can progress to hepatocellular carcinoma (HCC). The recent availability of direct acting anti-viral agents can eliminate HCV in up to 90% of patients[1]. However, the high cost of these drugs along with reports of viral genotype resistance, may limit their wide-spread use. Importantly, patients with liver cirrhosis cured of HCV may remain at risk of developing HCC, highlighting the need to understand host pathways playing a role in HCC development[2,3].

    Date de mise en ligne : Samedi 21 janvier 2017
    Emmanuel A. Tsochatzis, Alexander L. Gerbes
    Diagnosis and treatment of ascites
    Ascites is the most common complication of cirrhosis and its development is a sign of significant portal hypertension [1]. It becomes clinically detectable when in excess of 1.5 lt. Ascites in cirrhosis is the result of a vicious cycle involving arterial splanchnic vasodilation, decreased effective blood volume despite a compensatory increase in cardiac output, renal vasoconstriction with resulting sodium retention and finally extracellular fluid retention [2]. Systemic inflammation can exacerbate portal hypertension, contribute to the development of ascites and impair prognosis.

    Date de mise en ligne : Mardi 17 janvier 2017
    Eva-Carina Heier, Anna Meier, Henrike Julich-Haertel, Sonja Djudjaj, Monica Rau, Thomas Tschernig, Andreas Geier, Peter Boor, Frank Lammert, Veronika Lukacs-Kornek
    Murine CD103+ dendritic cells protect against steatosis progression towards steatohepatitis
    The prevalence of metabolic syndrome and non-alcoholic fatty liver disease (NAFLD) in the last decade has increased dramatically worldwide and affects both adults and children [1–3]. Non-alcoholic fatty liver (NAFL) is characterized by fat accumulation that can progress towards non-alcoholic steatohepatitis (NASH) distinguished by intrahepatic inflammation, increased steatosis with hepatocellular ballooning and cellular damage [4]. The chronic inflammatory response in NASH often results in progressive fibrosis and cirrhosis, which predisposes individuals to hepatocellular carcinoma [5,6].

    Date de mise en ligne : Mardi 17 janvier 2017
    Stefan Zeuzem, Masashi Mizokami, Stephen Pianko, Alessandra Mangia, Kwang-Hyub Han, Ross Martin, Evguenia Svarovskaia, Hadas Dvory-Sobol, Brian Doehle, Charlotte Hedskog, Chohee Yun, Diana M. Brainard, Steven Knox, John G. McHutchison, Michael D. Miller, Hongmei Mo, Wan-Long Chuang, Ira Jacobson, Gregory J. Dore, Mark Sulkowski
    NS5A Resistance-Associated Substitutions in Patients with Genotype 1 Hepatitis C Virus: Prevalence and Effect on Treatment Outcome
    Due to high rates of viral replication and an error prone HCV RNA polymerase, tremendous variability of HCV has been observed within infected patients (quasispecies) with all single mutations that do not abolish viral replication thought to be pre-existing [1]. As a result, NS5A RASs are observed at baseline in patients infected with chronic HCV. Deep sequencing enables detection of HCV substitutions, point deletions, or insertions within the quasispecies down to a frequency of 1%. However, commercially available assays based on standard population HCV sequencing or not cross-validated next generation, also called deep sequencing, report variants with a frequency of ⩾15% of the quasispecies.

    Date de mise en ligne : Vendredi 13 janvier 2017
    Ameet Dhar, Benjamin H. Mullish, Mark R. Thursz
    Anticoagulation in chronic liver disease
    In this Grand Round presentation, the case of a man with decompensated liver disease is described. He subsequently developed a fatal pulmonary embolism, which may not have occurred if he had been prescribed prophylactic anticoagulation to prevent venous thromboembolic disease. The burden of thrombotic disease in those with chronic liver disease is discussed, before a more detailed analysis of the current evidence, safety data, and clinical dilemmas regarding the use of anticoagulation in patients with chronic liver disease.

    Date de mise en ligne : Vendredi 13 janvier 2017
    Aveline Filliol, Claire Piquet-Pellorce, Céline Raguénès-Nicol, Sarah Dion, Muhammad Farooq, Catherine Lucas-Clerc, Peter Vandenabeele, Mathieu J.M. Bertrand, Jacques Le Seyec, Michel Samson
    RIPK1 protects hepatocytes from Kupffer cells-mediated TNF-induced apoptosis in mouse models of PAMP-induced hepatitis
    The liver is constantly exposed to bacterial pathogen associated molecular patterns (PAMPs) such as unmethylated CpG-DNA motifs or lipopolysaccharides (LPS) originating from the microbiota of the gastrointestinal tract. In physiological conditions, the intestinal barrier prevents the translocation of large amounts of bacterial by-products to the liver [1]. The low quantities of bacterial debris reaching the liver are efficiently cleared by phagocytic hepatic cells, avoiding induction of inflammation and harmful response [2].

    Date de mise en ligne : Vendredi 13 janvier 2017
    Maria Sandbothe, Reena Buurman, Nicole Reich, Luisa Greiwe, Beate Vajen, Engin Gürlevik, Vera Schäffer, Marlies Eilers, Florian Kühnel, Alejandro Vaquero, Thomas Longerich, Stephanie Roessler, Peter Schirmacher, Michael P. Manns, Thomas Illig, Brigitte Schlegelberger, Britta Skawran
    The microRNA-449 family inhibits TGF-β-mediated liver cancer cell migration by targeting SOX4
    Hepatocellular carcinoma (HCC) accounts for approximately 80% of all primary liver cancers [1]. It is the second most common cause of cancer-related death worldwide, estimated to be responsible for 745,000 deaths in 2012 alone [2]. While patients with early HCC benefit from interventional therapies such as resection or liver transplantation, patients with advanced HCC are mainly treated palliatively with very limited treatment options [3,4]. The only systemic therapy available for advanced HCC is the multikinase inhibitor Sorafenib [5].

    Date de mise en ligne : Vendredi 13 janvier 2017
    Jérôme Boursier, Victor de Ledinghen, Vincent Leroy, Rodolphe Anty, Sven Francque, Dominique Salmon, Adrien Lannes, Sandrine Bertrais, Frederic Oberti, Isabelle Fouchard-Hubert, Paul Calès
    A stepwise algorithm using a at-a-glance first-line test for the non-invasive diagnosis of advanced liver fibrosis and cirrhosis
    Chronic liver diseases (CLD) are very common: worldwide, an estimated 160 million people have chronic hepatitis C [1], 240 million have chronic hepatitis B [2], and 25% of the general population has non-alcoholic fatty liver disease (NAFLD) [3]. CLD can lead to a progressive accumulation of fibrosis in the liver which progressively evolves to cirrhosis and its life-threatening complications such as hepatocellular carcinoma (HCC), liver failure, variceal bleeding, or renal insufficiency. In 2012, driven by the growing worldwide burden of CLD, cirrhosis was responsible for more than 35 million years of lost life and thus became the eleventh leading cause of mortality among non-communicable diseases [4].

    Date de mise en ligne : Lundi 09 janvier 2017
    Thomas Klag, Julia Dietz, Christoph R. Werner, Julia M. Schwarz, Ulrich M. Lauer, Robert Beck, Nisar P. Malek, Christoph Sarrazin, Christoph P. Berg
    Hepatitis C “true” late relapse beyond 48weeks of sustained virologic response after direct acting antiviral therapy
    We read with great interest the 2016 EASL recommendations for treatment of hepatitis C [1]. These guidelines recommend that patients who achieve a sustained virologic response (SVR, defined as undetectable HCV RNA in blood 12 or 24weeks after end of treatment) should be retested for HCV RNA at 48weeks post end of treatment. When HCV RNA is then negative, hepatitis C is defined as being definitely cured, thereby terminating any further analysis for presence/absence of HCV RNA. Only in special risk groups, such as people who inject drugs or men who have sex with men, further HCV RNA testing should be performed beyond SVR48 on an annual basis [1].

    Date de mise en ligne : Lundi 09 janvier 2017
    Joanna Hanley, Dipok Kumar Dhar, Francesca Mazzacuva, Rebeca Fiadeiro, Jemima J. Burden, Anne-Marie Lyne, Holly Smith, Anna Straatman-Iwanowska, Blerida Banushi, Alex Virasami, Kevin Mills, Frédéric P. Lemaigre, A.S. Knisely, Steven Howe, Neil Sebire, Simon N. Waddington, Coen C. Paulusma, Peter Clayton, Paul Gissen
    Vps33b is crucial for structural and functional hepatocyte polarity
    In metazoans, the development of three-dimensional body structures depends on the generation of polarised epithelial layers. Polarisation of epithelial cells is a complex process that requires the cooperation of multiple factors including cell junction formation, extracellular matrix interactions and intracellular protein trafficking [1]. Correct interaction of these factors enables the establishment of discrete apical and basolateral membrane domains. This then promotes normal epithelial cell function by allowing directional solute absorption and secretion [2].

    Date de mise en ligne : Lundi 09 janvier 2017
    Michael Bitzer, Helmut R. Salih
    Reply to: “Histone deacetylase inhibitor for the treatment of hepatocellular carcinoma: Chemoimmunotherapeutic perspective and prospects”
    We thank Drs. Goto and Kato for their thoughtful comments on our study, in particular their remarks on possible immunotherapeutic consequences of treatment with histone deacetylase inhibitors [1]. They speculate that reinforcement of natural killer (NK) cell immunity may constitute an additional mechanism by which the histone deacetylase inhibitor (HDACi) resminostat, in combination with the tyrosine kinase inhibitor (TKI) sorafenib achieved a high disease control rate in our second line study in hepatocellular carcinoma (HCC) [2].

    Date de mise en ligne : Lundi 09 janvier 2017
    Kaku Goto, Naoya Kato
    Histone deacetylase inhibitor for the treatment of hepatocellular carcinoma: Chemoimmunotherapeutic perspective and prospects
    We are highly interested in the recent article by Bitzer et al. [1] on the SHELTER study, demonstrating the efficacy of the histone deacetylase (HDAC) inhibitor (HDACi) resminostat (RES) in combination with sorafenib (SOR) in patients with hepatocellular carcinoma (HCC), and published in the Journal of Hepatology. In addition to the chemotherapeutic effects discussed in this exploratory clinical study, the immunotherapeutic effects of the combination treatment can be considered as well.

    Date de mise en ligne : Vendredi 06 janvier 2017
    Wei-Tien Tai, Ann-Lii Cheng, Chung-Wai Shiau, Hsiang-Po Huang, Jui-Wen Huang, Pei-Jer Chen, Kuen-Feng Chen
    Corrigendum to “Signal transducer and activator of transcription 3 is a major kinase-independent target of sorafenib in hepatocellular carcinoma”
    After careful examination of the raw data included in this manuscript, we found that the Western blots of the internal control, actin, in Fig. 3B and C were the same as the Fig. 2D. We have corrected this error in the revised Fig. 3 below. In addition, the expression level of SOCS-1 and SOCS-3 in Fig. 4E should be under sorafenib 5μM and 10μM treatments, rather than sorafenib and SC-1 treatment. The corrected version of Fig. 4 is also included below.

    Date de mise en ligne : Jeudi 05 janvier 2017
    Dewei Ye, Kangmin Yang, Shufei Zang, Zhuofeng Lin, Hau-Tak Chau, Yudong Wang, Jialiang Zhang, Junping Shi, Aimin Xu, Shaoqiang Lin, Yu Wang
    Corrigendum to “Lipocalin-2 mediates non-alcoholic steatohepatitis by promoting neutrophil-macrophage crosstalk via the induction of CXCR2”
    An error was introduced in Fig. 6C of the original manuscript. During preparation of Fig. 6C, the representative image of “HFHC+Rm-LCN2-CXCR2 KO” group was inadvertently duplicated in lieu of the representative image for “SC-CXCR2 KO” group. The corrected immunohistochemistry images shown in the updated Fig. 6, are provided below. The authors apologize for any inconvenience caused.

    Date de mise en ligne : Samedi 31 décembre 2016
    Erfan Ayubi, Saeid Safiri, Mohadeseh Sani, Salman Khazaei, Kamyar Mansori
    Heavy daily alcohol intake at the population level predicts the weight of alcohol in cirrhosis burden worldwide: Methodological issues of confounding and prediction models
    We were interested to read paper entitled “Heavy daily alcohol intake at the population level predicts the weight of alcohol in cirrhosis burden worldwide”, published by Stein and colleagues in the Journal of Hepatology 2016 [1]. The authors aimed to evaluate the associations between population drinking, cirrhosis cofactors, and economic indicators and the burden of alcoholic cirrhosis on a population level. They found that heavy daily drinking had statistically significant effect on the weight of alcohol in the cirrhosis burden, however, the results suggested that higher gross domestic product (GDP) may decrease alcohol-attributable fraction (AAF) of cirrhosis [1].

    Date de mise en ligne : Samedi 31 décembre 2016
    Fanny Lebossé, Barbara Testoni, Judith Fresquet, Floriana Facchetti, Enrico Galmozzi, Maëlenn Fournier, Valérie Hervieu, Pascale Berthillon, Françoise Berby, Isabelle Bordes, David Durantel, Massimo Levrero, Pietro Lampertico, Fabien Zoulim
    Intrahepatic innate immune response pathways are downregulated in untreated chronic hepatitis B patients
    More than 240 million people are chronically infected with hepatitis B virus (HBV) worldwide [1]. Chronic hepatitis B (CHB) can evolve towards liver fibrosis, cirrhosis and hepatocellular carcinoma (HCC), which is responsible for over 0.5–1 million deaths per year [2]. Viral persistence is mostly ascribed to the intrahepatic pool of covalently closed circular DNA (cccDNA), which represents the unique template for HBV replication [3–5]. Currently available therapies fail to clear intrahepatic cccDNA.

    Date de mise en ligne : Samedi 31 décembre 2016
    Monica Cruz-Lemini, Jose Altamirano, Nambi Ndugga, Juan G. Abraldes, Ramon Bataller
    Reply to: “Heavy daily alcohol intake at the population level predicts the weight of alcohol in cirrhosis burden worldwide: Methodological issues of confounding and prediction models”
    We would like to thank Dr Ayubi and colleagues for their constructive comments on our paper [1]. First, they hypothesize that ethnicity might be confounding the association between gross domestic product (GDP) and alcohol-attributable fraction (AAF), since ethnicity might determine susceptibility to alcohol damage [2] and at the same time might be associated with GDP. Unfortunately, with the available data we cannot test this hypothesis, since the World Health Organization (WHO) data is grouped by country, and assigning a specific ethnicity to a country would be challenging.

    Date de mise en ligne : Mercredi 28 décembre 2016
    Thomas Karlas, David Petroff, Magali Sasso, Jian-Gao Fan, Yu-Qiang Mi, Victor de Lédinghen, Manoj Kumar, Monica Lupsor-Platon, Kwang-Hyub Han, Ana C. Cardoso, Giovanna Ferraioli, Wah-Kheong Chan, Vincent Wai-Sun Wong, Robert P. Myers, Kazuaki Chayama, Mireen Friedrich-Rust, Michel Beaugrand, Feng Shen, Jean-Baptiste Hiriart, Shiv K. Sarin, Radu Badea, Kyu Sik Jung, Patrick Marcellin, Carlo Filice, Sanjiv Mahadeva, Grace Lai-Hung Wong, Pam Crotty, Keiichi Masaki, Joerg Bojunga, Pierre Bedossa, Volker Keim, Johannes Wiegand
    Individual patient data meta-analysis of controlled attenuation parameter (CAP) technology for assessing steatosis
    Hepatic steatosis is a frequent finding in chronic liver diseases of different etiologies such as viral hepatitis and alcoholic liver disease, and its prevalence is increasing along with the worldwide epidemic of non-alcoholic fatty liver disease (NAFLD) [1–4].

    Date de mise en ligne : Mercredi 28 décembre 2016
    Bettina Langhans, Hans Dieter Nischalke, Benjamin Krämer, Annekristin Hausen, Leona Dold, Peer van Heteren, Robert Hüneburg, Jacob Nattermann, Christian P. Strassburg, Ulrich Spengler
    Increased peripheral CD4+ regulatory T cells persist after successful direct-acting antiviral treatment of chronic hepatitis C
    Chronic hepatitis C virus (HCV) infection is a major global health problem, because it leads to liver fibrosis, cirrhosis and liver cancer [1]. The T cell balance between stimulatory and immunosuppressive mechanisms seems to critically determine outcomes of HCV infection [2]. During chronic hepatitis C effector T cells become progressively exhausted and exhibit reduced antiviral activity, while CD4+ regulatory T cells (Tregs) gradually expand and accumulate in the liver [3]. Tregs suppress antiviral T cell responses [4–7], inhibit activation of natural killer (NK) cells [8], activate fibrogenesis in hepatic stellate cells [9,10] and ultimately facilitate liver cancer [11].

    Date de mise en ligne : Mercredi 28 décembre 2016
    Emmanuel Weiss, Pierre-Emmanuel Rautou, Magali Fasseu, Mikhael Giabicani, Marc de Chambrun, JingHong Wan, Charlotte Minsart, Thierry Gustot, Alain Couvineau, Rakhi Maiwall, Margarita Hurtado-Nedelec, Nathalie Pilard, Didier Lebrec, Dominique Valla, François Durand, Pierre de la Grange, Renato C. Monteiro, Catherine Paugam-Burtz, Sophie Lotersztajn, Richard Moreau
    Type I interferon signaling in systemic immune cells from patients with alcoholic cirrhosis and its association with outcome
    Type I interferons (IFNs) are a family of cytokines that play a crucial role in the immune response to viral pathogens [1]. They mediate virus detection by intracellular or extracellular sensors and the activation of antiviral mechanisms, via an autocrine/paracrine signaling (Fig. 1) [2]. IFNs engage canonical signaling pathways through a common heterodimeric receptor (IFNAR1/IFNAR2) [3]. Receptor subunits are associated with the kinases JAK1 and TYK2, and activation of these kinases results in phosphorylation of STAT1 and STAT2, which then associate with IFN regulatory factor (IRF)9 to form the IFN-stimulated gene factor (ISGF)3 complex activating the transcription of IFN-stimulated genes (ISGs) [4,5].

    Date de mise en ligne : Mardi 27 décembre 2016
    Inmaculada Fernández, Raquel Muñoz-Gómez, Juan M. Pascasio, Carme Baliellas, Natalia Polanco, Nuria Esforzado, Ana Arias, Martín Prieto, Lluis Castells, Valentín Cuervas-Mons, Olga Hernández, Javier Crespo, José L. Calleja, Xavier Forns, María-Carlota Londoño
    Efficacy and tolerability of interferon-free antiviral therapy in kidney transplant recipients with chronic hepatitis C
    Approximately 5 to 15% of kidney transplant (KT) recipients have chronic hepatitis C. Hepatitis C virus (HCV) infection is associated with an increased risk of mortality in these patients as a consequence of liver disease, higher infection rates and cardiovascular disease [1]. Moreover, HCV infection in KT patients is an independent risk factor for graft loss, and it is associated with proteinuria, chronic rejection, transplant glomerulopathy, post-transplant diabetes and HCV-associated glomerulonephritis [2,3].

    Date de mise en ligne : Samedi 24 décembre 2016
    Xin Yu, Peixiang Lan, Xuben Hou, Qiuju Han, Nan Lu, Tao Li, Chenwei Jiao, Jian Zhang, Cai Zhang, Zhigang Tian
    HBV inhibits LPS-induced NLRP3 inflammasome activation and IL-1β production via suppressing the NF-κB pathway and ROS production
    Hepatitis B virus (HBV), an enveloped DNA virus that belongs to the Hepadnaviridae family, chronically infects more than 400 million people worldwide. Its persistence is a major cause of liver cirrhosis and hepatocellular carcinoma (HCC). HBV is considered to be a “stealth virus” that induces negligible innate immune responses during the early phase of infection. Viral proteins (HBV polymerase, HBx, HBeAg and HBsAg), can inhibit distinct innate immune pathways, leading to immunosuppression and viral persistence [1,2].

    Date de mise en ligne : Samedi 24 décembre 2016
    Kyle A. Soltys, Kentaro Setoyama, Edgar N. Tafaleng, Alejandro Soto Gutiérrez, Jason Fong, Ken Fukumitsu, Taichiro Nishikawa, Masaki Nagaya, Rachel Sada, Kimberly Haberman, Roberto Gramignoli, Kenneth Dorko, Veysel Tahan, Alexandra Dreyzin, Kevin Baskin, John J. Crowley, Mubina A. Quader, Melvin Deutsch, Chethan Ashokkumar, Benjamin L. Shneider, Robert H. Squires, Sarangarajan Ranganathan, Miguel Reyes-Mugica, Steven F. Dobrowolski, George Mazariegos, Rajavel Elango, Donna B. Stolz, Stephen C. Strom, Gerard Vockley, Jayanta Roy-Chowdhury, Marilia Cascalho, Chandan Guha, Rakesh Sindhi, Jeffrey L. Platt, Ira J. Fox
    Host conditioning and rejection monitoring in hepatocyte transplantation in humans
    Transplantation of isolated hepatocytes has been proposed as a minimally invasive alternative to organ transplantation for acute liver failure and liver-based metabolic deficiencies [1]. Hepatocytes have been safely transplanted into the liver, have produced partial correction of Crigler-Najjar syndrome type 1 [2], factor VII deficiency [3], urea cycle disorders (UCD) [4,5], infantile Refsum’s disease [6], glycogen storage disease type 1 [7], and phenylketonuria (PKU) [8], and have been associated anecdotally with reversal of acute hepatic failure [1].

    Date de mise en ligne : Vendredi 23 décembre 2016
    Heng Wu, Tianpeng Zhang, Fei Pan, Clifford J. Steer, Zhuoyu Li, Xin Chen, Guisheng Song
    MicroRNA-206 prevents hepatosteatosis and hyperglycemia by facilitating insulin signaling and impairing lipogenesis
    Results from the American Heart Association showed that nearly 73% of U.S adults are overweight or obese. Obesity and its associated co-morbidities are among the most prevalent and challenging conditions confronting the medical profession in the past century. A major metabolic consequence of obesity is insulin resistance, which is a major risk factor of type 2 diabetes (T2D) and non-alcoholic fatty liver disease (NAFLD) [1]. NAFLD is the accumulation of excessive amounts of lipids within hepatocytes that is not caused by alcohol.

    Date de mise en ligne : Vendredi 23 décembre 2016
    Michaela Wittlich, Michael Dudek, Jan P. Böttcher, Oliver Schanz, Silke Hegenbarth, Tobias Bopp, Edgar Schmitt, Christian Kurts, Christoph Garbers, Stefan Rose John, Percy A. Knolle, Dirk Wohlleber
    Liver sinusoidal endothelial cell cross-priming is supported by CD4 T cell-derived IL-2
    Induction of antigen-specific immunity by CD8 T cells requires appropriate activation and maturation of antigen-presenting cells such as dendritic cells (DCs). Activation of DCs through Toll-like receptors or pro-inflammatory mediators like type I interferon induces their functional maturation, which is characterized by an upregulation of co-stimulatory molecules, e.g., CD80/CD86 or CD40, and increased expression of IL-12 [1,2]. Such functional maturation is operational in improving DC capacity to cross-prime naïve CD8 T cells towards soluble antigens and to mount protective immunity [3].

    Date de mise en ligne : Jeudi 22 décembre 2016
    Ranka Vukotic, Fabio Conti, Pietro Andreone
    Hepatitis C virus eradication in the elderly: The challenge worth a long-life elixir?
    Senectus enim insanabilis morbus est.Lucius Annaeus Seneca, c. 65 AD.

    Date de mise en ligne : Jeudi 22 décembre 2016
    Stefano Caruso, Julien Calderaro, Eric Letouzé, Jean-Charles Nault, Gabrielle Couchy, Anaïs Boulai, Alain Luciani, Elie-Serge Zafrani, Paulette Bioulac-Sage, Olivier Seror, Sandrine Imbeaud, Jessica Zucman-Rossi
    Germline and somatic DICER1 mutations in familial and sporadic liver tumors
    Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide and is related to different risk factors, including chronic hepatitis B (HBV) and C (HCV) virus infection, alcohol abuse, metabolic syndrome and other genetic disorders [1]. Only few studies reported familial clusters of HCC and most of them were described in areas with endemic HBV infection suggesting that the viral infection could participate to the familial aggregation of HCC [2–10]. However, growing evidence suggests that a family history of liver cancer significantly increases HCC risk, and a multifactorial inheritance could contribute to increasing this risk, regardless of viral hepatitis infection [11–13].

    Date de mise en ligne : Mercredi 21 décembre 2016
    Antje Mohs, Nadine Kuttkat, Johanna Reißing, Henning Wolfgang Zimmermann, Roland Sonntag, Amanda Proudfoot, Sameh A. Youssef, Alain de Bruin, Francisco Javier Cubero, Christian Trautwein
    Functional role of CCL5/RANTES for HCC progression during chronic liver disease
    Under physiological conditions the inflammatory response is a beneficial process to restore tissue injury and to protect against pathogenic causes. However, persistent liver damage triggers chronic inflammation leading to scar formation and enhances the susceptibility for cancer development [1]. Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death and the fifth most common solid tumor worldwide [2]. Most HCCs develop in the context of chronic liver inflammation [3–5].

    Date de mise en ligne : Mercredi 21 décembre 2016
    Martin F. Sprinzl, Peter R. Galle
    Current progress in immunotherapy of hepatocellular carcinoma
    During the last years, new immune-modulatory agents were introduced for oncological treatment, eventually leading to the clinical breakthrough of checkpoint inhibitors (CPI) targeting cytotoxic T lymphocyte antigen-4 (CTLA-4), programmed death-1 (PD-1) and programmed death-1 ligand (PD-1L) [1–5]. Under physiological conditions these molecules resolve T cell activation to maintain inflammatory homeostasis, protect tissue integrity and prevent unwanted auto-immunity [6]. CPI administration in tumor patients, however, unleashes tumor-directed cytotoxic T cells specific against an unknown spectrum of tumor-associated antigens (TAA).

    Date de mise en ligne : Vendredi 16 décembre 2016
    Philipp Schwabl, Eva Hambruch, Berit A. Seeland, Hubert Hayden, Michael Wagner, Lukas Garnys, Bastian Strobel, Tim-Lukas Schubert, Florian Riedl, Dieter Mitteregger, Michael Burnet, Patrick Starlinger, Georg Oberhuber, Ulrich Deuschle, Nataliya Rohr-Udilova, Bruno K. Podesser, Markus Peck-Radosavljevic, Thomas Reiberger, Claus Kremoser, Michael Trauner
    The FXR agonist PX20606 ameliorates portal hypertension by targeting vascular remodelling and sinusoidal dysfunction
    Patients with chronic liver disease ultimately develop cirrhosis and portal hypertension (PHT) [1] if the underlying etiology cannot be effectively treated [2]. Most severe complications occur in patients with advanced intrahepatic collagen deposition [3,4] and pronounced PHT [5]. PHT is primarily caused by increased intrahepatic vascular resistance that results from both structural remodelling (fibrogenesis and scarring) and functional alterations (contractile hepatic stellate cells and endothelial dysfunction).

    Date de mise en ligne : Lundi 12 décembre 2016
    Anna K. Kopec, Nikita Joshi, Holly Cline-Fedewa, Anna V. Wojcicki, Jessica L. Ray, Bradley P. Sullivan, John E. Froehlich, Brendan F. Johnson, Matthew J. Flick, James P. Luyendyk
    Fibrin(ogen) drives repair after acetaminophen-induced liver injury via leukocyte αMβ2 integrin-dependent upregulation of Mmp12
    Acute liver injury caused by acetaminophen (APAP) overdose in experimental animals is associated with activation of the coagulation cascade. Strong evidence also connects APAP-induced liver injury in humans to changes in the hemostatic system including thrombocytopenia, elevated plasma levels of thrombin-antithrombin (TAT), increased levels of procoagulant microvesicles, and a reduction in plasma fibrinogen concentration [1–3]. Prolongation of the prothrombin time-international normalized ratio (PT-INR) is linked with increased morbidity in patients with acute liver failure, whereas preservation of plasma fibrinogen is coupled to improved outcome [2,4–6].

    Date de mise en ligne : Lundi 12 décembre 2016
    Alessandra Mangia, Simone Susser, Valeria Piazzolla, Ernesto Agostinacchio, Giulio De Stefano, Vincenzo Palmieri, Giancarlo Spinzi, Immacolata Carraturo, Domenico Potenza, Ruggero Losappio, Andrea Arleo, Maria Miscio, Rosanna Santoro, Christoph Sarrazin, Massimiliano Copetti
    Sofosbuvir and ribavirin for genotype 2 HCV infected patients with cirrhosis: A real life experience
    Hepatitis C virus (HCV) genotype still represents the most important viral factor for selection of appropriate direct-acting antiviral agents (DAA) regimen and duration in chronic HCV infection. In the era of interferon-based therapies, genotype 2 (GT2) was considered easy to treat. Indeed, the first interferon free treatment, based on the combination of sofosbuvir (SOF) 400mg+ribavirin (RBV) 1000–1200mg daily, was investigated in patients infected with this genotype and until very recently [1] has represented the standard of care [2].

    Date de mise en ligne : Lundi 12 décembre 2016
    Eloi R. Verrier, Catherine Schuster, Thomas F. Baumert
    Advancing hepatitis B virus entry inhibitors
    Despite the effective antivirals and vaccines, chronic hepatitis B virus (HBV) infection remains a major public health problem worldwide [1,2]. Due to limited access, late or absent detection and vertical transmission, the prevalence of HBV infection is estimated to be 250–350 million infected individuals [1,3]. HBV infection is a leading cause of hepatocellular carcinoma worldwide. While current therapies, based on pegylated-interferon and nucleos(t)ide analogs effectively decrease viral load, viral elimination is rare.

    Date de mise en ligne : Lundi 12 décembre 2016
    Dorothee Schwinge, Franziska von Haxthausen, Alexander Quaas, Antonella Carambia, Benjamin Otto, Fabian Glaser, Benedikt Höh, Nina Thiele, Tanja Schoknecht, Samuel Huber, Niklas Steffens, Ansgar W. Lohse, Johannes Herkel, Christoph Schramm
    Dysfunction of hepatic regulatory T cells in experimental sclerosing cholangitis is related to IL-12 signaling
    Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease leading to fibrosis and obliteration of bile ducts, and eventually to liver cirrhosis [1]. In addition to liver disease, 60–80% of PSC patients have a history of associated inflammatory bowel disease [2,3]. There is currently no medical treatment available with a proven effect on disease progression, making PSC a major indication for liver transplantation [4]. The etiology of PSC is still unknown, but immune dysregulation is considered to be part of PSC pathogenesis [5].

    Date de mise en ligne : Lundi 12 décembre 2016
    Yi Ni, Stephan Urban
    Stem cell-derived hepatocytes: A promising novel tool to study hepatitis B virus infection
    Hepatitis B virus (HBV) infection affects 240 million people worldwide. HBV is the major cause for progressive liver diseases often leading to cirrhosis and hepatocellular carcinoma. After the isolation and genetic characterization of HBV, it became instantly clear that the virus essentially depends on species- and hepatocyte-specific host factors in its replication cycle [1]. Although hepatoma-derived cell lines support HBV replication and particle assembly following transfection of cloned viral genomes [2], only primary hepatocytes from humans (PHH) [3] or a tree shrew [4] support the full viral replication cycle.

    Date de mise en ligne : Lundi 12 décembre 2016
    Philippe Kolly, Jean-François Dufour
    Patients with hepatocellular carcinoma: Your address matters!
    One of the major goals of research on hepatocellular carcinoma (HCC) is to improve overall survival (OS), either by exploring new therapeutic options, improving patient selection for various treatment strategies, or enhancing early detection of HCC. The emergence of systemic therapies has contributed to the increase in OS of patients with advanced HCC since 2007, with evidence provided by the SHARP trial [1] and, very recently, by the RESORCE trial [2]. The European guidelines for the management of HCC suggest that patients at risk of HCC should be included in a surveillance program [3].

    Date de mise en ligne : Lundi 12 décembre 2016
    Yuanjun Shen, Bingfang Yan
    Covalent inhibition of carboxylesterase-2 by sofosbuvir and its effect on the hydrolytic activation of tenofovir disoproxil
    Sofosbuvir is considered as a paradigm shift in treating hepatitis C viral infection (HCV) [1]. Patients co-infected with human immunodeficiency virus (HIV) usually receive both anti-HCV and antiretroviral therapy [2]. Emerging evidence, recently reported by this and other journals, has linked sofosbuvir-containing regimens to liver or kidney toxicity when co-administered with anti-HIV drugs [2–6]. Interestingly, sofosbuvir and some anti-HIV drugs such as tenofovir disoproxil contain ester and/or amide bonds.

    Date de mise en ligne : Lundi 12 décembre 2016
    Kun Huang, Meng Du, Xin Tan, Ling Yang, Xiangrao Li, Yuhan Jiang, Cheng Wang, Fengxiao Zhang, Feng Zhu, Min Cheng, Qinglin Yang, Liqing Yu, Lin Wang, Dan Huang, Kai Huang
    PARP1-mediated PPARα poly(ADP-ribosyl)ation suppresses fatty acid oxidation in non-alcoholic fatty liver disease
    Non-alcoholic fatty liver disease (NAFLD) covers a broad spectrum of liver abnormalities ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis [1]. The prevalence of NAFLD is increasing globally, and becoming the predominant cause of chronic liver disease in many parts of the world [2]. The hallmark of NAFLD is an over-accumulation of triglycerides-rich lipid droplets in the hepatocytes of liver due to deregulation of hepatic lipid metabolism, including increased fatty acid (FA) uptake and synthesis as well as insufficient disposal (i.e., oxidation and secretion).

    Date de mise en ligne : Lundi 05 décembre 2016
    Hyun-seok Kim, Adaugo Ike, Justin Mathew
    Effect of exercise on the development of new fatty liver and the resolution of existing fatty liver
    We have read and are greatly intrigued by the article in a recent issue, written by Sung et al., showing evidence that there is a dose-dependent association between the amount of exercise with incidence and resolution of non-alcoholic fatty liver disease (NAFLD) [1]. The authors concluded that any amount of exercise was associated with a significant benefit for both a decrease in the incidence of new fatty liver and for improvement of existing fatty liver. This finding is supported by previous studies that suggest weight loss through exercise provides benefits in prevention and improvement in NAFLD [2,3].

    Date de mise en ligne : Samedi 03 décembre 2016
    David Wyles, Hadas Dvory-Sobol, Evguenia S. Svarovskaia, Brian P. Doehle, Ross Martin, Nezam H. Afdhal, Kris V. Kowdley, Eric Lawitz, Diana M. Brainard, Michael D. Miller, Hongmei Mo, Edward J. Gane
    Post-treatment resistance analysis of hepatitis C virus from phase II and III clinical trials of ledipasvir/sofosbuvir
    In recent years, direct-acting antiviral drugs (DAAs) developed for the treatment of hepatitis C virus (HCV) have replaced the previous standard of care of pegylated interferon and ribavirin. Inhibitors targeting the viral NS3/4A protease (telaprevir, boceprevir, simeprevir, paritaprevir and grazoprevir), NS5B polymerase (the nucleotide inhibitor sofosbuvir and the non-nucleoside inhibitor dasabuvir), and NS5A protein (ledipasvir, daclatasvir, ombitasvir and elbasvir) have been approved by the USA FDA, with more in late-phase clinical trials.

    Date de mise en ligne : Samedi 03 décembre 2016
    Sara Montagnese, Michele De Rui, Paolo Angeli, Piero Amodio
    Neuropsychiatric performance in patients with cirrhosis: Who is “normal”?
    In patients with cirrhosis a normal neuropsychiatric performance has been traditionally defined by the absence of any degree of hepatic encephalopathy and/or the absence of psychometric or neurophysiological abnormalities, compared with data from the healthy population. As the understanding and management of end-stage liver disease continues to change, it is our impression that the concept of normal neuropsychiatric performance also needs updating. This review explores novel and more pragmatic interpretations of neuropsychiatric “normality” compared with top personal performance, in terms of risk of overt hepatic encephalopathy or brain failure and in relation with events such as liver transplantation, decompensation, acute-on-chronic liver failure and transjugular intrahepatic portosystemic shunt placement.

    Date de mise en ligne : Mercredi 30 novembre 2016
    Valentin Le Guen, Jean-Paul Judor, Françoise Boeffard, Vanessa Gauttier, Nicolas Ferry, Jean-Paul Soulillou, Sophie Brouard, Sophie Conchon
    Alloantigen gene transfer to hepatocytes promotes tolerance to pancreatic islet graft by inducing CD8+ regulatory T cells
    Allogeneic transplantation remains the only treatment available for end-stage diseases of various organs, such as kidney, heart, liver, and pancreas. However, the donor-specific allogeneic immune response of the host requires life-long immunosuppression. Despite constant progress, these long-term treatments still carry serious side effects, from toxicity to increased risk of opportunistic infections and of neoplasia [1,2]. An ideal alternative to the need for long-term exposure to immunosuppressors would consist of the induction of a donor-specific immune tolerance, which, despite having been achieved experimentally, remains a challenge in the clinical arena.

    Date de mise en ligne : Mercredi 30 novembre 2016
    Deepak Joshi, Nitika Gupta, Marianne Samyn, Maesha Deheragoda, Fabienne Dobbels, Michael A. Heneghan
    The management of childhood liver diseases in adulthood
    An increasing number of patients with childhood liver disease survive into adulthood. These young adults are now entering adult services and require ongoing management. Aetiologies can be divided into liver diseases that develop in young adults which present to adult hepatologists i.e., biliary atresia and Alagille syndrome or liver diseases that occur in children/adolescents and adults i.e., autoimmune hepatitis or Wilson’s disease. To successfully manage these young adults, a dynamic and responsive transition service is essential.

    Date de mise en ligne : Mardi 29 novembre 2016
    Benjamin L. Woolbright, Hartmut Jaeschke
    Role of the inflammasome in acetaminophen-induced liver injury and acute liver failure
    Drug-induced acute liver failure carries a high morbidity and mortality rate. Acetaminophen overdose is the number one cause of acute liver failure and remains a major problem in Western medicine. Administration of N-acetyl cysteine is an effective antidote when given before the initial rise in toxicity; however, many patients present to the hospital after this stage occurs. As such, treatments which can alleviate late-stage acetaminophen-induced acute liver failure are imperative. While the initial mechanisms of toxicity are well described, a debate has recently occurred in the literature over whether there is a second phase of injury, mediated by inflammatory processes.

    Date de mise en ligne : Mardi 29 novembre 2016
    S Pischke, J Hartl, SD Pas, AW Lohse, BC Jacobs, AA van der Eijk
    Hepatitis E virus infection beyond the liver?
    Hepatitis E virus (HEV) infections are not limited to the liver but may also affect other organs. Several diseases, including Guillain-Barré syndrome, neuralgic amyotrophy, glomerulonephritis, cryoglobulinemia, pancreatitis, lymphoma, thrombopenia, meningitis, thyreoiditis and myocarditis have been observed in the context of hepatitis E. To date the definite pathophysiological links between HEV and extrahepatic manifestations are not yet established. However, it is suggested that HEV-infection might be causative based on serological studies, case series, in vitro data and animal models.

    Date de mise en ligne : Mardi 29 novembre 2016
    Katalin Dezső, András Rókusz, Edina Bugyik, Armanda Szücs, András Szuák, Bence Dorogi, Mátyás Kiss, Ágnes Nemeskéri, Péter Nagy, Sándor Paku
    Human liver regeneration in advanced cirrhosis is organized by the portal tree
    Cirrhosis is the final common outcome of all chronic liver diseases, resulting in patients’ suffering and a tremendous burden for health care systems [1]. It is characterized by the diffuse nodular transformation of the liver tissue and the deposition of collagen rich extracellular matrix. There are several in vivo experimental models for hepatic fibrosis/cirrhosis and the progression of the disease is well documented in human livers as well, thus the evolution of cirrhosis looks to be a well characterized straightforward process.

    Date de mise en ligne : Lundi 28 novembre 2016
    Eirini Kyrana, Anil Dhawan
    Minimal hepatic encephalopathy in children, uncommon or unrecognised? Time to act
    Hepatic encephalopathy has been defined as a spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction after exclusion of an intrinsic brain disease [1]. Minimal hepatic encephalopathy (MHE) has been used to describe a subset of patients with the mildest form of encephalopathy, not detected on clinical examination, but detected on psychometric testing [1,2]. The term applies to both patients with cirrhosis and patients with portosystemic shunts without intrinsic liver disease such as isolated portal vein thrombosis [1].

    Date de mise en ligne : Lundi 28 novembre 2016
    Mirjana Ziemer, Eleni Koukoulioti, Susanne Beyer, Jan C. Simon, Thomas Berg
    Managing immune checkpoint-inhibitor-induced severe autoimmune-like hepatitis by liver-directed topical steroids
    Immuno-oncology therapies are being increasingly used as a principle pharmacological cancer treatment. The CTLA4-antibody ipilimumab, and PD-1-antibodies pembrolizumab and nivolumab have revolutionized anti-neoplastic therapies [1–3]. They are licensed to treat for advanced melanoma, non-small-lung cancer and renal cell carcinoma, but are currently being evaluated in a broad spectrum of malignant diseases including hepatocellular carcinoma [4,5]. However, due to their mode of action, the blockade of T cell inhibition, these new class of drugs have a spectrum of adverse reactions, specifically the induction of autoimmune-like diseases [6,7].

    Date de mise en ligne : Samedi 26 novembre 2016
    Andrea Notarpaolo, Richard Layese, Paolo Magistri, Maria Gambato, Michele Colledan, Giulia Magini, Lucia Miglioresi, Alessandro Vitale, Giovanni Vennarecci, Cecilia D Ambrosio, Patrizia Burra, Fabrizio Di Benedetto, Stefano Fagiuoli, Marco Colasanti, Giuseppe Maria Ettorre, Arnoldo Andreoli, Umberto Cillo, Alexis Laurent, Sandrine Katsahian, Etienne Audureau, Françoise Roudot-Thoraval, Christophe Duvoux
    Validation of the AFP model as a predictor of HCC recurrence in patients with viral hepatitis-related cirrhosis who had received a liver transplant for HCC
    Liver transplantation (LT) is considered the best treatment of hepatocellular carcinoma (HCC). However, its efficacy is limited by the risk of tumor recurrence, which results in rapid death and graft loss in patients who are not selected appropriately, making LT futile.

    Date de mise en ligne : Vendredi 25 novembre 2016
    Carolin Lackner, Walter Spindelboeck, Johannes Haybaeck, Philipp Douschan, Florian Rainer, Luigi Terracciano, Josef Haas, Andrea Berghold, Ramon Bataller, Rudolf E. Stauber
    Histological parameters and alcohol abstinence determine long-term prognosis in patients with alcoholic liver disease
    Alcoholic liver disease (ALD) is a substantial burden on public health and is responsible for half of the cases of cirrhosis worldwide [1,2]. Despite its health and socioeconomic burden, there have not been major advances in the management of these patients. There are no widespread programs for early detection and the current therapy for its more severe form (i.e., prednisolone for alcoholic hepatitis) has not evolved since 1971 [3,4]. The complex pathogenesis of ALD, influenced by host and environmental factors, is only partially understood.

    Date de mise en ligne : Jeudi 24 novembre 2016
    Hidenori Toyoda, Takashi Kumada, Toshifumi Tada, Noritomo Shimada, Koichi Takaguchi, Tomonori Senoh, Kunihiko Tsuji, Yoshihiko Tachi, Atsushi Hiraoka, Toru Ishikawa, Toshihide Shima, Takeshi Okanoue
    Efficacy and tolerability of an IFN-free regimen with DCV/ASV for elderly patients infected with HCV genotype 1B
    Chronic hepatitis C virus (HCV) infection is a major cause of cirrhosis and hepatocellular carcinoma (HCC). The risk of these complications is reduced by the eradication of HCV using antiviral therapy, i.e., sustained virologic response (SVR) [1]. Interferon (IFN)-based therapies, usually in combination with ribavirin, have been administered to eradicate HCV. However, it is often difficult for aged patients to undergo these treatments due to the adverse effects of IFN and ribavirin [2–4].

    Date de mise en ligne : Jeudi 24 novembre 2016
    David J. Pinato, Clarence Yen, Rohini Sharma
    Reply to: ‘Validating the ALBI grade: Its current and future use in HCC prognostication’
    We thank Chan et al. for their kind comments outlined in their Letter to the Editor. A number of points are also highlighted for discussion pertaining to our manuscript “The ALBI grade provides objective hepatic reserve estimation across each BCLC stage of hepatocellular carcinoma” [1].

    Date de mise en ligne : Jeudi 24 novembre 2016
    Satomi Shimura, Koichi Watashi, Kento Fukano, Michael Peel, Ann Sluder, Fumihiro Kawai, Masashi Iwamoto, Senko Tsukuda, Junko S. Takeuchi, Takeshi Miyake, Masaya Sugiyama, Yuki Ogasawara, Sam-Yong Park, Yasuhito Tanaka, Hiroyuki Kusuhara, Masashi Mizokami, Camille Sureau, Takaji Wakita
    Cyclosporin derivatives inhibit hepatitis B virus entry without interfering with NTCP transporter activity
    Hepatitis B virus (HBV) infection is a worldwide public health problem, which is estimated to chronically infect approximately 240 million individuals [1,2]. Chronic HBV infection elevates the risk of developing liver cirrhosis and hepatocellular carcinoma [3–5]. Current clinical treatments for HBV infection include interferons (IFN)s and nucleos(t)ide analogs (NAs) [6–8]. IFNα and its pegylated form (PegIFNα) modulate host immune response to viral infection and directly inhibit HBV replication in hepatocytes.

    Date de mise en ligne : Jeudi 24 novembre 2016
    Gladys Ferrere, Laura Wrzosek, Frédéric Cailleux, Williams Turpin, Virginie Puchois, Madeleine Spatz, Dragos Ciocan, Dominique Rainteau, Lydie Humbert, Cindy Hugot, Françoise Gaudin, Marie-Louise Noordine, Véronique Robert, Dominique Berrebi, Muriel Thomas, Sylvie Naveau, Gabriel Perlemuter, Anne-Marie Cassard
    Fecal microbiota manipulation prevents dysbiosis and alcohol-induced liver injury in mice
    Chronic alcohol consumption is the major cause of chronic liver disease in the world. Most long-term heavy drinkers develop steatosis, but only 10–35% develop liver inflammation (hepatitis), of which 8–20% ultimately progresses to cirrhosis [1]. Thus, factors other than alcohol intake influence the onset and progression of alcoholic liver disease (ALD). Among these, the intestinal microbiota (IM) plays a role in the pathogenesis of ALD [2,3]. The IM is involved in host homeostasis and maintenance of the intestinal barrier by several mechanisms such as preventing colonization by pathogenic bacteria and by cooperating with the intestinal epithelium to produce mucin 2 [3–6].

    Date de mise en ligne : Jeudi 24 novembre 2016
    Anthony W.H. Chan, Howard H.W. Leung, Charing C.N. Chong, Stephen L. Chan
    Validating the ALBI grade: Its current and future use in HCC prognostication
    We have read with interest the article from Pinato et al., who validated the prognostication of the albumin-bilirubin (ALBI) grade in an international cohort of 2426 patients with hepatocellular carcinoma (HCC) from Europe, the United States and Asia [1]. The authors confirmed that the ALBI grade was an independent prognostic factor among different treatment modalities, geographical location and time of study recruitment across each Barcelona Clinic Liver Cancer (BCLC) stage. In this letter, we would like to raise two interesting points for discussion.

    Date de mise en ligne : Lundi 21 novembre 2016
    Maria J. Monte, Marta Alonso-Peña, Oscar Briz, Elisa Herraez, Carmen Berasain, Josepmaria Argemi, Jesus Prieto, Jose J.G. Marin
    ACOX2 deficiency: An inborn error of bile acid synthesis identified in an adolescent with persistent hypertransaminasemia
    Bile acids play essential digestive functions and are critical signaling molecules that modulate intermediate metabolism and liver tissue homeostasis. They are synthetized by hepatocytes from cholesterol [1,2] through two main pathways involving enzymes located at the endoplasmic reticulum, cytosol, mitochondria and peroxisomes. These enzymes are responsible for modifying the sterol nucleus of cholesterol and shortening its side-chain [3,4]. Inborn errors of bile acid synthesis are rare autosomal recessive diseases accounting for 1–2% of cholestatic disorders in children [5].

    Date de mise en ligne : Vendredi 18 novembre 2016
    Teresa Ramirez, Yong-Mei Li, Shi Yin, Ming-Jiang Xu, Dechun Feng, Zhou Zhou, Mengwei Zang, Partha Mukhopadhyay, Zoltan V. Varga, Pal Pacher, Bin Gao, Hua Wang
    Aging aggravates alcoholic liver injury and fibrosis in mice by downregulating sirtuin 1 expression
    Alcoholic liver disease (ALD) is considered to be a major cause of morbidity and mortality nationwide [1–5]. It has an array of liver pathology that ranges from simple fatty liver to more severe forms of liver injury such as steatohepatitis, cirrhosis, and hepatocellular carcinoma. Many factors have been shown to affect the development and progression of ALD, including age, gender, ethnicity, genetic factors, drinking pattern, type of alcohol consumed, dose, duration, obesity, viral hepatitis infection, and environment [1–5].

    Date de mise en ligne : Jeudi 17 novembre 2016
    Elisabetta Ceni, Tommaso Mello, Simone Polvani, Mireille Vasseur-Cognet, Mirko Tarocchi, Sara Tempesti, Duccio Cavalieri, Luca Beltrame, Giada Marroncini, Massimo Pinzani, Stefano Milani, Andrea Galli
    The orphan nuclear receptor COUP-TFII coordinates hypoxia-independent proangiogenic responses in hepatic stellate cells
    An exuberant wound healing response to chronic liver injury culminates in excessive and altered deposition of extracellular matrix (ECM) components. It is temporally and spatially linked with vascular remodelling of hepatic sinusoids, angiogenesis and recruitment of inflammatory cells [1]. Hepatic stellate cells (HSC) play an important role in the physiological homeostasis of ECM in the liver, and are the precursors of activated myofibroblast-like cells responsible for the development of liver fibrosis.

    Date de mise en ligne : Mardi 15 novembre 2016
    Thomas Reiberger, Mattias Mandorfer
    Beta adrenergic blockade and decompensated cirrhosis
    Non-selective betablockers (NSBBs) remain the cornerstone of medical treatment of portal hypertension. The evidence for their efficacy to prevent variceal bleeding is derived from prospective trials, which largely excluded patients with refractory ascites and renal failure. In parallel to the increasing knowledge on portal hypertension-induced changes in systemic hemodynamics, cardiac function, and renal perfusion, emerging studies have raised concerns about harmful effects of NSBBs. Clinicians are facing an ongoing controversy on the use of NSBBs in patients with advanced cirrhosis.

    Date de mise en ligne : Samedi 05 novembre 2016
    Veronika Lukacs-Kornek, Frank Lammert
    The progenitor cell dilemma: Cellular and functional heterogeneity in assistance or escalation of liver injury
    Liver progenitor cells (LPCs) are quiescent cells that are activated during liver injury and thought to give rise to hepatocytes and cholangiocytes in order to support liver regeneration and tissue restitution. While hepatocytes are capable of self-renewal, during most chronic injuries the proliferative capacity of hepatocytes is inhibited, thus LPCs provide main source for regeneration. Despite extensive lineage tracing studies, their role and involvement in these processes are often controversial.

    Date de mise en ligne : Samedi 05 novembre 2016
    Carlo Spirli, Valeria Mariotti, Ambra Villani, Luca Fabris, Romina Fiorotto, Mario Strazzabosco
    Adenylyl cyclase 5 links changes in calcium homeostasis to cAMP-dependent cyst growth in polycystic liver disease
    Autosomal dominant polycystic kidney disease (ADPKD) is characterized by formation of multiple cysts in the kidney, liver and pancreas [1]. In the liver (polycystic liver disease [PLD]-ADPKD), multiple fluid-filled cysts progressively dilate and grow until their complications mandate surgery or liver transplantation [2,3]. PLD-ADPKD is associated with mutations in one of two genes: PKD1, and PKD2, that code for polycystin-1 (PC1) and polycystin-2 (PC2), respectively. These two proteins are involved in intracellular signaling, cell differentiation and epithelial morphogenesis [4].

    Date de mise en ligne : Samedi 05 novembre 2016
    Vincent Mallet, Kamal Hamed, Michaël Schwarzinger
    Prognosis of patients with chronic hepatitis B in France (2008–2013): A nationwide, observational and hospital-based study
    Approximately 3.61% of the global population is chronically infected with hepatitis B virus (HBV) [1]. A fraction of these will progress to a liver-related complication, including end-stage liver disease (ESLD) and hepatocellular carcinoma (HCC), and will contribute to more than half of liver deaths worldwide [2,3].

    Date de mise en ligne : Jeudi 03 novembre 2016
    Naveed Z. Janjua, Mei Chong, Margot Kuo, Ryan Woods, Jason Wong, Eric M. Yoshida, Morris Sherman, Zahid A. Butt, Hasina Samji, Darrel Cook, Amanda Yu, Maria Alvarez, Mark Tyndall, Mel Krajden
    Long-term effect of sustained virological response on hepatocellular carcinoma in patients with hepatitis C in Canada
    Hepatitis C virus (HCV) infection is a major global health concern with about 184 million people infected worldwide [1]. In North America, about two-thirds of chronic infections are among people born between 1945–1965 and, having acquired the virus decades ago, are now increasingly being diagnosed with serious liver-related illnesses including decompensated cirrhosis and hepatocellular carcinoma (HCC) [2–4]. Due to the low uptake and effectiveness (∼50% cured), interferon-based treatments resulted in limited population level impact [5,6].

    Date de mise en ligne : Mercredi 02 novembre 2016
    Austin G. Duffy, Susanna V. Ulahannan, Oxana Makorova-Rusher, Osama Rahma, Heiner Wedemeyer, Drew Pratt, Jeremy L. Davis, Marybeth S. Hughes, Theo Heller, Mei ElGindi, Ashish Uppala, Firouzeh Korangy, David E. Kleiner, William D. Figg, David Venzon, Seth M. Steinberg, Aradhana M. Venkatesan, Venkatesh Krishnasamy, Nadine Abi-Jaoudeh, Elliot Levy, Brad J. Wood, Tim F. Greten
    Tremelimumab in combination with ablation in patients with advanced hepatocellular carcinoma
    Hepatocellular carcinoma (HCC) is one of the most frequently occurring cancers worldwide, ranked 3rd in global incidence by the International Agency for Research on Cancer [1]. HCC typically occurs in the setting of chronic inflammation, such as that induced by viral hepatitis. In contrast to other types of cancer, where surgery, radiation and chemotherapies dominate the therapeutic landscape, in HCC locoregional treatments are widely applied, either with curative (ablative procedures, surgery) or palliative (arterial chemoembolization) intent [2].

    Date de mise en ligne : Mardi 01 novembre 2016
    Anshu Srivastava, Saurabh Chaturvedi, Rakesh Kumar Gupta, Rohan Malik, Amrita Mathias, Naranamangalam R. Jagannathan, Sunil Jain, Chandra Mani Pandey, Surender Kumar Yachha, Ram Kishor Singh Rathore
    Minimal hepatic encephalopathy in children with chronic liver disease: Prevalence, pathogenesis and magnetic resonance-based diagnosis
    Minimal hepatic encephalopathy (MHE) represents the mildest form of hepatic encephalopathy (HE) seen in patients with liver dysfunction and/or portosystemic shunting [1]. MHE is characterized by subtle motor and cognitive deficits, affecting attention, speed of information processing, motor abilities and co-ordination [1,2]. The prevalence of MHE in adults with chronic liver disease (CLD) ranges from 30–84% [2,3]. This variation is attributed to differences in severity of liver disease, extent of portosystemic shunting, and cut-offs for abnormal neuropsychological tests (NPT) for diagnosing MHE [2].

    Date de mise en ligne : Vendredi 28 octobre 2016
    Florence Wong, Paolo Angeli
    New diagnostic criteria and management of acute kidney injury
    Traditionally, the diagnosis of renal dysfunction in cirrhosis is defined as a 50% increase in serum creatinine (SCr) with a final SCr of ⩾1.5mg/dl (133μmol/L) [1]. However, smaller rises in SCr have also been shown to have a negative prognostic impact in decompensated cirrhosis, especially in patients with infection [2]. Therefore, the International Club of Ascites, in line with other subspecialty communities, formally adapted the term acute kidney injury (AKI) to represent renal dysfunction in cirrhosis [3].

    Date de mise en ligne : Vendredi 28 octobre 2016
    Partha Mukhopadhyay, Béla Horváth, Mohanraj Rajesh, Zoltán V. Varga, Karim Gariani, Dongryeol Ryu, Zongxian Cao, Eileen Holovac, Ogyi Park, Zhou Zhou, Ming-Jiang Xu, Wei Wang, Grzegorz Godlewski, Janos Paloczi, Balazs Tamas Nemeth, Yuri Persidsky, Lucas Liaudet, György Haskó, Peter Bai, A. Hamid Boulares, Johan Auwerx, Bin Gao, Pal Pacher
    PARP inhibition protects against alcoholic and non-alcoholic steatohepatitis
    Chronic alcoholism is a leading cause of liver disease worldwide. The development of alcoholic steatohepatitis involves alcohol and acetaldehyde-induced direct hepatocyte injury and death by increasing reactive oxygen and nitrogen species (ROS/RNS) production, lipid peroxidation and oxidative DNA injury, coupled with overactivation of hepatic inflammatory processes (both innate and adaptive immunity) and reprograming of lipid metabolism by promoting hepatic lipid accumulation [1–4]. Non-alcoholic fatty liver disease (NAFLD) may also progress to steatohepatitis (non-alcoholic steatohepatitis; NASH).

    Date de mise en ligne : Samedi 22 octobre 2016
    Adriaan J. van der Meer, Jordan J. Feld, Harald Hofer, Piero L. Almasio, Vincenza Calvaruso, Conrado M. Fernández-Rodríguez, Soo Aleman, Nathalie Ganne-Carrié, Roberta D’Ambrosio, Stanislas Pol, Maria Trapero-Marugan, Raoel Maan, Ricardo Moreno-Otero, Vincent Mallet, Rolf Hultcrantz, Ola Weiland, Karoline Rutter, Vito Di Marco, Sonia Alonso, Savino Bruno, Massimo Colombo, Robert J. de Knegt, Bart J. Veldt, Bettina E. Hansen, Harry L.A. Janssen
    Risk of cirrhosis-related complications in patients with advanced fibrosis following hepatitis C virus eradication
    Chronic infection with the hepatitis C virus (HCV) may lead to the development of hepatic fibrosis, which can ultimately progress to cirrhosis. Patients with cirrhosis have an increased risk to develop end-stage liver disease and hepatocellular carcinoma (HCC) [1]. A recent meta-analysis found that chronic HCV-infected patients with advanced hepatic fibrosis had an overall annual risk of 2.9% to experience liver failure, 3.2% to develop HCC and 2.7% to die of liver-related causes [2]. According to the current guidelines these patients should be included in HCC surveillance programs [3,4].

    Date de mise en ligne : Jeudi 20 octobre 2016
    Nathalie Goutté, Philippe Sogni, Noelle Bendersky, Jean Claude Barbare, Bruno Falissard, Olivier Farges
    Geographical variations in incidence, management and survival of hepatocellular carcinoma in a Western country
    Liver cancer, which is overrepresented by hepatocellular carcinoma (HCC), is the fifth most common cancer in men, the seventh most common cancer in women, and the second most common cause of cancer-related death worldwide [1,2]. Most cases of HCC occur in Sub-Saharan Africa and Eastern Asia, where incidence rates are high. South European countries have intermediate incidence rates, and the incidence in northern Europe, North America, and South America is low. Since the 1980s, the incidence of HCC has decreased in Asia, whereas it has increased in areas of low incidence such as North America and northern Europe [2].

    Date de mise en ligne : Mercredi 19 octobre 2016
    Magda Langiewicz, Andrea Schlegel, Enrica Saponara, Michael Linecker, Pieter Borger, Rolf Graf, Bostjan Humar, Pierre A. Clavien
    Hedgehog pathway mediates early acceleration of liver regeneration induced by a novel two-staged hepatectomy in mice
    The liver is unique with regards to its regenerative capacity. Its ability to regrow after tissue loss has permitted the surgical removal of large or multiple liver tumors with curative intent. Physiological limits to liver regeneration nevertheless exist. When the functional liver remnant is too small, the liver cannot recover vital function due to deficient hepatocyte proliferation [1,2]. In the clinic, resection-induced liver failure is known as the small-for-size syndrome (SFSS) and represents the most frequent cause of death due to liver surgery [3,4].

    Date de mise en ligne : Mercredi 19 octobre 2016
    Maud Lemoine, Mark R. Thursz
    Battlefield against hepatitis B infection and HCC in Africa
    Despite effective and safe hepatitis B virus (HBV) vaccine and antiviral therapies, HBV-related hepatocellular carcinoma (HCC) remains a major cause of deaths in young adults in Africa. There are multiple barriers to control the burden of HBV infection and HCC. In comparison to other major infectious diseases, HBV infection and liver diseases have received remarkably little attention from the global health community. There is an urgent need to improve birth dose vaccine coverage and implementing screening and treatment interventions.

    Date de mise en ligne : Jeudi 13 octobre 2016
    Yuchen Xia, Arnaud Carpentier, Xiaoming Cheng, Peter Daniel Block, Yao Zhao, Zhensheng Zhang, Ulrike Protzer, T. Jake Liang
    Human stem cell-derived hepatocytes as a model for hepatitis B virus infection, spreading and virus-host interactions
    Hepatitis B virus (HBV) remains a major public health threat with more than 240 million individuals chronically infected worldwide who are then at a high risk of developing liver cirrhosis and hepatocellular carcinoma (HCC) [1,2]. Currently, there are two classes of approved treatments: nucleos(t)ide analogs (NUC) and interferon-α (IFN-α). NUC targets viral polymerase, which limits virus replication, but cannot clear virus infection. Thus, patients need to take life-long treatment with the risk of developing drug resistance.

    Date de mise en ligne : Samedi 01 octobre 2016
    Christoph Roderburg, Christian Trautwein
    Cell-specific functions of miRNA in the liver
    miRNAs play essential roles in virtually all cellular and biological processes including liver development, differentiation and homeostasis [1,2]. Altered expression levels of miRNAs were observed in patients with liver diseases e.g., liver steatosis, cirrhosis and hepatocellular carcinoma (HCC) [1,3]. Expression pattern of miRNAs are organ- and tissue-specific. In the liver, miRNAs are not homogeneously distributed but are selectively expressed and regulated in distinct hepatic cell types. For certain miRNAs, opposite regulation were described between the different liver cell compartments.

    Date de mise en ligne : Lundi 18 février 2013
    Shunji Nagai, Marcelo Facciuto, Shozo Mori, Mizuki Ninomiya, Juan P. Rocca, Alan Contreras-Saldivar, Myron E. Schwartz, Sander S. Florman
    WITHDRAWN: Recurrence prediction of hepatocellular carcinoma after liver transplantation by ischemia time and tumor characteristics
    This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at http://www.elsevier.com/locate/withdrawalpolicy.

    Date de mise en ligne : Jeudi 01 janvier 1970
    EASL membership

    Date de mise en ligne : Jeudi 01 janvier 1970
    Richard Moreau, Ramon Bataller, Thomas Berg, Jessica Zucman-Rossi, Rajiv Jalan
    From the Editor’s desk...
    An intriguing paper in this issue investigates the mechanisms by which aging exacerbates the progression of alcoholic liver disease (ALD). Ramirez el al. demonstrate that, compared to young mice, middle-aged and old mice are more susceptible to alcohol-induced liver injury. Importantly, restoring hepatic expression of sirtuin 1 (Gene Symbol: Sirt1), which is markedly lower in older mice, ameliorates subacute liver injury induced by alcohol and also improves the fibrogenic response to chronic liver injury.

    Date de mise en ligne : Jeudi 01 janvier 1970

    Date de mise en ligne : Jeudi 01 janvier 1970
    EASL Clinical School of Hepatology: Course 28: Controversies in end-stage liver diseases. Madrid, Spain. 2017

    Date de mise en ligne : Jeudi 01 janvier 1970
    EASL Andrew K. Burroughs Short-term Training Fellowship

    Date de mise en ligne : Jeudi 01 janvier 1970
    EASL Monothematic Conference: Cholangiocytes in health and disease: From basic science to novel treatments. Oslo, Norway. 2017

    Date de mise en ligne : Jeudi 01 janvier 1970
    The International Liver Congress. Amsterdam, The Netherlands. 2017

    Date de mise en ligne : Jeudi 01 janvier 1970
    Editorial Board