Keratin 19 marks poor differentiation and a more aggressive behaviour in canine and human hepatocellular tumours

Keratin 19 marks poor differentiation and a more aggressive behaviour in canine and human hepatocellular tumours Renee GHM van Sprundel1, Ted SGAM van den Ingh2, Valeer J Desmet3, Azeam Katoonizadeh3, Louis C Penning1, Jan Rothuizen1, Tania Roskams3 and Bart Spee13* * Corresponding author: Bart Spee [email protected] Author Affiliations 1 Department of Clinical Sciences of Companion Animals, Faculty of Veterinary medicine, Utrecht University, Utrecht, The Netherlands 2 TCCI Consultancy BV, Utrecht, The Netherlands 3 Department of Morphology and Molecular Pathology, University Hospitals Leuven, Leuven, Belgium For all author emails, please log on. Comparative Hepatology 2010, 9:4 doi:10.1186/1476-5926-9-4 The electronic version of this article is the complete one and can be found online at: http://www.comparative-hepatology.com/content/9/1/4 Received: 23 November 2009 Accepted: 18 February 2010 Published: 18 February 2010 © 2010 van Sprundel et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

Flucloxacillin-associated hepatic injury

Eleven cases of hepatic injury attributed to the intake of flucloxacillin were reported to the Netherlands Center for Monitoring of Adverse Reactions to Drugs between 1982 and 1992. They concerned four men and seven women, with a mean age of 57 years, treated for 2-28 days with an oral dose varying from 1500-4000 mg per day. Symptoms mostly appeared 10 to 30 days after starting treatment with flucloxacillin. Biochemically, the pattern was compatible with cholestatic hepatitis in seven cases, with a mixed cholestatic-hepatocellular type of injury in one case, a hepatocellular pattern in two cases, and mild liver enzyme elevations in one patient. Two patients died, one due to fatal bleeding from the liver after biopsy, and the second patient to a combination of hepatic and cardiac failure. The other patients recovered, on average 72 days after peaking of serum aminotransferase values. Histology in seven cases showed cholestatic hepatitis in five, with cholangitis or cholangiolitis in four of these patients. In the other two patients, there was centrilobular cholestasis with extensive bridging fibrosis and portal-central bridging necrosis, respectively