J S McMillan, D S Bowden, P W Angus, G W McCaughan, S A Locarnini – 1 December 1996 – Recurrent hepatitis B virus (HBV) infection is a major problem in patients undergoing liver transplantation. Previously, we reported that infection with HBV strains containing a mutation in the precore region (G‐to‐A at nucleotide 1896) was associated with severe recurrent disease posttransplantation. In this study we investigated other mutations in the precore/core gene and core promoter which may be associated with this severe recurrence.

M Pirlich, O Selberg, K Boker, M Schwarze, M J Muller – 1 December 1996 – The creatinine‐method to estimate muscle mass is frequently used in clinical studies, although the validity of this approach is uncertain in patients with cirrhosis. In this study 102 patients with cirrhosis differing in cause, clinical state, liver, and renal function were investigated to determine whether reduced liver or renal function may explain in part the low levels of urinary creatinine excretion frequently observed in these patients.

P Sauer, L Theilmann, S Herrmann, T Bruckner, T Roeren, G Richter, W Stremmel, A Stiehl – 1 December 1996 – Development of stenosis or occlusion of the transjugular intrahepatic portosystemic stent shunt (TIPSS) is one of the major limiting factors in the long‐term viability of this procedure. The efficacy of anticoagulation with heparin which is used in different centers is still unclear.

N A Terrault, S Zhou, C Combs, J A Hahn, J R Lake, J P Roberts, N L Ascher, T L Wright – 1 December 1996 – Prophylactic hepatitis B immunoglobulin (HBIg) reduces the risk of reinfection in hepatitis B surface antigen (HBsAg)‐positive liver transplant recipients. In the medical center of this study, high‐dose HBIg immunoprophylaxis is administered at a fixed dose of 10,000 IU monthly, and in this study, the long‐term efficacy of this treatment regimen was examined.

A Robert, O Chazouilleres – 1 December 1996 – Prothrombin time (PT) is a universal indicator of liver disease severity. However, variability in thromboplastin reagents leads to large interlaboratory differences in PT results. The aim of this study was to determine whether the use of the international normalized ratio (INR) or other modes of expression might achieve PT standardization in patients with liver failure.

D E Cohen, M Fuchs – 1 December 1996

D J Hillebrand, B A Runyon, W G Yasmineh, G P Rynders – 1 December 1996 – Tuberculous peritonitis, although common in Third World countries, remains an uncommon cause of ascites in the United States. Ascitic fluid adenosine deaminase (ADA) activity has been proposed as a useful diagnostic test. The aim of this retrospective study was to determine the clinical utility of ascitic fluid ADA activity in diagnosing tuberculous peritonitis in a U.S. patient population.

S Eguchi, A Kamlot, J Ljubimova, W R Hewitt, L T Lebow, A A Demetriou, J Rozga – 1 December 1996 – A reproducible experimental animal model of fulminant hepatic failure (FHF) resembling the clinical condition is needed. We have developed such a model in the rat by combining resection of the two anterior liver lobes (68% liver mass) with ligation of the right lobes pedicle (24% liver mass), resulting in liver necrosis; the remaining two omental lobes (8% liver mass) are left intact. Adult Sprague‐Dawley rats (250‐300 g) were used. Survival time was determined in 60 rats.

P Muller, T Pomorski, S Porwoli, R Tauber, A Herrmann – 1 December 1996 – The redistribution of spin‐labeled phospholipid analogs across the plasma membrane of HepG2 cells, either in suspension or grown as monolayers, was investigated. After incorporation into the outer membrane leaflet spin‐labeled aminophospholipids phosphatidylserine (PS) and phosphatidylethanolamine (PE) moved rapidly to the inner monolayer, whereas the analog of phosphatidylcholine (PC) disappeared more slowly from the outer leaflet.

H C Geiss, M M Ritter, W O Richter, P Schwandt, R Zachoval – 1 December 1996 – High serum concentrations of lipoprotein (a) [Lp(a)] are considered a risk factor for premature atherosclerosis. Besides apolipoprotein B‐100, Lp(a) consists of apolipoprotein (a) [apo(a)], which shows a remarkable size polymorphism. The serum concentration of Lp(a) is considerably influenced by this apo(a) phenotype. Because Lp(a) is synthesized in the liver, we wondered whether and to what extent Lp(a) levels might be affected by acute liver disease.