Elie Serge Zafrani – 1 February 1990 – A patient with acute myeloblastic leukaemia developed jaundice revealing peliosis hepatis after receiving 6‐thioguanine for two months. Peliosis hepatis was severe and was associated with mild lesions of centrilobular veins. Withdrawal of 6‐thioguanine was followed by a progressive improvement of liver dysfunction. This report shows that 6‐thioguanine, a thiopurine already reported to be responsible for veno‐occlusive disease of the liver, can induce peliosis hepatis.

Dieter Häussinger, Thomas Stehle, Florian Lang – 1 February 1990 – The present study has been performed to elucidate the mechanisms of volume regulation in isolated perfused liver. Reduction of extracellular osmolarity by 80 mOsm/L leads to a release of potassium and a sustained alkalinization of effluent. Reexposure to isotonic perfusate leads to reuptake of potassium by the liver and acidification of effluent. Part of the alkalinization could be due to release of bicarbonate parallel to potassium release.

Jonathan A. Leighton, Michael K. Bay, Alma L. Maldonado, Raymond F. Johnson, Steven Schenker, K. V. Speeg – 1 February 1990 – Recent work has shown that colchicine may benefit patients with primary biliary or alcoholic cirrhosis. However, very little is known about its pharmacokinetics in the presence of impaired liver function. To study this we examined the effects of three models of experimental liver dysfunction and one of cytochrome P‐450 inhibition on colchicine elimination in the rat.

Charles S. Lieber, Alessandro Casini, Leonore M. Decarli, Cho‐Il Kim, Nancy Lowe, Rika Sasaki, Maria A. Leo – 1 February 1990 – Chronic ethanol consumption by baboons (50% of energy from a liquid diet) for 18 to 36 mo resulted in significant depletion of hepatic S‐adenosyl‐L‐methionine concentration: 74.6 ± 2.4 nmol/gm vs. 108.9 ± 8.2 nmol/gm liver in controls (p < 0.005). The depletion was corrected with S‐adenosyl‐L‐methionine (0.4 mg/kcal) administration (102.1 ± 15.4 nmol/gm after S‐adenosyl‐L‐methionine–ethanol, with 121.4 ± 11.9 nmol/gm in controls).

Robin D. Hughes, Christopher D. Gove, Roger Williams, Hirohita Tsubouchi, Yasushi Daikuhara – 1 February 1990

Rowen K. Zetterman – 1 February 1990

Elspeth M. Jack, Philip Bentley, Francoise Bieri, Samar F. Muakkassah‐Kelly, Willy Stäubli, Joseph Suter, Felix Waechter, Luis M. Cruz‐Orive – 1 February 1990 – Gamma‐glutamyltranspeptidase‐positive hepatocyte foci were produced in female rats given a single dose of diethylnitrosamine neonatally after birth and, after weaning, a diet containing phenobarbitone for 30 wk. The nucleator method, a new stereological approach, provided an efficient, unbiased estimate of mean cell volume in focal lesions and extrafocal areas.

David Kershenobich, Marcos Rojkind, Alfonso Quiroga, Jorge Alcocer‐Varela – 1 February 1990 – Lymphocyte and monocyte function was investigated in eight patients with primary biliary cirrhosis and in age‐matched and sex‐matched controls. In three of the eight cirrhotic patients, two were in the late stage of the disease (stage III) and concanavalin A‐induced suppressor cell function was markedly decreased; it returned to normal levels after 1 mo of treatment consisting of 5 mg per week of orally administered colchicine.

Yasushi Shiratori, Mitsugu Tanaka, Kenji Hai1, Tateo Kawase, Shuichiro Shiina, Tsuneaki Sugimoto – 1 February 1990 – Although administration of 100 mg galactosamine caused severe hepatic injury in C3H/HeN mice, splenectomy reduced the grade of this hepatotoxicity. However, this hepatic injury was scarcely detected in the endotoxin‐resistant C3H/HeJ mice. In addition, in contrast to high lethality in C3H/HeN mice with a combined administration of galactosamine and endotoxin, splenectomy rendered C3H/HeN mice slightly resistant to this treatment.

Shashi Kumar, Rudolf E. Stauber, Judith S. Gavaler, Michael H. Basista, Vincents J. Dindzans, Robert R. Schade, Mordechai Rabinovitz, Ralph E. Tarter, Robert Gordon, Thomas E. Starzl, David H. Van Thiel – 1 February 1990 – Alcohol abuse is the most common cause of end‐stage liver disease in the United States, but many transplant centers are unwilling to accept alcoholic patients because of their supposed potential for recidivism, poor compliance with the required immunosuppression regimen and resulting failure of the allograft.