Salvatore Badalamenti, Francesco Salerno – 1 February 1992 – We compared the clinical efficacy and safety of large‐volume paracentesis and dialytic ultrafiltration in the treatment of refractory ascites in cirrhotic patients. A group of cirrhotic subjects (age 49–80 years) were randomly allocated to either continuous paracentesis (1–1.5 l/hour) or dialytic ultrafiltration until disappearance of ascites. Each patient was maintained on bed rest, fluid restriction (1 l/day) and a low (25 mmol/day) sodium diet for 14 days.

Thomas L. Treadwell – 1 February 1992

J. Michael Henderson, Gregory J. Mackay, Alan B. Lumsden, Hussein M. Atta, Richard Brouillard, Michael H. Kutner – 1 January 1992 – This study tested the hypothesis that the denervated liver is more susceptible to hypovolemic shock than the normal liver. Fourteen swine, seven nondenervated and seven after liver denervation, were studied during hypovolemic shock to 50% of baseline blood pressure. Hepatic artery and portal vein flows were measured using transonic flow probes, and cardiac output and central venous pressure were measured using Swan‐Ganz catheters.

Peter Schirmacher, Albert Geerts, Antonello Pietrangelo, Hans P. Dienes, Charles E. Rogler – 1 January 1992 – Hepatocyte growth factor/hepatopoietin A is a complete mitogen for parenchymal liver cells, and its expression is increased as an early response to acute liver injury. To identify the liver cell population responsible for hepatocyte growth factor gene expression, we investigated tissue sections and isolated and purified cell fractions from normal rat liver by in situ and Northern blot hybridization.

Howard C. Thomas – 1 January 1992 – Background. A nosocomial outbreak of fulminant hepatitis B occurred in five patients in Haifa, Israel. Previous investigations identified the suspected source as a carrier of hepatitis B surface antigen who was positive for antibodies to hepatitis B e antigen and had chronic liver disease. We examined the strain of hepatitis B virus (HBV) that caused this epidemic, in order to identify specific mutations in the precore or core region.

Raymond S. Koff – 1 January 1992

Makoto Hashizume, Seigo Kitano, Nobuhiro Koyanagi, Kazuo Tanoue, Masayuki Ohta, Hiroya Wada, Hirohiko Yamaga, Hidefumi Higashi, Yasunori Iso, Tetsuya Iwanaga, Keizo Sugimachi – 1 January 1992 – We report here the results of endoscopic injection sclerotherapy performed in 1,000 consecutively treated Japanese patients with esophageal varices. This prospective study covered the period from 1982 to 1990. Variceal bleeding was controlled in 215 (97.7%) of 220 patients. Esophageal varices were completely eradicated in 778 patients (77.8%); the mean number of sessions was 4.2.

John G. McHutchison, John L. Person, Sugantha Govindarajan, Boontar Valinluck, Tessie Gore, Steven R. Lee, Mitchell Nelles, Alan Polito, David Chien, Robert DiNello, Stella Quan, George Kuo, Allan G. Redeker – 1 January 1992 – Sera from 483 patients at high (group 1, n = 313) and lower (group 2, n = 170) risk for exposure to hepatitis C were tested for antibodies to hepatitis C using first‐generation (c100‐3) and second‐generation enzyme‐linked immunosorbent assays and four‐antigen recombinant immunoblot assay.

Jean‐Claude Trinchet, Beverley Balkau, Renée E. Poupon, François Heintzmann, Patrice Callard, Cécile Gotheil, Jean‐Didier Grange, Denis Vetter, Arnaud Pauwels, Hélène Labadie, Olivier Chazouilleres, Philippe Mavier, Hervé Desmorat, Jean‐Pierre Zarski, Jean‐Claude Barbare, Jean‐françois Chambre, E. Alexandre Pariente, Dominique Roulot, Michel Beaugrand – 1 January 1992 – Severe alcoholic hepatitis is still a therapeutic challenge. It has been recently advocated that a 3‐wk infusion with insulin and glucagon reduces its short‐term mortality rate.

Marie‐Anne Loriot, Patrick Marcellin, Eric Bismuth, Michèle Martinot‐Peignoux, Nathalie Boyer, Claude Degott, Serge Erlinger, Jean‐Pierre Benhamou – 1 January 1992 – The objective was to determine the proportion of patients with chronic hepatitis B in whom hepatitis B virus DNA is demonstrated by polymerase chain reaction after HBeAg to anti‐HBe or HBsAg to anti‐HBs spontaneous or therapeutically induced seroconversion.