Screening in liver disease: Report of an AASLD clinical workshop

Paul C. Adams, Michael J. Arthur, Thomas D. Boyer, Laurie D. DeLeve, Adrian M. Di Bisceglie, Mark Hall, Theodore R. Levin, Dawn Provenzale, Leonard Seeff – 26 April 2004 – This report summarizes an AASLD Clinical Workshop that was presented at Digestive Diseases Week 2003 on screening in liver diseases. As newer diagnostic tests become available, many liver diseases and complications of liver disease can be detected at an early asymptomatic stage. In many cases, early detection can lead to earlier treatment and an improved outcome.

Hepatic adducts, circulating antibodies, and cytokine polymorphisms in patients with diclofenac hepatotoxicity

Guruprasad P. Aithal, Lesley Ramsay, Ann K. Daly, Nhareet Sonchit, Julian B. S. Leathart, Graeme Alexander, J. Gerald Kenna, John Caldwell, Christopher P. Day – 26 April 2004 – Diclofenac is a nonsteroidal anti‐inflammatory drug that causes rare but serious hepatotoxicity, the mechanism of which is unclear. The purpose of the present study was to explore the potential role played by the immune processes.

Angiogenesis in chronic inflammatory liver disease

Jesús Medina, Alicia G. Arroyo, Francisco Sánchez‐Madrid, Ricardo Moreno‐Otero – 26 April 2004 – Intrahepatic hypoxia may occur during the inflammatory and fibrotic processes that characterize several chronic liver diseases of viral and autoimmune origin. As a consequence, new vascular structures are formed to provide oxygen and nutrients. Angiogenesis involves a tightly regulated network of cellular and molecular mechanisms that result in the formation of functional vessels.

Activation of hepatic Nrf2 in vivo by acetaminophen in CD‐1 mice

Christopher E. P. Goldring, Neil R. Kitteringham, Robert Elsby, Laura E. Randle, Yuri N. Clement, Dominic P. Williams, Michael McMahon, John D. Hayes, Ken Itoh, Masayuki Yamamoto, B. Kevin Park – 26 April 2004 – The transcription factor NF‐E2‐related factor 2 (Nrf2) plays an essential role in the mammalian response to chemical and oxidative stress through induction of hepatic phase II detoxification enzymes and regulation of glutathione (GSH).

Steatosis and liver cell apoptosis in chronic hepatitis C: A mechanism for increased liver injury

Meagan J. Walsh, Daina M. Vanags, Andrew D. Clouston, Michelle M. Richardson, David M. Purdie, Julie R. Jonsson, Elizabeth E. Powell – 26 April 2004 – Steatosis is increasingly recognized as a cofactor influencing the progression of fibrosis in chronic hepatitis C; however, the mechanisms by which it contributes to liver injury remain uncertain.

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