Michael Phillips, Laurence M. Cummins – 1 May 1988 – Recent studies have demonstrated that commercial preparations of hepatitis B immune globulin often contain antibody to the human immunodeficiency virus. The presence of this antibody has aroused concerns that treatment with hepatitis B immune globulin might passively induce human immunodeficiency virus antibody seropositivity, leading to incorrect diagnoses of human immunodeficiency virus exposure.

Min Chan Lai, Myron J. Tong, Marek J. Nowicki, Shou‐Dong Lee – 1 May 1988 – Seventy HBsAg‐positive patients, including 24 with primary hepatocellular carcinoma, 34 with chronic active hepatitis, 12 with chronic persistent hepatitis and 30 asymptomatic healthy hepatitis B virus carriers were tested for anti‐HBc IgM using the Corzyme‐M test. Anti‐HBc IgM was detected in 50% of the primary hepatocellular carcinoma patients, 26.5% of the chronic active hepatitis patients, 25% of the chronic persistent hepatitis patients, but in none of the healthy hepatitis B virus carriers.

Jen‐Yang Chen, Tim J. Harrison, Chue‐Shue Lee, Ding‐Shinn Chen, Arie J. Zuckerman – 1 May 1988 – We have previously reported an analysis of DNA extracted from 31 primary liver tumors where, in 25 cases, we found chromosomal integration of hepatitis B virus DNA sequences. We describe here an investigation of the extent of the viral genome at each integration site in 15 of the hepatitis B virus DNA‐positive tumors using subgenomic fragments of the viral genome as probes.

Joachim Limmer, Wolfgang E. Fleig, Dorothea Leupold, Reinhard Bittner, Hans Ditschuneit, Hans‐Günter Berger – 1 May 1988 – Patients suffering from Type I glycogen storage disease frequently develop hepatic tumors. Some of these were classified as carcinoma, with the majority of tumors representing benign adenomata. However, no evidence exists of malignant transformation of adenomata in these patients.

Mark E. Marotto, Ronald G. Thurman, John J. Lemasters – 1 May 1988 – Trypan blue uptake and lactate dehydrogenase release were measured as indices of irreversible cell damage in isolated, perfused rat livers during low‐flow hypoxia. In livers from fasted rats perfused in the anterograde direction, trypan blue uptake took place beginning at about 45 min of hypoxia. Cells which took up trypan blue first were located in narrow bands at the border between anoxic pericentral areas and normoxic periportal regions of the liver lobule.

Mauro Pirovino, Otfried Müller, Thomas Zysset, Ueli Honegger – 1 May 1988 – Morphological and biochemical investigations were performed in guinea pigs after 1, 3, 5 and 16 weeks of amiodarone feeding. The most prominent morphological finding was an increase in dense bodies in hepatocytes, Kupffer cells and in bile duct epithelia, reaching a maximum after 5 weeks of treatment according to morphometric analysis. Similar time courses were observed for the serum and liver tissue concentrations of amiodarone and desethylamiodarone and the—albeit minimal—extent of hepatocellular necrosis.

Helmut Keller, Vera Bezjak, Beatrice Stegaru, Jan Buss, Eggert Holm, Dieter L. Heene – 1 May 1988 – Cardiovascular alterations such as increased heart rate, high cardiac output, reduced systemic vascular resistance, and in most of the cases, increased contractility parameters have been recognized in patients with advanced liver disease.

1 May 1988

Yi‐Ming Chen, Cheng‐Po Hu, Pao‐Huei Chen, Ming‐Huey H. Chu, Yang‐Te Tsai, Shou‐Dong Lee, Chungming Chang – 1 May 1988 – In order to study hepatocellular carcinoma‐associated antigens, screening of sera and ascites was done from hepatocellular carcinoma patients having antibodies reactive with three hepatocellular carcinoma cell lines (PLC/PRF/5, Hep 3B and HA22T/VGH). The indirect immunofluorescent antibody test was used.

William C. Duane, Ingemar Björkhem, Jan Neal Hamilton, Susan M. Mueller – 1 May 1988 – During biosynthesis of bile acid, carbons 25–26–27 are removed from the cholesterol side chain. Side‐chain oxidation begins either with hydroxylation at the 26‐position, in which case the three‐carbon fragment is released as propionic acid, or with hydroxylation at the 25‐position, in which case the three‐carbon fragment is released as acetone.