Pediatric fulminant hepatic failure in endemic areas of hepatitis B infection: 15 years after universal hepatitis B vaccination

Huey‐Ling Chen, Chee‐Jen Chang, Man‐Shan Kong, Fu‐Chen Huang, Hung‐Chang Lee, Chieh‐Chung Lin, Ching‐Chuan Liu, I‐Hsien Lee, Tzee‐Chung Wu, Shu‐Fen Wu, Yen‐Hsuan Ni, Hong‐Yuan Hsu, Ding‐Shinn Chen, Mei‐Hwei Chang – 5 January 2004 – To investigate the role of hepatitis B virus (HBV) infection in pediatric fulminant hepatic failure (FHF) after the launch of universal HBV vaccination, the authors analyzed the data from patients with FHF collected from a nationwide collaborative study group.

Long‐term outcome (35 years) of hepatitis C after acquisition of infection through mini transfusions of blood given at birth

Maria Antonietta Casiraghi, Massimo De Paschale, Luisa Romanò, Renato Biffi, Agnese Assi, Giorgio Binelli, Alessandro Remo Zanetti – 5 January 2004 – Long‐term follow up studies of hepatitis C virus (HCV) infection rarely exceed 20–25 yr. We studied the outcome of HCV infection in 35‐yr‐old adults infected at birth (1968) through mini transfusions of blood. A retrospective‐prospective study was carried out. The cohort included 31 individuals who were given mini blood transfusions (21–30 ml) collected from a donor subsequently revealed to be HCV infected.

Over‐expression of the ribosomal protein L36a gene is associated with cellular proliferation in hepatocellular carcinoma

Jong‐Hyun Kim, Kyung‐Ran You, In Hee Kim, Baik‐Hwan Cho, Chan‐Young Kim, Dae‐Ghon Kim – 5 January 2004 – Using messenger RNA (mRNA) differential display, we identified a single complementary DNA (cDNA) fragment (HG23T1) that was over‐expressed in a hepatocellular carcinoma (HCC) specimen. We cloned the full‐length HG23T1 gene by the rapid amplification of cDNA end (RACE) polymerase chain reaction (PCR) method. It perfectly matched the gene encoding human ribosomal protein L36a (RPL36A also referred to as RPL44).

Genipin enhances Mrp2 (Abcc2)‐mediated bile formation and organic anion transport in rat liver

Junichi Shoda, Tetsuo Miura, Hirotoshi Utsunomiya, Koji Oda, Masahiro Yamamoto, Masahito Kano, Tadashi Ikegami, Naomi Tanaka, Hidetaka Akita, Kousei Ito, Hiroshi Suzuki, Yuichi Sugiyama – 5 January 2004 – Inchin‐ko‐to (ICKT), an herbal medicine, and its ingredients exert potent choleretic effects by a “bile acid‐independent” mechanism. The current study was designed to determine whether ICKT or its ingredients potentiate multidrug resistance‐associated protein 2 (Mrp2; Abcc2)‐mediated choleresis in vivo.

Vascular involvement of the liver in Turner's syndrome

Dominique Roulot, Claude Degott, Olivier Chazouillères, Frédéric Oberti, Paul Calès, Nicolas Carbonell, Said Benferhat, Solange Bresson‐Hadni, Dominique Valla – 5 January 2004 – Unexplained liver test abnormalities are frequent in patients with Turner's syndrome. This cohort study was performed to clarify the histopathologic features, causes, and long‐term outcome of liver involvement in these patients. Thirty patients with persistently abnormal liver test results were followed‐up for 8.8 ± 5.2 years. Liver specimens were available in 27 patients.

A pilot study of pioglitazone treatment for nonalcoholic steatohepatitis

Kittichai Promrat, Glen Lutchman, Gabriel I. Uwaifo, Renee J. Freedman, Alejandro Soza, Theo Heller, Edward Doo, Marc Ghany, Ahalya Premkumar, Yoon Park, T. Jake Liang, Jack A. Yanovski, David E. Kleiner, Jay H. Hoofnagle – 5 January 2004 – Nonalcoholic steatohepatitis (NASH) is a common chronic liver disease for which there is no known effective therapy. A proportion of patients with NASH progress to advanced fibrosis and cirrhosis. NASH is considered one of the clinical features of the metabolic syndrome in which insulin resistance plays a central role.

Cholestasis shuts down calcium signaling in cholangiocytes

Juliette Martin, Jean‐François Dufour – 5 January 2004 – Background & Aims: Cholestasis is one of the principal manifestations of liver disease and often results from disorders involving bile duct epithelia rather than hepatocytes. A range of disorders affects biliary epithelia, and no unifying pathophysiologic event in these cells has been identified as the cause of cholestasis.

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