James H. Lewis, Hyman J. Zimmerman, Carlton T. Garrett, Elliot Rosenberg – 1 November 1982 – The administration of high‐dose valproic acid (VPA) (750 mg per kg) consistently produced significant microvesicular steatosis in mature Sprague‐Dawley rats after 48 hr. Similar changes occurred in animals pretreated with phenobarbital which received a lower dose of VPA (350 mg per kg), but no steatosis was seen in animals treated with the low‐dose VPA alone. The steatogenic effect of VPA is most likely mediated by a toxic metabolite.

George W. Mihaly, Richard A. Smallwood, Jeanette D. Anderson, D. Brian Jones, Lorraine K. Webster, Frank J. Vajda – 1 November 1982 – The effect of four H2‐receptor antagonists (Cimetidine, burimamide, oxmetidine, and ranitidine) on antipyrine elimination was studied in the isolated perfused rat liver. The first three drugs are substituted imidazoles, whereas ranitidine contains a furanyl nucleus. Isolated livers were perfused using a 100‐ml, recycling, constant flow circuit for 4 hr. Antipyrine elimination was studied with or without an H2‐receptor antagonist present.

Jay H. Hoofnagle, Gerald Y. Minuk, Geoffrey M. Dusheiko, Daniel F. Schafer, Rodney Johnson, Stephen Straus, E. Anthony Jones, John L. Gerin, Kamal Ishak – 1 November 1982 – Six patients with chronic type B hepatitis were treated with adenine arabinoside 5′‐monophosphate at a dosage of 10 to 15 mg per kg per day for 10 days. All demonstrated an immediate and marked decrease in serum hepatitis B virus DNA and DNA polymerase, and 5 of the 6 became negative for both markers by the end of the period of therapy.

Anne‐Marie Jezequel, Patrizia Bonazzi, Piera Amabili, Cinzia Venturini, Francesco Orlandi – 1 November 1982 – Ultrastructural studies of the liver of rats given diethylmaleate (DEM) (0.7 ml per kg body, i.p.) weight revealed marked alterations of the configuration of the Golgi complex in all hepatocytes. This consisted in dilatation of the cisternae leading to the formation of large cysts. The alteration was more prominent 15 min after administration of the drug, coincident with a 2‐fold increase of bile flow and a decrease of hepatic glutathione to 15% of controls.

Joseph R. Bloomer, Claus A. Pierach – 1 November 1982 – Hepatic damage in protoporphyria appears to be caused by a toxic effect of excess protoporphyrin. Therapy which reduces the formation of excess protoporphyrin may, therefore, be helpful. We examined the effects of hematin administered i.v. to two patients with protoporphyria and decompensated cirrhosis. Neither patient had side effects from the compound or manifested signs of toxicity. The vascular disappearance of hematin in one patient was similar to that in patients with porphyria who do not have structural liver disease.

Solko W. Schalm, Rudolf A. Heijtink – 1 November 1982 – In 20 patients with HBsAg‐and HBeAg‐positive chronic active hepatitis, we determined the long‐term effect of human leukocyte interferon as well as placebo treatment. During the 2‐year follow‐up period, HBsAg remained present in all patients, but the Dane particle markers HBeAg and DNA polymerase disappeared in two of 10 patients who had received interferon, and in 4 of 10 patients from the placebo group.

John C. Hoefs – 1 November 1982

Maxwell Finland – 1 November 1982

A. Roelof Janssens, Cornelis J. A. Van Den Hamer – 1 November 1982 – To assess the pathogenetic mechanisms involved in the accumulation of copper in primary biliary cirrhosis (PBC), the kinetics of 64Copper (64Cu) were studied in 6 healthy volunteers, 3 patients with PBC (Stages I to III) and a normal liver copper, and 7 patients with PBC (Stages II to IV) and a high liver copper. The kinetics of oral and i.v. administered 64Cu in patients with a normal liver copper were similar to those in controls.

Victor M. Rosenoer – 1 November 1982