Early viral load and recipient interleukin‐28B rs12979860 genotype are predictors of the progression of hepatitis C after liver transplantation

Ivo W. Graziadei, Heinz M. Zoller, Anna Schloegl, Karin Nachbaur, Karl‐Peter Pfeiffer, Walter Mark, Gregor Mikuz, Johann Pratschke, Raimund Margreiter, Wolfgang Vogel – 2 February 2012 – There have been few detailed studies of viral kinetics after liver transplantation (LT), and conflicting data have been reported on viral loads and the severity of recurrent hepatitis C virus (HCV) disease.

Sinusoidal C4d deposits in liver allografts indicate an antibody‐mediated response: Diagnostic considerations in the evaluation of liver allografts

Tomasz Kozlowski, Kenneth Andreoni, John Schmitz, Paul Hideo Hayashi, Volker Nickeleit – 2 February 2012 – There is a paucity of data concerning the correlation of complement component 4d (C4d) staining in liver allografts and antibody‐mediated rejection. Data about the location and character of C4d deposits in native and allograft liver tissues are inconsistent.

Cannabinoid receptor 2 agonist ameliorates mesenteric angiogenesis and portosystemic collaterals in cirrhotic rats

Hui‐Chun Huang, Sun‐Sang Wang, I‐Fang Hsin, Ching‐Chih Chang, Fa‐Yauh Lee, Han‐Chieh Lin, Chiao‐Lin Chuang, Jing‐Yi Lee, Hsian‐Guey Hsieh, Shou‐Dong Lee – 30 January 2012 – Angiogenesis in liver cirrhosis leads to splanchnic hyperemia, increased portal inflow, and portosystemic collaterals formation, which may induce lethal complications, such as gastroesophageal variceal hemorrhage and hepatic encephalopathy. Cannabinoids (CBs) inhibit angiogenesis, but the relevant influences in cirrhosis are unknown.

Outcomes of living donor liver transplantation for patients with preoperative type 1 hepatorenal syndrome and acute hepatic decompensation

Kenneth S. H. Chok, James Y. Y. Fung, See Ching Chan, Tan To Cheung, William W. Sharr, Albert C. Y. Chan, Sheung Tat Fan, Chung Mau Lo – 30 January 2012 – This study investigated the outcomes of living donor liver transplantation (LDLT) for patients with preoperative type 1 hepatorenal syndrome (HRS) and acute hepatic decompensation. Prospectively collected data for 104 patients who had fulminant hepatic failure, acute decompensation of cirrhosis, or an acute flare of chronic hepatitis B were analyzed.

Disruption of phospholipid and bile acid homeostasis in mice with nonalcoholic steatohepatitis

Naoki Tanaka, Tsutomu Matsubara, Kristopher W. Krausz, Andrew D. Patterson, Frank J. Gonzalez – 30 January 2012 – Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease that can develop into cirrhosis, hepatic failure, and hepatocellular carcinoma. Although several metabolic pathways are disrupted and endogenous metabolites may change in NASH, the alterations in serum metabolites during NASH development remain unclear.

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