The prediction of acute cellular rejection in orthotopic liver transplantation

Andrew J. Bathgate, Paula Hynd, David Sommerville, Peter C. Hayes – 30 December 2003 – The occurrence of acute cellular rejection after orthotopic liver transplantation is common. At present, no allowance is made in immunosuppressive regimens for parameters other than weight. We investigated parameters in 121 consecutive patients receiving their primary allograft to determine if there are pretransplantation factors predicting the occurrence of acute cellular rejection after transplantation.

Acute liver failure associated with prolonged use of bromfenac leading to liver transplantation

Robert J. Fontana, Timothy M. McCashland, Kent G. Benner, Henry D. Appelman, Naresh T. Gunartanam, James L. Wisecarver, John M. Rabkin, William M. Lee, Acute Liver Failure Study Group – 30 December 2003 – Bromfenac, a nonnarcotic analgesic nonsteroidal anti‐inflammatory drug, was associated with reversible, minor elevations in serum aminotransferase levels during clinical trials.

Cytochrome P‐450 content and activity after cold storage of rat hepatocytes in university of wisconsin and sodium‐lactobionate‐sucrose solutions

Halima Serrar, Ayman El‐Kadi, Patrick Du Souich, Pierre Haddad – 30 December 2003 – We compared the capacity of University of Wisconsin (UW) and of sodium‐lactobionate‐sucrose (SLS) hypothermic preservation solutions to maintain the integrity of the hepatic cytochrome P‐450–dependent mono‐oxygenase system. Isolated rat hepatocytes were stored for 0, 10, 24, and 48 hours in UW or SLS solution and were subsequently cultured shortly at 37°C.

Budd‐chiari syndrome associated with factor V leiden mutation: A report of 6 patients

Ron Hoffman, Assy Nimer, Naomi Lanir, Benjamin Brenner, Yaacov Baruch – 30 December 2003 – Budd‐Chiari syndrome is characterized by hepatic venous outflow obstruction. Although myeloproliferative disorders are usually responsible for this severe thrombotic disorder, deficiency or dysfunction of the natural anticoagulants can be involved. Resistance to activated protein C caused by factor V Leiden mutation has been recently identified as a major cause of thrombophilia.

Mycophenolate mofetil, microemulsion cyclosporine, and prednisone as primary immunosuppression for pediatric liver transplant recipients

John F. Renz, Jennifer Lightdale, Christine Mudge, Peter Bacchetti, Jennifer Watson, Nancy L. Ascher, Jean C. Emond, Philip Rosenthal, John P. Roberts – 30 December 2003 – Triple immunosuppressive therapy using mycophenolate mofetil (MMF), microemulsion cyclosporine (me‐CsA), and prednisone offers the potential for potent immunosuppression without intravenous drug therapy or anti–T‐cell antibody induction therapy.

Hereditary hemochromatosis in liver transplantation

M. Isabel Fiel, Thomas D. Schiano, Henry C. Bodenheimer, Swan N. Thung, Thomas W. King, C. Rathna Varma, Charles M. Miller, Elizabeth M. Brunt, Steven Starnes, Cynthia Prass, Roger K. Wolff, Bruce R. Bacon – 30 December 2003 – A candidate gene, HFE, was recently described in patients with hereditary hemochromatosis (HH) and found to contain a missense mutation leading to a cysteine to tyrosine substitution (C282Y). A second mutation, H63D, was also found in the gene.

CD40L (CD154) expression in human liver allografts during chronic ductopenic rejection

Anderson S. Gaweco, Russell H. Wiesner, Sherri Yong, Ruud Krom, Michael Porayko, Gregorio Chejfec, Kenneth D. McClatchey – 30 December 2003 – The CD40‐CD40L (CD154) interaction plays a pivotal role in the effector mechanisms of allograft rejection. Blockade of the CD40/CD40L costimulatory pathway prevents the development of chronic allograft rejection in several animal transplant models. The relevance of in situ CD40 and CD40L expression in human liver allografts was assessed by immunohistochemistry during ductopenic chronic rejection (CR).

Post–liver transplantation myocardial dysfunction

Priya Sampathkumar, Amir Lerman, Barbara Youngmee Kim, Bradley J. Narr, John J. Poterucha, Laurence C. Torsher, David J. Plevak – 30 December 2003 – Patients with end‐stage liver disease usually show a hyperdynamic circulatory state. It has previously been reported that patients who develop myocardial depression in the early post–liver transplantation period are more prone to organ failure and death.

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