Vijayan Balan, Kennetii P. Batts, Michael K. Porayko, Ruud A. F. Krom, Jurgen Ludwig, Russell H. Wiesner – 1 December 1993 – Whether primary biliary cirrhosis recurs after orthotopic liver transplantation remains a controversial issue. Sixty consecutive patients with primary biliary cirrhosis with at least 1 yr of follow‐up after liver transplantation were studied. All patients were treated with triple‐drug immunosuppression (cyclospoine, prednisone, azathioprine).

Andreas Gardemann, Thomas Zimmermann, Georg Machnik, Rolf Dargel, Kurt Jungermann – 1 December 1993

Stuart C. Gordon, Richard S. Elloway, John C. Long, Carl F. Dmuchowski – 1 December 1993 – We reviewed the clinical records of 140 consecutively evaluated patients with chronic hepatitis C infection. One hundred twenty‐four patients (89%) contracted infection through blood transfusion or intravenous drug use. The liver biopsy specimens of 83 patients (43 blood transfusion cases and 40 intravenous drug abuse cases) were examined without knowledge of the mode of disease transmission.

Carl T. McGary, Judith Yannariello‐Brown, Dennis W. Kim, Tami C. Stinson, Paul H. Weige – 1 December 1993 – The release and intracellular accumulation of 125I‐hyaluronan degradation products was studied in cultured liver endothelial cells with hyaluronan oligosaccharides (relative molecular mass = approximately 44,000) uniquely modified and radiolabeled at the terminal reducing sugar. Two methods were combined to measure 125I‐hyaluronan degradation by liver endothelial cells.

Giorgio Saracco, Floriano Rosina, Maria Lorena Abate, Livio Chiandussi, Vittorio Gallo, Elena Cerutti, Angelo Di Napoli, Antonio Solinas, Angelo Deplano, Andreina Tocco, Pierangela Cossu, David Chien, George Kuo, Alan Polito, Amy J. Weiner, Michael Houghton, Giorgio Verme, Ferruccio Bonino, Mario Rizzetto – 1 December 1993 – Eighty patients with chronic hepatitis C who completed a previously reported randomized controlled trial on the efficacy of interferon‐α2b were followed up for at least 36 mo after therapy discontinuation.

Janet Quinn, Austin G. Diamond, Jeremy M. Palmer, Margaret F. Bassendine, Oliver F. W. James, Stephen J. Yeaman – 1 December 1993 – Approximately 95% of patients with primary biliary cirrhosis have antimitochondrial antibodies against the E2 component of the pyruvate dehydrogenase complex (E2p). Immunodominant sites on E2p have been localized to the inner lipoyl domain, which serves as a covalent attachment site for the essential cofactor, lipoic acid. However, it is not clear whether the presence of lipoic acid is necessary for autoimmune recognition of human E2p.

Ulrich Marti – 1 December 1993 – In the aged liver, cell proliferation and induction of DNA synthesis by epidermal growth factor is impaired. Changes in the hepatic handling of epidermal growth factor may be important for these effects. I compared epidermal growth factor handling in the livers of young and old rats. Epidermal growth factor binding capacity of plasma membranes was reduced from 1.30 ± 0.15 to 0.51 ± 0.19 pmol/mg in young and old animals, respectively.

Gerhard P. Püschel, Ursula Hespeling, Martin Oppermann, Peter Dieter – 1 December 1993 – Human anaphylatoxin C3a increases glycogenolysis in perfused rat liver. This action is inhibited by prostanoid synthesis inhibitors and prostanoid antagonists. Because prostanoids but not anaphylatoxin C3a can increase glycogenolysis in hepatocytes, it has been proposed that prostanoid formation in nonparenchymal cells represents an important step in the C3a‐dependent increase in hepatic glycogenolysis.

Makoto Nakamuta, Masao Ohashi, Yuichi Tanabe, Kaichiro Hiroshige, Hajime Nawata – 1 December 1993 – Plasma myeloperoxidase levels in patients with cirrhosis were compared with those in patients with chronic hepatitis and healthy controls by means of a specific radioimmunoassay for myeloperoxidase. The mean concentration of plasma myeloperoxidase in cirrhotic patients (309.1 ± 17.2 ng/ml, n = 41) was markedly higher than that in chronic hepatitis patients (222.6 ± 17.2 ng/ml, n = 21) (p < 0.01) and normal controls (219.5 ± 5.7 ng/ml, n = 50) (p < 0.01).

Peter Widler, Hans U. Fisch, Peter Schoch, Arthur Zimmermann, Thomas E. Schläpfer, Jürg Reichen – 1 December 1993 – Increased levels of natural benzodiazepine receptor agonists, produced in the body (endogenous) or ingested with food (exogenous) have been proposed as one of the factors causing hepatic encephalopathy in both experimental animals and human subjects. However, the divergent response of hepatic encephalopathy to benzodiazepine antagonists sheds doubt on this attractive hypothesis.