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Publication Information
Affiliation
Northwestern University, Chicago, Illinois, USA. gcote@im.wustl.edu
Authors
Acute Liver Failure Study Group, Avant L, Barakat F, Bernard T, Blei AT, Brown R Jr, Campbell M, Casson D, Chung R, Coté GA, Coultrup S, Crippin JS, Daud A, Davern TJ, Emre S, Fontana RJ, 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, Lee WM, 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
Citation
Coté GA, Gottstein JH, Daud A, Blei AT, Acute Liver Failure Study Group. The role of etiology in the hyperamylasemia of acute liver failure. Am J Gastroenterol 2009 Mar;104(3):592-7. Epub 2009 Feb 17.Abstract
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.