J Heathcote – 1 May 1996

P K Yuet, D Blankschtein, J M Donovan – 1 April 1996 – To accurately determine the cholesterol (Ch) distribution between mixed micelles and vesicles in lithogenic bile, both ultracentrifugation and gel chromatography with the correct intermixed micellar/vesicular bile salt concentration (IMC) have been proposed. We have systematically compared both separation techniques with physiological model biles to ascertain their quantitative separation ability.

P H McGuinness, G A Bishop, D M Painter, R Chan, G W McCaughan – 1 April 1996 – The balance between a direct cytopathic effect by hepatitis C virus (HCV) and immune‐mediated injury remains unclear. This report aims to test the following hypotheses: (1) that intrahepatic HCV load would correlate with the degree of liver injury; (2) that interferon alfa (IFN‐α) would decrease intrahepatic HCV‐RNA levels. Liver tissues (n = 56) were obtained from 47 patients with chronic HCV (9 before and after IFN‐α therapy).

G V Gregorio, P Jara, L Hierro, C Diaz, A de la Vega, A Vegnente, R Iorio, F Bortolotti, C Crivellaro, L Zancan, H Daniels, B Portmann, G Mieli‐Vergani – 1 April 1996 – The comparative efficacy of prednisolone followed by interferon alfa (IFN‐α) versus IFN‐α alone in enhancing the rate of antibody to hepatitis B e antigen (anti‐HBe) seroconversion has not been evaluated in a large cohort of white children.

K Sone, M Maeda, K Wakabayashi, N Takeichi, M Mori, T Sugimura, M Nagao – 1 April 1996 – Trientine dihydrochloride (trientine) is an alternative medicinal copper chelating agent for patients with Wilson's disease of penicillamine intolerance. We examined the effects of trientine on the spontaneous development of hepatitis and hepatic tumors, by its short‐ term and long‐term administration to Long‐Evans cinnamon (LEC) rats with an accumulation of copper in the liver, as animal models of Wilson's disease.

J G Wagner, P E Ganey, R A Roth – 1 April 1996 – Polymorphonuclear leukocytes (PMNS) have been implicated as cellular mediators of hepatic injury in models of inflammation in vivo. In vitro, hepatocyte killing by activated PMNs is mediated in part by proteases, but the role of nitric oxide is unknown. NO is produced by PMNs and hepatocytes and can act either to damage or protect in various models of toxicity. Therefore, we tested the hypothesis that NO is important in PMN‐mediated hepatocyte killing in vitro.

P Portincasa, K J van Erpecum, A Jansen, W Renooij, M Gadellaa, G P van Berge‐Henegouwen – 1 April 1996 – Besides classical plate‐like cholesterol monohydrate crystals, a variety of crystal shapes have recently been described in model biles but their relevance for human gallstone formation is unknown. We therefore studied crystallization behavior in gallbladder bile from cholesterol stone patients (54 untreated, 13 ursodeoxycholate‐treated) and 6 pigment stone patients.

C L Booth, G M Pollack, K L Brouwer – 1 April 1996 – Previous work in this laboratory has suggested that the nonlinear disposition of valproic acid (VPA) in the rat may be due to nonlinear distribution of VPA into the liver. The present study was undertaken to elucidate further the hepatobiliary disposition of VPA. VPA (0.1‐2 mmol/L) was incubated with isolated rat hepatocytes in vitro. Uptake of [3H]‐VPA was linear from 10 to 50 seconds, with minimal (<7 percent) biotransformation.

P C Adams, S Agnew – 1 April 1996 – The relationship between alcoholism and hereditary hemochromatosis remains controversial. Previous studies have included patients with alcoholic siderosis rather than hereditary hemochromatosis. In this retrospective study, the clinical features, iron status, alcohol history, liver histology, and long‐term survival were reviewed in 105 homozygotes for hemochromatosis using rigid diagnostic criteria including an HLA identical sibling with iron overload. Heavy alcohol consumption (>80 g ethanol/day) was found in 15% of hemochromatosis patients.

N Chalasani, C M Wilcox – 1 April 1996 – Although liver test abnormalities are frequently identified in patients with acquired immunodeficiency syndrome (AIDS), the causes, evaluation, and outcome of jaundice in these patients have not been systematically evaluated. From August 1, 1990 through September 1, 1994, all human immunodeficiency virus (HIV)‐infected patients with liver test abnormalities seen by the gastroenterology service at a large, inner‐city hospital were prospectively identified. Jaundice was defined as a serum bilirubin concentration ≥ 3 mg/dL.