Rifaat Safadi, Daniel Shouval, Ran Tur Kaspa, Yaffa Ashur, Yaron Ilan – 1 July 1996 – Mixed cryoglobulinemia is a well‐known complication after hepatitis C virus (HCV) infection. We report five cases in which cryoglobulinemia appeared or grossly exacerbated following orthotopic liver transplantation (OLT). Cryoglobulinemia and the associated clinical symptoms resolved or improved in two patients treated with ribavirin after liver transplantation, while plasmapheresis was ineffective in another patient.

1 July 1996

Giuseppe Francesco Stefanini, Francesco Giuseppe Foschi, Lorenzo Marsigli, Cristiana Fumelli, Gian Luca Grazi, Gunnar Söderdahl, Ole Suhr, Gösta Holmgren, Gustaf Herlenius, Bo‐Göran Ericzon, Jean‐Francois Desjardins, Jean‐Piere Campion, Bruno Clement, Pierre‐Alain Clavien – 1 July 1996

G Nardone, M Romano, A Calabrò, P V Pedone, I de Sio, M Persico, G Budillon, C B Bruni, A Riccio, R Zarrilli – 1 June 1996 – Increased prevalence of hepatitis C virus (HCV) infection has been found in patients with hepatocellular carcinoma (HCC). The expression of insulinlike growth factor II (IGF‐II) has been linked to hepatocarcinogenesis in the experimental animal and in humans.

C Colombo, P M Battezzati, M Podda, N Bettinardi, A Giunta – 1 June 1996 – Liver disease is increasingly recognized as a major cause of morbidity in cystic fibrosis (CF). Preliminary data suggest that ursodeoxycholic acid (UDCA) may be beneficial for treatment of this manifestation. We performed a double‐blind, multicenter trial in these patients to establish efficacy and safety of UDCA in terms of the improvement of clinical and nutritional indicators besides standard liver function tests.

P J De Bleser, C D Scott, T Niki, G Xu, E Wisse, A Geerts – 1 June 1996 – The liver is reported to be the main source of soluble insulin‐like growth factor‐II/mannose 6‐phosphate (IGF‐II/M6P) receptor in adults. In view of the role of this receptor in the activation of transforming growth factor β (TGF‐β) during hepatic fibrogenesis, we have investigated the correlation between serum levels and tissue expression of the receptor during acute CCl4 intoxication of the rat.

T Niki, P J De Bleser, G Xu, K Van der Berg, E Wisse, A Geerts – 1 June 1996 – Fat‐storing cells are the major producers of extracellular matrix in the liver. A good immunocytochemical marker is, however, still lacking for this cell type. Desmin, frequently used by most investigators, fails to stain many pericentral fat‐storing cells in normal rat liver. The aim of the present study is to evaluate glial fibrillary acidic protein (GFAP) as an alternative marker of fat‐storing cells.

M Moriyama, I Makiyama, M Shiota, K Uesugi, Y Kannan, M Ohta, K Kimura, T Sugano – 1 June 1996 – Ureagenesis from ammonia, alanine, and glutamine in the liver after partial hepatectomy (PH) was determined by using the liver‐perfusion system. The maximum rate of ureagenesis from ammonium chloride (10 mmol/L) in hepatectomized (HX) rats at 24 hours after surgery was obtained in the presence of ornithine, lactate, and pyruvate, and it was almost identical to that in sham‐operated (SO) rats.

C R Leveille‐Webster, J Rogers, I M Arias – 1 June 1996 – The hepatic asialoglycoprotein receptor is responsible for rapid clearance of desiaylated glycoproteins from the circulation by receptor‐ mediated endocytosis. Previous in vitro studies in hepatocyte preparations from rats subjected to partial hepatectomy (PH) of 70% to stimulate hepatic regeneration showed decreased asialoglycoprotein (ASGP) receptor binding. We used an ASGP receptor‐targeted hepatic magnetic resonance imaging (MRI) agent, BMS 180550, to demonstrate similar changes in receptor biology in vivo.

H Takikawa, Y Sugiyama, J C Fernandez‐Checa, J Kuhlenkamp, M Ookhtens, N Kaplowitz – 1 June 1996 – We previously identified that Y′ bile acid binders (3α‐ hydroxysteroid dehydrogenases) interact with bile acids in intact rat hepatocytes using [3β‐3H, C24‐14C]bile acids and that indomethacin, a competitive inhibitor of 3α‐hydroxysteroid dehydrogenase, inhibits 3H‐loss from the C3‐position of bile acids as well as inhibits hepatic bile acid removal and excretion.