Outcome of acute idiosyncratic drug‐induced liver injury: Long‐term follow‐up in a hepatotoxicity registry

Raúl J. Andrade, M. Isabel Lucena, Neil Kaplowitz, Beatriz García‐Muņoz, Yolanda Borraz, Ketevan Pachkoria, Miren García‐Cortés, M. Carmen Fernández, Gloria Pelaez, Luis Rodrigo, José A. Durán, Joan Costa, Ramón Planas, Anabel Barriocanal, Carlos Guarner, Manuel Romero‐Gomez, Teresa Muņoz‐Yagüe, Javier Salmerón, Ramón Hidalgo – 28 November 2006 – A chronic adverse reaction may occur in some instances of drug‐induced liver injury (DILI), even despite drug cessation.

Aquaporin‐1 and aquaporin‐2 urinary excretion in cirrhosis: Relationship with ascites and hepatorenal syndrome

Christina Esteva‐Font, Maria E. Baccaro, Patricia Fernández‐Llama, Laia Sans, Monica Guevara, Elisabet Ars, Wladimiro Jiménez, Vicente Arroyo, Jose A. Ballarín, Pere Ginès – 28 November 2006 – Several experimental models of cirrhosis have shown dysregulation of renal aquaporins in different phases of liver disease. We investigated the urinary excretion of both aquaporin‐1 and aquaporin‐2 in patients with cirrhosis at different stages of the disease.

Genomics and complex liver disease: Challenges and opportunities

Brian D. Juran, Konstantinos N. Lazaridis – 28 November 2006 – The concept of genetic susceptibility in the contribution to human disease is not new. What is new is the emerging ability of the field of genomics to detect, assess, and interpret genetic variation in the study of susceptibility to development of disease. Deciphering the human genome sequence and the publication of the human haplotype map are key elements of this effort.

Hepatic precursors derived from murine embryonic stem cells contribute to regeneration of injured liver

Jeonghoon Heo, Valentina M. Factor, Tania Uren, Yasushi Takahama, Ju‐Seog Lee, Marian Major, Stephen M. Feinstone, Snorri S. Thorgeirsson – 28 November 2006 – We established an efficient system for differentiation, expansion and isolation of hepatic progenitor cells from mouse embryonic stem (ES) cells and evaluated their capacity to repopulate injured liver.

JunD is a profibrogenic transcription factor regulated by Jun N‐terminal kinase‐independent phosphorylation

David E. Smart, Karen Green, Fiona Oakley, Jonathan B. Weitzman, Moshe Yaniv, Gary Reynolds, Jelena Mann, Harry Millward‐Sadler, Derek A. Mann – 28 November 2006 – JunD is implicated in the regulation of hepatic stellate cell (HSC) activation and liver fibrosis via its transcriptional regulation of the tissue inhibitor of metalloproteinases‐1 (TIMP‐1) gene. In the present study we found in vivo evidence of a role for JunD in fibrogenesis. Expression of JunD was demonstrated in alpha‐SMA‐positive activated HSCs of fibrotic rodents and human livers.

Hyponatremia in cirrhosis: Results of a patient population survey

Paolo Angeli, Florence Wong, Hugh Watson, Pere Ginès, CAPPS Investigators – 28 November 2006 – Low serum sodium concentration is an independent predictor of mortality in patients with cirrhosis, but its prevalence and clinical significance is unclear. To evaluate prospectively the prevalence of low serum sodium concentration and the association between serum sodium levels and severity of ascites and complications of cirrhosis, prospective data were collected on 997 consecutive patients from 28 centers in Europe, North and South America, and Asia for a period of 28 days.

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