Jeffrey S. Plotkin,, R. Michael Benitez, Paul C. Kuo, Mary J. Njoku, Linda A. Ridge, James W. Lim, Charles D. Howell, Jacqueline M. Laurin, Lynt B. Johnson – 30 December 2003 – This study attempts to evaluate the efficacy of dobutamine stress echocardiography for preoperative cardiac risk stratification in patients undergoing orthotopic liver transplantation. Two hundred twenty consecutively submitted patients were evaluated in preparation for orthotopic liver transplantation. Dobutamine stress echocardiography was performed in 80 patients with known or suspected coronary artery disease.

Annarosa Floreani,, Walter Fries, Giovanni Luisetto, Patrizia Burra, Stefano Fagiuoli, Patrizia Boccagni, Giovanni Roselli Della Rovere, Mario Plebani, Antonio Piccoli, Remo Naccarato – 30 December 2003 – Bone mineral density (BMD) and mineral metabolism were assessed in 54 patients with end‐stage liver disease who were evaluated for orthotopic liver transplantation (OLT) and assessed 3, 6, and 12 months after surgery in 26 patients who underwent OLT.

Gideon Hirshfield, Jane D. Collier, Karen Brown, Craig Taylor, Thomas Frick, Trevor P. Baglin, Graeme J.M. Alexander – 30 December 2003 – The most commonly detected hypercoagulable state involves an abnormal factor V protein synthesized by the liver in which arginine at position 506 is replaced by glutamine as a result of a single‐point mutation in the factor V gene (factor V Leiden). Liver transplantation is complicated by hepatic vascular thrombosis in up to 15% of cases, resulting in graft loss in most instances.

Alison L. Doughty, Jenean D. Spencer, Yvonne E. Cossart, Geoffrey W. McCaughan – 30 December 2003 – Viral recurrence is universal after transplantation for hepatitis C infection. This may lead to difficulties in differentiating allograft dysfunction caused by chronic rejection from hepatitis C virus (HCV) recurrence. Cases of severe cholestatic hepatitis have also been reported in conjunction with reinfection of the graft with HCV. Patients receiving transplants for HCV‐related liver disease were studied before and after transplantation by HCV RNA quantitation of serial serum samples.

Kenneth E. Sherman, Maria Sjogren, Robin L. Creager, Melissa A. Damiano, Stephen Freeman, Scot Lewey, Dirk Davis, Spencer Root, Frederick L. Weber, Kamal G. Ishak, Zachary D. Goodman – 30 December 2003 – Hepatitis C is a major cause of liver disease leading to cirrhosis. Although interferon (IFN) is the only approved therapy, treatment is characterized by low response rates and dose‐limiting side effects.

William Bernal, Julia Wendon, Mohamed Rela, Nigel Heaton, Roger Williams – 30 December 2003 – Once defined clinical criteria are fulfilled in acetaminophen‐induced hepatotoxicity, prognosis without orthotopic liver transplantation (OLT) may be very poor. In the present study, we examined the application and outcome of OLT in 548 patients admitted to a single center between 1990 and 1996. Four hundred twenty‐four (77%) of the patients studied did not fulfill transplantation criteria, and 396 of these (93%) survived.

Shigeru Taketani, Stephan Immenschuh, Sien Go, Peter R. Sinclair, Richard J. Stockert, H. Heng Liem, Ursula Muller Eberhard – 30 December 2003 – Hemopexin (Hx) binds heme with a very high affinity (Kd<0.1 pmol/L). It has been implicated as a major vehicle for the transport of heme into liver cells, involving a receptor‐mediated recycling mechanism.

Koji Nagano, Kimitoshi Nakamura, Ken‐Ich Urakami, Kazuhiro Umeyama, Hideki Uchiyama, Kazunori Koiwai, Shinzaburo Hattori, Tetsuro Yamamoto, Ichiro Matsuda, Fumio Endo – 30 December 2003 – In patients with Wilson's disease, both copper incorporation into ceruloplasmin and excretion of this metal into bile are impaired. These conditions are caused by a genetic defect in the Wilson's disease gene (ATP7B).

Carol R. Gardner, Diane E. Heck, Chung S. Yang, Paul E. Thomas, Xu‐Jie Zhang, George L. DeGeorge, Jeffrey D. Laskin, Debra L. Laskin – 30 December 2003 – Acetaminophen is a mild analgesic and antipyretic agent known to cause centrilobular hepatic necrosis at toxic doses. Although this may be due to a direct interaction of reactive acetaminophen metabolites with hepatocyte proteins, recent studies have suggested that cytotoxic mediators produced by parenchymal and nonparenchymal cells also contribute to the pathophysiological process.

Milena Rizzardini, Massimo Zappone, Pia Villa, Paola Gnocchi, Marina Sironi, Luisa Diomede, Cristina Meazza, Mario Monshouwer, Lavinia Cantoni – 30 December 2003 – The heme oxygenase 1 (HO‐1) gene is rapidly activated in the liver after lipopolysaccharide (LPS) treatment. Ninety minutes after LPS treatment (0.1 mg/kg, intraperitoneally) hepatic HO‐1 messenger RNA (mRNA) of mice was 40 times the control value.