Ponni Perumalswami, David E. Kleiner, Glen Lutchman, Theo Heller, Brian Borg, Yoon Park, T. Jake Liang, Jay H. Hoofnagle, Marc G. Ghany – 23 March 2006 – Hepatic steatosis is common in patients with chronic hepatitis C (CHC) and is reported to be a risk factor for progression of fibrosis. The aims of this study were to evaluate the interactions between hepatic steatosis and fibrosis in a well‐defined cohort of patients with CHC.

Sathish Kumar Natarajan, Prabhu Ramamoorthy, Simmy Thomas, Jayasree Basivireddy, Gagandeep Kang, Anup Ramachandran, Anna B Pulimood, K.A. Balasubramanian – 23 March 2006 – Spontaneous bacterial peritonitis is a major cause of mortality after liver cirrhosis. Altered permeability of the mucosa and deficiencies in host immune defenses through bacterial translocation from the intestine due to intestinal bacterial overgrowth have been implicated in the development of this complication. Molecular mechanisms underlying the process are not well known.

Peter F. Whitington – 23 March 2006

Matthias Engelke, Kerry Mills, Stefan Seitz, Petra Simon, Philippe Gripon, Martina Schnölzer, Stephan Urban – 23 March 2006 – Insights into the early infection events of the human hepatitis B (HBV) and hepatitis delta virus (HDV) have been limited because of the lack of a cell culture system supporting the full replication cycle for these important pathogens. The human hepatoma cell line HepaRG allows the experimental induction of a differentiated state, thereby gaining susceptibility toward HBV and HDV infection.

Jan Paeshuyse, Artur Kaul, Erik De Clercq, Brigitte Rosenwirth, Jean‐Maurice Dumont, Pietro Scalfaro, Ralf Bartenschlager, Johan Neyts – 23 March 2006 – Cyclosporin A (CsA) inhibits the in vitro replication of HCV subgenomic replicons. We here report on the potent anti‐HCV activity of the non‐immunosuppressive cyclosporin DEBIO‐025. The 50% effective concentration for inhibition of HCV subgenomic replicon replication in Huh 5‐2 cells (luciferase assay) by DEBIO‐025 was 0.27 ± 0.03 μg/mL and for CsA 2.8 ± 0.4 μg/mL.

Arun J. Sanyal, Colin Banas, Carol Sargeant, Velimir A. Luketic, Richard K. Sterling, Richard T. Stravitz, Mitchell L. Shiffman, Douglas Heuman, Adrian Coterrell, Robert A. Fisher, Melissa J. Contos, Alan S. Mills – 23 March 2006 – The objective of this study was to prospectively define outcomes of cirrhosis due to nonalcoholic steatohepatitis (NASH) and compare them with those associated with hepatitis C virus (HCV) infection. We compared 152 patients with cirrhosis due to NASH with 150 matched patients with cirrhosis due to HCV.

Lucy E. Wilson, Michael Torbenson, Jacquie Astemborski, Hawazin Faruki, Charles Spoler, Rudra Rai, Shruti Mehta, Gregory D. Kirk, Kenrad Nelson, Nezam Afdhal, David L. Thomas – 23 March 2006 – Although most hepatitis C virus (HCV) infections are acquired by injection drug use, prospective data on the progression of liver fibrosis are sparse. Baseline liver biopsies were obtained (1996–1998) on a random sample of 210 out of 1667 HCV‐positive injection drug users (IDUs). Subjects were followed biannually, with a second biopsy offered to those eligible.

23 March 2006

Pen‐Chung Tan, Ming‐Chih Hou, Han‐Chieh Lin, Tsu‐Te Liu, Fa‐Yauh Lee, Full‐Young Chang, Shou‐Dong Lee – 23 March 2006 – Progression of gastric variceal hemorrhage (GVH) is poorer than esophageal variceal bleeding. However, data on its optimal treatment are limited. We designed a prospective study to compare the efficacy of endoscopic band ligation (GVL) and endoscopic N‐butyl‐2‐cyanoacrylate injection (GVO). Liver patients with cirrhosis with or without concomitant hepatocellular carcinoma (HCC) and patients presenting with acute GVH were randomized into two treatment groups.

Jun Yu, Emilia Ip, Aileen dela Peña, Jing Yun Hou, Jayshree Sesha, Natasha Pera, Pauline Hall, Richard Kirsch, Isabelle Leclercq, Geoffrey C. Farrell – 23 March 2006 – The underlying mechanisms that perpetuate liver inflammation in nonalcoholic steatohepatitis are poorly understood. We explored the hypothesis that cyclooxygenase‐2 (COX‐2) can exert pro‐inflammatory effects in metabolic forms of fatty liver disease.