Pigment gallstone disease: Summary of the national institutes of health—international workshop

Bruce W. Trotman, Roger D. Soloway – 1 November 1982 – This report summarizes the proceedings of the first National Institutes of Health—International Workshop on Pigment Gallstone Disease. The meeting held at the University of Pennsylvania in May, 1981 consisted of eight sessions in which the following aspects of pigment gallstone disease were discussed: (a) classification; (b) epidemiology; (c) radiographic assessment; (d) gallstone composition; (e) composition of bile; (f) pathogenesis; (g) animal models, genetics, and computer analysis, and (h) medical treatment.

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.

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