Acute Exacerbation of Chronic Hepatitis B Virus Infection After Withdrawal of Lamivudine Therapy

Pieter Honkoop, Robert A. de Man, Hubert G.M. Niesters, Pieter E. Zondervan, Solko W. Schalm – 30 December 2003 – Acute exacerbations of chronic hepatitis B virus (HBV) infection occur after withdrawal of lamivudine therapy in approximately 16% of patients and are considered of little clinical significance. We observed “lamivudine withdrawal hepatitis” accompanied by jaundice and incipient liver failure, but also followed by complete recovery and viral clearance.

Hepatocyte growth factor promotes cell survival from Fas‐mediated cell death in hepatocellular carcinoma cells via Akt activation and Fas‐death–inducing signaling complex suppression

Atsushi Suzuki, Midori Hayashida, Hirokazu Kawano, Kazushi Sugimoto, Takeshi Nakano, Katsuya Shiraki – 30 December 2003 – The Akt/PI‐3 kinase pathway is a system essential for cell survival. In the current study, we showed that hepatocyte growth factor (HGF) activates the Akt/PI‐3 kinase pathway to suppress Fas‐mediated cell death in human hepatocellular carcinoma (HCC; 3 lines; SK‐Hep1, HLE, and Chang Liver cell lines), hepatoblastoma (1 line; HepG2), and embryonic hepatocyte (1 line; WRL). Five tested cell lines showed the resistance to Fas‐mediated cell death by the pretreatment of HGF.

Randomized, double‐blind, placebo‐controlled trial of interferon Alfa2a with and without amantadine as initial treatment for chronic hepatitis C

Stefan Zeuzem, Gerlinde Teuber, Uta Naumann, Thomas Berg, Jochen Raedle, Susanne Hartmann, Uwe Hopf – 30 December 2003 – Although the antiviral effects of amantadine sulphate (1‐aminoadamantan sulphate) have not been characterized for the hepatitis C virus (HCV), previous pilot studies have suggested promising results in patients with chronic hepatitis C. The aim of the present study was to compare the efficacy, safety, and health‐related quality of life (HRQOL) of interferon alfa (IFN‐α) alone or in combination with oral amantadine for treatment of chronic hepatitis C.

γ‐Glutamyltranspeptidase–deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial function, and cellular function

Yvonne Will, Kay A. Fischer, Robert A. Horton, Rhonda S. Kaetzel, Marda K. Brown, Olaf Hedstrom, Michael W. Lieberman, Donald J. Reed – 30 December 2003 – γ‐Glutamyltranspeptidase (GGT)‐deficient mice (GGT−/−) display chronic glutathione (GSH) deficiency, growth retardation, and die at a young age (<20 weeks). Using livers from these mice, we investigated the relationship between GSH content, especially mitochondrial, and mitochondrial and cellular function.

Heparan sulfate proteoglycans initiate dengue virus infection of hepatocytes

Philip Hilgard, Richard Stockert – 30 December 2003 – Dengue viruses (DEN) cause a broad spectrum of clinical manifestations including potentially life‐threatening conditions such as hemorrhagic shock syndrome and less frequently acute hepatitis with liver failure and encephalopathy. In addition, dengue viruses provide a potential model to understand the initiation of hepatocyte infection by the structurally closely related hepatitis C virus (HCV), because this virus at present cannot be grown in cell culture.

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