William J. Sandborn, George M. Lawson, Timothy J. Cody, Michael K. Porayko, J. Eileen Hay, Gregory J. Gores, Jeffery L. Steers, Ruud A. F. Krom, Russell H. Wiesner – 1 January 1995 – We have previously reported that low hepatic tissue cyclosporine levels correlate with early cellular rejectionafter liver transplantation. The aim of this study is to determine whether there is a similar relationship in patients treated with FK506.

1 January 1995

Patricia A. Sheiner, Myron E. Schwartz, Eytan Mor, Leona K. Schluger, Neil Theise, Keiji Kishikawa, Vadim Kolesnikov, Henry Bodenheimer, Sukru Emre, Charles M. Miller – 1 January 1995 – Recurrent hepatitis C causes significant morbidity after liver transplantation. Because immunosuppression is associated with enhanced viral replication, we postulated that clinical recurrence of the disease may be associated with augmented immunosuppression for rejection.

Siddhartha Datta Gupta, Mark Hudson, Andrew K. Burroughs, Richard Morris, Keith Rolles, Peter Amlot, Peter J. Scheuer, Amar P. Dhillon – 1 January 1995 – All 684 post‐orthotopic liver transplantation (OLT) liver biopsies performed at the Royal Free Hospital (RFH) between 1988 and 1993, from 120 patients, were reviewed in order to try to define the relative importance of the histological features of immunosuppressionresponsive cellular rejection.

John J. Poterucha, Michael J. Krowka, E. Rolland Dickson, Denis A. Cortese, Anthony W. Stanson, Ruud A. F. Krom – 1 January 1995 – The hepatopulmonary syndrome is an uncommon accompaniment of chronic liver disease. The outcome of this disorder after orthotopic liver transplantation is varibable. We describe a patient with the hepatopulmonary syndrome who underwent orthotopic liver transplantation for autoimmune hepatitis. Her platypnea and orthodeoxia failed to improve postoperatively.

Clifford A. Brass, Milan G. Mody – 1 January 1995 – With emerging data that endothelial cell (EC) injury is the limiting factor in liver preservation and hepatic function, a simple and reliable biochemical technique for monitoring EC injury is needed. Measurement of purine nucleoside phosphorylase (PNP) release into the circulation from perfused liver has been proposed as such a method. However, our experiments with perfused rat liver did not display a clear or direct relationship between PNP release and endothelial cell injury.

Olivier Soubrane, Mahmoud El Meteini, Denis Devictor, Olivier Bernard, Didier Houssin – 1 January 1995 – The aim of this study was to assess the risk and prognostic factors of gut perforation after orthotopic liver transplantation in children with biliary atresia using univariate and stepwise regression analysis. Among 51 pediatric recipients who underwent transplantation because of biliary atresia after failure of portoenterostomy, 10 patients (20%) had 19 episodes of gut perforations after 14 transplantations. The median delay between transplantation and perforation was 13 days.

Gongliang Jin, Kenric M. Murayama, Jon S. Thompson, Layton F. Rikkers – 1 January 1995 – Pancreatic complications after the distal splenorenal shunt have not been commonly recognized. Between January 1978 and June 1993, 154 patients underwent a distal splenorenal shunt, and 11 patients (7%) developed pancreatic complications, of which 4 had pancreatitis alone, and 7 developed pancreatitis‐related complications. Etiology of cirrhosis, Child's classification and timing of surgery were not predictive of pancreatic complications.

Conrado M. Fernández‐Rodriguez, Jesús Prieto, Jorge Quiroga, José Manuel Zozoya, Amalia Andrade, Marina Núñez, Bruno Sangro, José Penas – 1 January 1995 – The mediators of the hyperdynamic circulation of liver cirrhosis are not well characterized. Substance P is a potent vasodilatory peptide produced by the enteric nervous system and partly cleared by the liver. In this work we have investigated the plasma levels of substance P and their relationship to the hemodynamic, neurohormonal, and renal function changes occurring in patients with cirrhosis.

Florian Gantner, Marcel Leist, Ansgar Wilhelm Lohse, Paul Georg Germann, Gisa Tiegs – 1 January 1995 – Concanavalin A activates T lymphocytes in vitro and causes T‐cell‐dependent hepatic injury in mice. T lymphocytes were previously identified as effector cells of concanavalin A‐induced liver injury. Here we report that hepatic injury is characterized by apoptotic cell death. On concanavalin A challenge, the cytokines tumor necrosis factor‐α (TNF α), interleukin‐2, granulocyte macrophage‐colony stimulating factor, and interferon‐γ were detectable in the circulation of the mice.