Eike Walter, Hubert E. Blum, Peter Meier, Martin Huonker, Martin Schmid, Klaus‐Peter Maier, Wolf‐Bernhard Offensperger, Silke Offensperger, Wolfgang Gerok – 1 July 1988 – Hepatocellular carcinoma tissues from HBsAg‐negative patients with chronic alcoholic liver disease were investigated for the presence of hepatitis B virus DNA. Southern blot analyses of DNA extracted from the hepatocellular carcinomas were negative for hepatitis B virus DNA in all 17 patients examined, at a level of sensitivity of less than 0.01 genome equivalent per cell.

Lars Berglund, Bo Angelin, Rolf Blomstrand, George Drummond, Attallah Kappas – 1 May 1988 – Sn‐protoporphyrin, a potent competitive inhibitor of heme oxygenase, the rate‐limiting enzyme in the degradation of heme to bile pigment, was administered to 10 normal volunteers: 8 males and 2 females. A significant decrease in the levels of serum (mean decrease; 38%) and biliary bilirubin (mean decrease: 47%) was demonstrated in all 10 subjects. The decrease in these parameters lasted for a minimum of 4 days after administration of the metalloporphyrin.

Yun‐Fan Liaw, Dar‐In Tai, Chia‐Ming Chu, Tong‐Jong Chen – 1 May 1988 – The incidence and contributing factors of cirrhosis developing in patients with chronic type B hepatitis were assessed prospectively in 684 clinicopathologically verified patients, of which 509 were HBeAg positive and 175 were anti‐HBe positive at entry into the study. During an average follow‐up period of 35.3 months, cirrhosis occurred 6 to 64 months after entry in 35 HBeAg‐positive and 7 anti‐HBe positive patients with a calculated annual incidence of 2.4 and 1.3%, respectively (p > 0.05).

1 May 1988

I. Michael Samloff – 1 May 1988 – To characterize bleeding from gastric red spots in patients with cirrhosis, three groups of patients were studied: (a) 11 cirrhotic patients bleeding from gastric red spots, (b) 18 nonbleeding cirrhotic patients without gastric red spots, and (c) 13 non‐cirrhotic patients with endoscopic normal mucosa (controls). Histologic examination of antral biopsy specimens revealed a diffuse capillary ectasia without inflammation in 8 of the 11 cirrhotic patients with gastric lesions.

Russell H. Wiesner, Patricia M. Grambsch, Keith D. Lindor, Jurgen Ludwig, E. Rolland Dickson – 1 May 1988 – Primary biliary cirrhosis is a chronic, progressive, cholestatic liver disease thought to be related to abnormalities in immune regulation. The disease is associated with granulomatous bile duct destruction, cholestasis, hepatic copper overloading and the development of hepatic fibrosis or cirrhosis or both. There have been numerous therapeutic trials evaluating immunosuppres‐sive, antifibrotic and cupruretic agents.

Fenton Schaffner – 1 May 1988 – One hundred and fifty‐four patients with histologically verified non‐alcoholic chronic liver disease were randomized to azathioprine or prednisone treatment. After a median of 91 months observation time, the cause of death was assessed retrospectively. Autopsy was performed in 82% of 71 deaths. In the azathioprine group 33% (13/39) died from malignant neoplasia, and in the prednisone group (13%) (4/32) (p = 0.08).

J. Donald Ostrow – 1 May 1988

Minoru Sukigara, Masahiko Ohata, Toshiro Komazaki, Ryozo Omoto – 1 May 1988 – The effect of spontaneous respiration on esophageal variceal flow was evaluated using 5 MHz color flow Doppler echography. Twenty‐one patients with esophageal varices, of whom 19 had liver cirrhosis (95%), were examined with a convex array transesophageal transducer. The direction and velocity of the variceal flow during inhalation and exhalation could be inferred from the color, its brightness or the Doppler time‐velocity spectrum.

Reidar Albrechtsen, Ulla M. Wewer, Snorri S. Thorgeirsson – 1 May 1988 – De novo formation of laminin‐positive basement membranes was found to be a distinct morphologic feature of diethylnitrosamine/phenobarbital‐induced hepatocellular carcinomas of the rat. The first appearance of extracellularly located laminin occurred in the pre‐neoplastic liver lesions (corresponding to neoplastic nodules), and this feature became successively more prominent during the course of hepatocellular carcinoma development.