The non‐immunosuppressive cyclosporin DEBIO‐025 is a potent inhibitor of hepatitis C virus replication in vitro

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.

Similarities and differences in outcomes of cirrhosis due to nonalcoholic steatohepatitis and hepatitis C

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.

Progression of liver fibrosis among injection drug users with chronic hepatitis C

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.

A randomized trial of endoscopic treatment of acute gastric variceal hemorrhage: N‐Butyl‐2‐Cyanoacrylate injection versus band ligation

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.

COX‐2 induction in mice with experimental nutritional steatohepatitis: Role as pro‐inflammatory mediator

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.

Coinheritance of Gilbert syndrome–associated UGT1A1 mutation increases gallstone risk in cystic fibrosis

Hermann E. Wasmuth, Hildegard Keppeler, Ulrike Herrmann, Ramin Schirin‐Sokhan, Michael Barker, Frank Lammert – 23 March 2006 – The prevalence of “black” pigment gallstones is increased in patients with cystic fibrosis (CF). Bile acid malabsorption with augmented bilirubin uptake from the intestine and the development of “hyperbilirubinbilia” have been proposed as key factors in gallstone formation in CF patients.

Progression of fibrosis in hepatitis C with and without schistosomiasis: Correlation with serum markers of fibrosis

Sanaa M. Kamal, Bradley Turner, Qi He, Jens Rasenack, Leonardo Bianchi, Ahmed Al Tawil, Ahmed Nooman, Mahmoud Massoud, Margaret James Koziel, Nezam H. Afdhal – 23 March 2006 – Serial liver biopsies are the gold standard by which the progression of fibrosis is evaluated. This longitudinal cohort study assessed the different rates in the progression of fibrosis using serial liver biopsies and serum fibrosis markers YKL‐40 and PIIINP and the cytokines, transforming growth factor beta (TGF‐β) and tumor necrosis factor alpha (TNF−α).

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