Kinetics of 64copper in primary biliary cirrhosis

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.

Viral infections of humans. Epidemiology and control. Edited by Alfred S. Evans, professor of epidemiology and public health, Yale University School of Public Health. Second edition, completely revised and expanded. xxxvi + 720 pp. New York and London: Pl

Spontaneous disappearance of viral replication and liver cell inflammation in HBsAg‐positive chronic active hepatitis: Results of a placebo vs. interferon trial

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.

Effect of hematin administration to patients with protoporphyria and liver disease

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.

Changes of the golgi apparatus induced by diethylmaleate in rat hepatocytes

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.

Adenine arabinoside 5′‐monophosphate treatment of chronic type B hepatitis

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.

H2‐receptor antagonists and hepatic drug disposition

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.

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