Hepatic venous outflow obstruction in pediatric living donor liver transplantation using left‐sided lobe grafts: Kyoto university experience

Seisuke Sakamoto, Hiroto Egawa, Hiroyuki Kanazawa, Toshiya Shibata, Aya Miyagawa‐Hayashino, Hironori Haga, Yasuhiro Ogura, Mureo Kasahara, Koichi Tanaka, Sinji Uemoto – 29 July 2010 – The goals of this study were to evaluate the incidence of hepatic venous outflow obstruction (HVOO) in pediatric patients after living donor liver transplantation (LDLT) using left‐sided lobe grafts and to assess the therapeutic modalities used for the treatment of this complication at a single center.

Mycobacterium tuberculosis infection in liver transplantation

Baligh R. Yehia, Emily A. Blumberg – 29 July 2010 – Mycobacterium tuberculosis can cause significant infections in liver transplant candidates and recipients. Its nonspecific clinical features and prolonged growth time in culture make the diagnosis difficult, and treating tuberculosis (TB) remains challenging because of significant toxicities and drug‐drug interactions. The diagnosis of a latent TB infection may be accomplished with tuberculin skin testing and with the newer interferon‐γ release assays, although this infection may be underrecognized because of host factors.

Phosphoinositide 3‐kinase/protein kinase B signaling pathway is involved in estradiol 17β‐d‐glucuronide–induced cholestasis: Complementarity with classical protein kinase c

Andrea C. Boaglio, Andrés E. Zucchetti, Enrique J. Sánchez Pozzi, José M. Pellegrino, Justina Elena Ochoa, Aldo D. Mottino, Mary Vore, Fernando A. Crocenzi, Marcelo G. Roma – 29 July 2010 – Estradiol 17β‐D‐glucuronide (E217G) is an endogenous, cholestatic metabolite that induces endocytic internalization of the canalicular transporters relevant to bile secretion: bile salt export pump (Bsep) and multidrug resistance–associated protein 2 (Mrp2). We assessed whether phosphoinositide 3‐kinase (PI3K) is involved in E217G‐induced cholestasis.

Raised hepatic bile acid concentrations during pregnancy in mice are associated with reduced farnesoid X receptor function

Alexandra Milona, Bryn M. Owen, Jeremy F. L. Cobbold, Ellen C. L. Willemsen, Isobel J. Cox, Mohamed Boudjelal, William Cairns, Kristina Schoonjans, Simon D. Taylor‐Robinson, Leo W. J. Klomp, Malcolm G. Parker, Roger White, Saskia W. C. van Mil, Catherine Williamson – 29 July 2010 – Pregnancy alters bile acid homeostasis and can unmask cholestatic disease in genetically predisposed but otherwise asymptomatic individuals. In this report, we show that normal pregnant mice have raised hepatic bile acid levels in the presence of procholestatic gene expression.

Endotoxin accumulation prevents carcinogen‐induced apoptosis and promotes liver tumorigenesis in rodents

Le‐Xing Yu, He‐Xin Yan, Qiong Liu, Wen Yang, Hong‐Ping Wu, Wei Dong, Liang Tang, Yan Lin, Ya‐Qin He, Shan‐Shan Zou, Chao Wang, Hui‐Lu Zhang, Guang‐Wen Cao, Meng‐Chao Wu, Hong‐Yang Wang – 29 July 2010 – Increasing evidence suggests that the presence of endotoxemia is of substantial clinical relevance to patients with cirrhosis, but it is unclear whether and how gut‐derived LPS amplifies the tumorigenic response of the liver. We found that the circulating levels of LPS were elevated in animal models of carcinogen‐induced hepatocarcinogenesis.

Putting flesh and polish on autoimmune hepatitis and moving the disease of exclusion to inclusion

Albert J. Czaja – 29 July 2010 – Autoimmune hepatitis emerged during an era when concepts of neonatal immune tolerance, clonal selection of lymphocytes, and “forbidden clones” of activated immune cells were forming. The diagnosis had to be deduced from circumstantial evidence and by exclusion of other conditions. The goals of this review are to demonstrate how a clinician nonscientist can contribute to the maturation of autoimmune hepatitis and to illustrate the principles of clinical investigation that can be applied broadly to other projects.

Risk factors for infection during treatment with peginterferon alfa and ribavirin for chronic hepatitis C

Robert Roomer, Bettina E. Hansen, Harry L. A. Janssen, Robert J. de Knegt – 29 July 2010 – Neutropenia during treatment with peginterferon alfa and ribavirin for chronic hepatitis C virus (HCV) infection is a common cause of dose reductions of peginterferon alfa. These reductions are performed to prevent bacterial and fungal infections, which are common during HCV treatment and can be attributed to neutropenia. The aims of this study were to investigate the occurrence of infections and their relation to neutropenia and to identify potential risk factors for infections during HCV treatment.

Subscribe to