PubMed ID:
19223884
Public Release Type:
Journal
Publication Year: 2009
Affiliation: Northwestern University, Chicago, Illinois, USA. gcote@im.wustl.edu
DOI:
https://doi.org/10.1038/ajg.2008.84
Authors:
Fontana RJ,
Lee WM,
Acute Liver Failure Study Group,
Avant L,
Barakat F,
Bernard T,
Blei AT,
Blei AT,
Brown R Jr,
Campbell M,
Casson D,
Chung R,
Coté GA,
Coultrup S,
Crippin JS,
Daud A,
Davern TJ,
Emre S,
Gerstle L,
Gottstein J,
Gottstein JH,
Groettum C,
Han S,
Harrison ME,
Hassanein T,
Hay JE,
Huntley N,
Hynan LS,
Ingram K,
Lalani E,
Larson AM,
McCashland TM,
McGuire B,
Misra C,
Morton D,
Munroz S,
Murray N,
Partovi K,
Peacock V,
Pezzia C,
Polson J,
Prosser C,
Reddy R,
Reisch JS,
Reuben A,
Rossaro L,
Rush R,
Salvatori J,
Sanders C,
Satyanarayana R,
Schilsky M,
Schwartz J,
Senkbeil L,
Shakil AO,
Smith A,
Stravitz T,
Taylor W,
Welch S,
Zaman A
Studies:
Acute Liver Failure Study Group: Adult Acute Liver Failure Study
Hyperamylasemia (HA) is often reported in patients with acute liver failure (ALF). Direct toxic effects of acetaminophen on the pancreas have been postulated, but the occurrence of HA in other etiologies raises the question of whether multiorgan failure is part of the pathogenesis of HA in this setting. Our main aim was to describe and analyze the incidence, clinical characteristics, and outcomes of HA in ALF of different etiologies.