Bernard Guigui, Sylvain Perrot, Jean Pierre Berry, Jocelyne Fleury‐Feith, Nadine Martin, Jean Michel Métreau, Daniel Dhumeaux, Elie Serge Zafrani – 1 September 1988 – In order to study the relationship between amiodarone‐induced hepatic phospholipidosis and liver disease, liver biopsies obtained from 13 patients treated with amiodarone for 4 months to 15 years were investigated by light and electron microscopy. Light microscopy showed pseudoalcoholic liver lesions that were probably related to amiodarone in four cases, various alterations (i.e.

Giulio Marchesini, Vincenzo Bua, Alessandra Brunori, Giampaolo Bianchi, Paolo Pisi, Andrea Fabbri, Marco Zoli, Emilio Pisi – 1 September 1988 – The galactose elimination capacity, a measure of the functional liver cell mass, and liver volume were measured in 50 normal subjects of five different age groups (<50, 51 to 60, 61 to 70, 71 to 80 and >81 years). The volume of the liver was evaluated by ultrasonography. All subjects had normal routine liver function tests and no history of liver disease.

Pei‐Jer Chen, Ding‐Shinn Chen, Chiou‐Rong Chen, Yu‐Ying Chen, Hsu‐Mei Hsu Chen, Ming‐Yang Lai, Juei‐Low Sung – 1 September 1988 – We examined the prevalence of serum anti‐δ antibody among 769 intravenous drug abusers in Taiwan. δ infection was found extremely common in the HBsAg‐positive carriers with drug abuse, because 128 (85%) of 151 carriers were positive for anti‐δ. However, most of antibody titers were low (<1:5,000). By molecular hybridization, δ RNA genomes were detectable in only five (4%) of 128 asymptomatic carriers positive for anti‐δ.

Joseph N. Benoit, D. Neil Granger – 1 September 1988 – Catecholamines, which are elevated during alcohol withdrawal, can alter hepatic blood flow and increase hepatic oxygen consumption. We hypothesized that, in the withdrawal state, hepatic oxygen consumption and delivery could be altered in relation to an increased sympathetic activity. Thirteen chronic alcoholics were studied 34–72 h after withdrawal and 10 days later (control period) using conventional hemodynamic methods.

1 September 1988

Pierre Ayotte, Gabriel L. Plaa – 1 September 1988 – We previously showed that alterations of the bile canalicular membrane are likely to occur following a cholestatic regimen composed sequentially of manganese and bilirubin. The present study was designed primarily to investigate the biliary excretion of organic bile constituents following administration of the manganese‐bilirubin combination. Experiments in hyperbilirubinemic Gunn rats were also performed to determine whether the unconjugated or the conjugated form of bilirubin is involved in this cholestatic interaction.

Peter F. Barnes, Cecilia Arevalo, Linda S. Chan, Sandra F. Wong, Telfer B. Reynolds – 1 September 1988 – We prospectively studied 51 consecutive bacteremic patients with chronic liver disease in order to evaluate their clinical presentation and to assess the relationship of various clinical parameters to mortality. Forty‐two patients had alcoholic liver disease and 40 were in Class C, by the Pugh modification of Child's criteria.

Bruce A. Runyon, John C. Hoefs, Timothy R. Morgan – 1 September 1988 – A prospective study identified 45 patients with malignancy‐related ascites among 448 ascites patients (10% of the total). Patients were categorized into five subgroups based on the pathophysiology of ascites formation. Each subgroup had a distinctive ascitic fluid analysis.

Peter Skov Olsen, Steen Boesby, Preben Kirkegaard, Kim Therkelsen, Thomas Almdal, Steen Seier Poulsen, Ebba Nexø – 1 September 1988 – The role of epidermal growth factor on liver regeneration after partial hepatectomy in rats was investigated. After a 70% hepatectomy in rats, the concentration of epidermal growth factor in portal venous blood was unchanged compared with unoperated controls. However, small amounts of epidermal growth factor could be identified in portal venous blood after intestinal instillation of epidermal growth factor.

Debra L. Laskin, Fredika M. Robertson, Anne M. Pilaro, Jeffrey D. Laskin – 1 September 1988 – Phenobarbital is a potent inducer of hepatic cytochrome P‐450 and is a tumor promoter in the two‐stage model of liver carcinogenesis. In the present studies, we show that phenobarbital also induces an accumulation of activated macrophages in the livers of treated rats. These macrophages are larger and more stellate than resident Kupffer cells and are highly vacuolated.