Small gallstones, preserved gallbladder motility, and fast crystallization are associated with pancreatitis

Niels G. Venneman, Willem Renooij, Jens F. Rehfeld, Gerard P. vanBerge‐Henegouwen, Peter M. N. Y. H. Go, Ivo A. M. J. Broeders, Karel J. van Erpecum – 25 March 2005 – Acute pancreatitis is a severe complication of gallstones with considerable mortality. We sought to explore the potential risk factors for biliary pancreatitis.

Late liver‐related mortality from complications of transfusion‐acquired hepatitis C

Hiroshi Kamitsukasa, Hideharu Harada, Hideo Tanaka, Michiyasu Yagura, Hajime Tokita, Akira Ohbayashi – 25 March 2005 – Although several cohort studies have been reported in individuals with chronic hepatitis C virus (HCV) infection, little is known about liver‐related mortality among the elderly. We conducted a cohort study in 302 patients with tuberculosis sequelae who had received a blood transfusion at a young age and had subsequently been treated at a chest clinic.

Fibrosis correlates with a ductular reaction in hepatitis C: Roles of impaired replication, progenitor cells and steatosis

Andrew D. Clouston, Elizabeth E. Powell, Meagan J. Walsh, Michelle M. Richardson, A. Jake Demetris, Julie R. Jonsson – 25 March 2005 – The mechanisms for progressive fibrosis and exacerbation by steatosis in patients with chronic hepatitis C (HCV) are still unknown. We hypothesized that proliferative blockade in HCV‐infected and steatotic hepatocytes results in the default activation of hepatic progenitor cells (HPC), capable of differentiating into both biliary and hepatocyte lineages, and that the resultant ductular reaction promotes portal fibrosis.

Suppressive effect of ursodeoxycholic acid on type IIA phospholipase A2 expression in HepG2 cells

Tadashi Ikegami, Yasushi Matsuzaki, Sugano Fukushima, Junichi Shoda, Jean Luc Olivier, Bernard Bouscarel, Naomi Tanaka – 25 March 2005 – Phospholipase A2 IIA (PLA2IIA), which plays a crucial role in arachidonic acid metabolism and in inflammation, is upregulated under various pathological conditions, including in the gallbladder and gallbladder bile from patients with multiple cholesterol gallstones, in the liver and kidney of rats with cirrhosis, as well as in the colonic tissue of animals treated with a chemical carcinogen.

Prevalence and significance of neurocognitive dysfunction in hepatitis C in the absence of correlated risk factors

Mary Pat McAndrews, Karl Farcnik, Peter Carlen, Andrei Damyanovich, Mirela Mrkonjic, Susan Jones, E. Jenny Heathcote – 25 March 2005 – Neurocognitive morbidity has been reported in individuals with chronic hepatitis C virus (HCV) infection, but the magnitude of such dysfunction in the absence of disease‐correlated factors known to affect the central nervous system (e.g., substance abuse, cirrhosis, depression, interferon treatment) and the impact of any such change on functioning is unclear.

A biphasic response of hepatobiliary cholesterol metabolism to dietary fat at the onset of obesity in the mouse

Suheeta Roy, Hideyuki Hyogo, Suresh K. Yadav, Michele K. Wu, Linda A. Jelicks, Joseph D. Locker, Philippe G. Frank, Michael P. Lisanti, David L. Silver, David E. Cohen – 25 March 2005 – Human obesity is associated with abnormal hepatic cholesterol homeostasis and resistance to leptin action. Because leptin administration to rodents promotes the biliary elimination of plasma cholesterol, this study was designed to elucidate a pathophysiological role for leptin during the development of obesity. We fed mice diets containing high or low saturated fat contents.

Abnormal concentrations of esterified carnitine in bile: A feature of pediatric acute liver failure with poor prognosis

Benjamin L. Shneider, Piero Rinaldo, Sukru Emre, John Bucuvalas, Robert Squires, Michael Narkewicz, Gabriel Gondolesi, Margret Magid, Raffaella Morotti, Linda S. Hynan – 24 March 2005 – The etiology of acute liver failure in children is unknown in a large number of cases. Defects in fatty acid oxidation have been shown to lead to severe liver injury. This retrospective analysis examined the bile acylcarnitine profiles of 27 children with acute liver failure who underwent liver transplantation or died.

Two common PFIC2 mutations are associated with the impaired membrane trafficking of BSEP/ABCB11

Hisamitsu Hayashi, Tappei Takada, Hiroshi Suzuki, Hidetaka Akita, Yuichi Sugiyama – 24 March 2005 – Progressive familial intrahepatic cholestasis type 2 (PFIC2) is caused by a mutation in the bile salt export pump (BSEP/ABCB11) gene. However, the mechanisms for the deficiency in the function of two mutations (E297G and D482G), which are frequently found in European patients, have not yet been identified. In the present study, we examined the transport activity and cellular localization of these two mutants in human embryonic kidney 293 and Madin‐Darby canine kidney II cells, respectively.

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