The potent bile acid sequestrant colesevelam is not effective in cholestatic pruritus: Results of a double‐blind, randomized, placebo‐controlled trial

Edith M. M. Kuiper, Karel J. van Erpecum, Ulrich Beuers, Bettina E. Hansen, H. Bing Thio, Robert A. de Man, Harry L. A. Janssen, Henk R. van Buuren – 30 June 2010 – Colesevelam is an anion‐exchange resin with a 7‐fold higher bile acid–binding capacity and fewer side effects than cholestyramine, the current first‐line treatment option for cholestatic pruritus. The aim of this trial was to compare the effects of colesevelam and a placebo in patients with cholestatic pruritus.

Liver‐enriched transcription factors regulate MicroRNA‐122 that targets CUTL1 during liver development

Hui Xu, Jie‐Hua He, Zhen‐Dong Xiao, Qian‐Qian Zhang, Yue‐Qin Chen, Hui Zhou, Liang‐Hu Qu – 30 June 2010 – MicroRNA‐122 (miR‐122) is a liver‐specific microRNA whose expression is specifically turned on in the mouse liver during embryogenesis, thus it is expected to be involved in liver development. However, the role of miR‐122 in liver development and its potential underlying mechanism remain unclear.

Acute liver failure due to antitubercular therapy: Strategy for antitubercular treatment before and after liver transplantation

Philippe Ichai, Faouzi Saliba, Fadi Antoun, Daniel Azoulay, Mylène Sebagh, Teresa Maria Antonini, Lélia Escaut, Delvart Valérie, Denis Castaing, Didier Samuel – 30 June 2010 – The standard antitubercular treatment (ATT), which consists of isoniazid (INH), rifampicin (RIF), ethambutol, and pyrazinamide (PZA), is the best available treatment for tuberculosis (TB). However, the hepatotoxicity of INH and PZA can be severe, and even after drug withdrawal, patients may require liver transplantation (LT). In these cases, the strategy for the treatment of TB is poorly defined.

Randomized trial of peginterferon alfa‐2b and ribavirin for 48 or 72 weeks in patients with hepatitis C virus genotype 1 and slow virologic response

Maria Buti, Yoav Lurie, Natalia G. Zakharova, Natalia P. Blokhina, Andrzej Horban, Gerlinde Teuber, Christoph Sarrazin, Ligita Balciuniene, Saya V. Feinman, Rab Faruqi, Lisa D. Pedicone, Rafael Esteban, for the SUCCESS Study Investigators – 30 June 2010 – The benefit of extending treatment duration with peginterferon (PEG‐IFN) and ribavirin (RBV) from 48 weeks to 72 weeks for patients with chronic hepatitis C genotype 1 infection has not been well established.

I148M patatin‐like phospholipase domain‐containing 3 gene variant and severity of pediatric nonalcoholic fatty liver disease

Luca Valenti, Anna Alisi, Enrico Galmozzi, Andrea Bartuli, Benedetta Del Menico, Arianna Alterio, Paola Dongiovanni, Silvia Fargion, Valerio Nobili – 30 June 2010 – Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease in children. Genetic variability, which is a main player in NAFLD, is especially characterized by polymorphisms in genes involved in the development and progression of the disease to nonalcoholic steatohepatitis (NASH).

Virologic response rates of weight‐based taribavirin versus ribavirin in treatment‐naive patients with genotype 1 chronic hepatitis C

Fred Poordad, Eric Lawitz, Mitchell L. Shiffman, Tarek Hassanein, Andrew J. Muir, Bruce R. Bacon, Jamie Heise, Deanine Halliman, Eric Chun, Janet Hammond – 30 June 2010 – Ribavirin‐induced hemolytic anemia can prompt dose reductions and lower sustained virologic response (SVR) rates in the treatment of patients with chronic hepatitis C. The study aimed to determine if weight‐based dosing of taribavirin (TBV), an oral prodrug of ribavirin (RBV), demonstrated efficacy comparable to RBV while maintaining its previously demonstrated anemia advantage with fixed dose administration. A U.S.

Defective bone morphogenic protein signaling underlies hepcidin deficiency in HFE hereditary hemochromatosis

John D. Ryan, Eleanor Ryan, Aurelie Fabre, Matthew W. Lawless, John Crowe – 30 June 2010 – Hereditary hemochromatosis (HH) is a common inherited iron overload disorder. The vast majority of patients carry the missense Cys282Tyr mutation of the HFE gene. Hepcidin, the central regulator of iron homeostasis, is deficient in HH, leading to unchecked iron absorption and subsequent iron overload. The bone morphogenic protein (BMP)/small mothers against decapentaplegic (Smad) signaling cascade is central to the regulation of hepcidin.

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