Quantitative liver function tests improve the prediction of clinical outcomes in chronic hepatitis C: Results from the hepatitis C antiviral long‐term treatment against cirrhosis trial

Gregory T. Everson, Mitchell L. Shiffman, John C. Hoefs, Timothy R. Morgan, Richard K. Sterling, David A. Wagner, Shannon Lauriski, Teresa M. Curto, Anne Stoddard, Elizabeth C. Wright, the HALT‐C Trial Group – 26 October 2011 – Risk for future clinical outcomes is proportional to the severity of liver disease in patients with chronic hepatitis C virus (HCV). We measured disease severity by quantitative liver function tests (QLFTs) to determine cutoffs for QLFTs that identified patients who were at low and high risk for a clinical outcome.

Claudin‐1 involved in neonatal ichthyosis sclerosing cholangitis syndrome regulates hepatic paracellular permeability

Brigitte Grosse, Doris Cassio, Nadya Yousef, Céline Bernardo, Emmanuel Jacquemin, Emmanuel Gonzales – 26 October 2011 – Neonatal ichthyosis and sclerosing cholangitis (NISCH) syndrome is a liver disease caused by mutations of CLDN1 encoding Claudin‐1, a tight‐junction (TJ) protein. In this syndrome, it is speculated that cholestasis is caused by Claudin‐1 absence, leading to increased paracellular permeability and liver injuries secondary to paracellular bile regurgitation. We studied the role of claudin‐1 in hepatic paracellular permeability.

Thrombocytopenia, splenomegaly, and portal blood flow in patients who have undergone liver transplantation for cirrhosis

Daniel Eyraud, Benjamin Granger, Christian Ionescu, Silvia Fratéa, Sabine Darnat, Jean‐Christophe Vaillant, Jean‐Michel Siksik, Laurent Hannoun, Pierre Coriat – 17 October 2011 – The platelet count (PC), the spleen size (SS), and the portal blood flow (PBF) have been independently studied in the perioperative period after orthotopic liver transplantation (OLT) for cirrhosis, but these parameters have not been described and analyzed in combination.

Hepatitis E virus (HEV)‐specific T‐cell responses are associated with control of HEV infection

Pothakamuri Venkata Suneetha, Sven Pischke, Verena Schlaphoff, Jan Grabowski, Paraskevi Fytili, Anna Gronert, Birgit Bremer, Antoaneta Markova, Jerzy Jaroszewicz, Christoph Bara, Michael P. Manns, Markus Cornberg, Heiner Wedemeyer – 17 October 2011 – Hepatitis E virus (HEV) infection is usually self‐limited but may lead to acute hepatitis and rarely to fulminant hepatic failure. Persistent HEV infections have recently been described in organ transplant recipients receiving immunosuppressive medications, suggesting that HEV is controlled by adaptive immune responses.

The protease inhibitor, GS‐9256, and non‐nucleoside polymerase inhibitor tegobuvir alone, with ribavirin, or pegylated interferon plus ribavirin in hepatitis C

Stefan Zeuzem, Peter Buggisch, Kosh Agarwal, Patrick Marcellin, Daniel Sereni, Hartwig Klinker, Christophe Moreno, Jean‐Pierre Zarski, Yves Horsmans, Hongmei Mo, Sarah Arterburn, Steven Knox, David Oldach, John G. McHutchison, Michael P. Manns, Graham R. Foster – 17 October 2011 – Tegobuvir (GS‐9190), a non‐nucleoside nonstructural protein (NS)5B polymerase inhibitor, and GS‐9256, an NS3 serine protease inhibitor, individually have activity against hepatitis C virus (HCV) genotype 1.

Subscribe to