Marsha Y. Morgan, Angela M. Madden, Clare T. Soulsby, Richard W. Morris – 27 September 2006 – Accurate assessments of nutritional status are difficult to obtain in patients with cirrhosis. The aim of this study was to devise and validate a global nutritional assessment scheme for use in this patient population.
Hiroki Kawamura, Sugantha Govindarajan, Fred Aswad, Keigo Machida, Michael M.C. Lai, Vicky M.‐H. Sung, Gunther Dennert – 27 September 2006 – Hepatitis C virus (HCV) infection causes acute and chronic liver disease often leading to liver cirrhosis and hepatocellular carcinoma. Numerous studies have shown that despite induction of virus specific immunity, a curative response is often not attained; this has led to the hypothesis that HCV genes modulate immunity, thereby enabling chronic infections.
27 September 2006
Mattias Ekstedt, Lennart E. Franzén, Ulrik L. Mathiesen, Lars Thorelius, Marika Holmqvist, Göran Bodemar, Stergios Kechagias – 27 September 2006 – Nonalcoholic fatty liver disease (NAFLD) is the most common cause of elevated liver enzymes in patients of developed countries. We determined the long‐term clinical and histological courses of such patients. In a cohort study, 129 consecutively enrolled patients diagnosed with biopsy‐proven NAFLD were reevaluated. Survival and causes of death were compared with a matched reference population.
Rui Sun, Ogyi Park, Norio Horiguchi, Shailin Kulkarni, Won‐Il Jeong, Hao‐Yu Sun, Svetlana Radaeva, Bin Gao – 27 September 2006 – Increasing evidence suggests that liver regeneration is suppressed in patients with chronic HCV infection; however, the underlying mechanisms remain unclear. Previously, we demonstrated that injection of the synthetic double‐stranded RNA (dsRNA) poly I:C to mimic viral infection suppresses liver regeneration in the partial hepatectomy (PHx) model, whereby IFN‐γ contributes to the inhibition.
Raphael B. Merriman, Linda D. Ferrell, Marco G. Patti, Shiobhan R. Weston, Mark S. Pabst, Bradley E. Aouizerat, Nathan M. Bass – 27 September 2006 – In the absence of surrogate markers, the evaluation of suspected nonalcoholic fatty liver disease (NAFLD) is highly dependent on histological examination. The extent of sampling variability affecting the reliability of a single liver biopsy in patients with suspected NAFLD is poorly characterized.
Christiane Pauli‐Magnus, Peter J. Meier – 27 September 2006 – Drug‐induced liver injury is an important clinical problem with significant morbidity and mortality. Whereas for most hepatocellular forms of drug‐induced hepatic injury the underlying pathophysiological mechanism is poorly understood, there is increasing evidence that cholestatic forms of drug‐induced liver damage result from a drug‐ or metabolite‐mediated inhibition of hepatobiliary transporter systems.
Felix J. Frey – 27 September 2006 – Exaggerated renal sodium retention with concomitant potassium loss is a hallmark of cirrhosis and contributes to the accumulation of fluid as ascites, pleural effusion, or edema. This apparent mineralocorticoid effect is only partially explained by increased aldosterone concentrations. I present evidence supporting the hypothesis that cortisol confers mineralocorticoid action in cirrhosis.
Joanna W. Y. Ho, Roberta W. C. Pang, Cecilia Lau, Chris K. Sun, Wan Ching Yu, Sheung Tat Fan, Ronnie T. P. Poon – 27 September 2006 – This study evaluated the significance of circulating bone marrow‐derived endothelial progenitor cells (EPCs) in patients with hepatocellular carcinoma (HCC), a solid tumor with rich neovasculature. Eighty patients with HCC were recruited for the study, and 16 patients with liver cirrhosis and 14 healthy subjects were also included for comparison. Blood samples were taken before treatment.
Andrew L. Mason – 27 September 2006 – Primary biliary cirrhosis (PBC) is an autoimmune disease with a strong genetic component characterized by biliary ductular inflammation with eventual liver cirrhosis. The serologic hallmark of PBC is antimitochondrial antibodies that react with the pyruvate dehydrogenase complex, targeting the inner lipoyl domain of the E2 subunit (anti‐PDC‐E2). Herein we demonstrate that NOD.c3c4 mice congenically derived from the non‐obese diabetic strain develop an autoimmune biliary disease (ABD) that models human PBC.