The role of etiology in the hyperamylasemia of acute liver failure

Gregory A. Coté, Jeanne H. Gottstein, Amna Daud, William M. Lee, Andres T. Blei, Julie Polson, Carla Pezzia, Ezmina Lalani, Corron Sanders, Linda S. Hynan, Joan S. Reisch, Anne M. Larson, Hao Do, Jeffrey S. Crippin, Laura Gerstle, Timothy J. Davern, Kristine Partovi, Sukru Emre, Timothy M. McCashland, Tamara BernardJ. Eileen Hay, Cindy Groettum, Natalie Murray, Sonnya Coultrup, A. Obaid Shakil, Diane Morton, Jeanne Gottstein, Atif Zaman, Jonathan M. Schwartz, Ken Ingram, Steven Han, Val Peacock, Robert J. Fontana, Suzanne Welch, Brendan McGuire, Linda Avant, Raymond Chung, Deborah Casson, Robert Brown, Michael Schilsky, Lauren Senkbeil, M. Edwyn Harrison, Rebecca Rush, Adrian Reuben, Nancy Huntley, Santiago Munoz, Chandra Misra, Todd Stravitz, Jennifer Salvatori, Lorenzo Rossaro, Colette Prosser, Raj Satyanarayana, Wendy Taylor, Raj Reddy, Mical Campbell, Tarek Hassanein, Fatma Barakat, Alistair Smith

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

OBJECTIVES: 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. METHODS: Patients enrolled in the Acute Liver Failure Study Group registry with an admission amylase value available were included. For the purpose of this analysis, HA was defined as ≥3x upper limits of normal. Patients were classified as having acetaminophen (APAP)- or non-APAP-induced ALF, and by amylase group: normal (<115), mildly elevated (115-345), or HA (>345). Significant variables identified by univariate analysis were added to a multiple linear regression model. The primary outcome was overall survival. RESULTS: In total, 622 eligible patients were identified in the database, including 287 (46%) with APAP-induced ALF; 76 (12%) patients met the criteria for HA. Among patients with HA, 7 (9%) had documented clinical pancreatitis. The incidence of HA was similar among APAP (13%) and non-APAP (12%) patients. Although HA was associated with renal failure and greater Model for End-stage Liver Disease scores for both groups, HA was not an independent predictor of mortality in multivariate analysis. CONCLUSIONS: Although not an independent predictor of mortality, HA in ALF was present in all etiologies and was associated with diminished overall survival. HA appeared to be related to renal dysfunction in both groups and multiorgan failure in non-APAP ALF.

Original languageEnglish (US)
Pages (from-to)592-597
Number of pages6
JournalAmerican Journal of Gastroenterology
Volume104
Issue number3
DOIs
StatePublished - Mar 2009
Externally publishedYes

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Hyperamylasemia
Acute Liver Failure
Acetaminophen
Amylases
Linear Models
End Stage Liver Disease
Survival
Mortality
Poisons
Incidence
Pancreatitis
Renal Insufficiency
Registries

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Coté, G. A., Gottstein, J. H., Daud, A., Lee, W. M., Blei, A. T., Polson, J., ... Smith, A. (2009). The role of etiology in the hyperamylasemia of acute liver failure. American Journal of Gastroenterology, 104(3), 592-597. https://doi.org/10.1038/ajg.2008.84

The role of etiology in the hyperamylasemia of acute liver failure. / Coté, Gregory A.; Gottstein, Jeanne H.; Daud, Amna; Lee, William M.; Blei, Andres T.; Polson, Julie; Pezzia, Carla; Lalani, Ezmina; Sanders, Corron; Hynan, Linda S.; Reisch, Joan S.; Larson, Anne M.; Do, Hao; Crippin, Jeffrey S.; Gerstle, Laura; Davern, Timothy J.; Partovi, Kristine; Emre, Sukru; McCashland, Timothy M.; Bernard, Tamara; Hay, J. Eileen; Groettum, Cindy; Murray, Natalie; Coultrup, Sonnya; Shakil, A. Obaid; Morton, Diane; Gottstein, Jeanne; Zaman, Atif; Schwartz, Jonathan M.; Ingram, Ken; Han, Steven; Peacock, Val; Fontana, Robert J.; Welch, Suzanne; McGuire, Brendan; Avant, Linda; Chung, Raymond; Casson, Deborah; Brown, Robert; Schilsky, Michael; Senkbeil, Lauren; Harrison, M. Edwyn; Rush, Rebecca; Reuben, Adrian; Huntley, Nancy; Munoz, Santiago; Misra, Chandra; Stravitz, Todd; Salvatori, Jennifer; Rossaro, Lorenzo; Prosser, Colette; Satyanarayana, Raj; Taylor, Wendy; Reddy, Raj; Campbell, Mical; Hassanein, Tarek; Barakat, Fatma; Smith, Alistair.

In: American Journal of Gastroenterology, Vol. 104, No. 3, 03.2009, p. 592-597.

Research output: Contribution to journalArticle

Coté, GA, Gottstein, JH, Daud, A, Lee, WM, Blei, AT, Polson, J, Pezzia, C, Lalani, E, Sanders, C, Hynan, LS, Reisch, JS, Larson, AM, Do, H, Crippin, JS, Gerstle, L, Davern, TJ, Partovi, K, Emre, S, McCashland, TM, Bernard, T, Hay, JE, Groettum, C, Murray, N, Coultrup, S, Shakil, AO, Morton, D, Gottstein, J, Zaman, A, Schwartz, JM, Ingram, K, Han, S, Peacock, V, Fontana, RJ, Welch, S, McGuire, B, Avant, L, Chung, R, Casson, D, Brown, R, Schilsky, M, Senkbeil, L, Harrison, ME, Rush, R, Reuben, A, Huntley, N, Munoz, S, Misra, C, Stravitz, T, Salvatori, J, Rossaro, L, Prosser, C, Satyanarayana, R, Taylor, W, Reddy, R, Campbell, M, Hassanein, T, Barakat, F & Smith, A 2009, 'The role of etiology in the hyperamylasemia of acute liver failure', American Journal of Gastroenterology, vol. 104, no. 3, pp. 592-597. https://doi.org/10.1038/ajg.2008.84
Coté GA, Gottstein JH, Daud A, Lee WM, Blei AT, Polson J et al. The role of etiology in the hyperamylasemia of acute liver failure. American Journal of Gastroenterology. 2009 Mar;104(3):592-597. https://doi.org/10.1038/ajg.2008.84
Coté, Gregory A. ; Gottstein, Jeanne H. ; Daud, Amna ; Lee, William M. ; Blei, Andres T. ; Polson, Julie ; Pezzia, Carla ; Lalani, Ezmina ; Sanders, Corron ; Hynan, Linda S. ; Reisch, Joan S. ; Larson, Anne M. ; Do, Hao ; Crippin, Jeffrey S. ; Gerstle, Laura ; Davern, Timothy J. ; Partovi, Kristine ; Emre, Sukru ; McCashland, Timothy M. ; Bernard, Tamara ; Hay, J. Eileen ; Groettum, Cindy ; Murray, Natalie ; Coultrup, Sonnya ; Shakil, A. Obaid ; Morton, Diane ; Gottstein, Jeanne ; Zaman, Atif ; Schwartz, Jonathan M. ; Ingram, Ken ; Han, Steven ; Peacock, Val ; Fontana, Robert J. ; Welch, Suzanne ; McGuire, Brendan ; Avant, Linda ; Chung, Raymond ; Casson, Deborah ; Brown, Robert ; Schilsky, Michael ; Senkbeil, Lauren ; Harrison, M. Edwyn ; Rush, Rebecca ; Reuben, Adrian ; Huntley, Nancy ; Munoz, Santiago ; Misra, Chandra ; Stravitz, Todd ; Salvatori, Jennifer ; Rossaro, Lorenzo ; Prosser, Colette ; Satyanarayana, Raj ; Taylor, Wendy ; Reddy, Raj ; Campbell, Mical ; Hassanein, Tarek ; Barakat, Fatma ; Smith, Alistair. / The role of etiology in the hyperamylasemia of acute liver failure. In: American Journal of Gastroenterology. 2009 ; Vol. 104, No. 3. pp. 592-597.
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abstract = "OBJECTIVES: 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. METHODS: Patients enrolled in the Acute Liver Failure Study Group registry with an admission amylase value available were included. For the purpose of this analysis, HA was defined as ≥3x upper limits of normal. Patients were classified as having acetaminophen (APAP)- or non-APAP-induced ALF, and by amylase group: normal (<115), mildly elevated (115-345), or HA (>345). Significant variables identified by univariate analysis were added to a multiple linear regression model. The primary outcome was overall survival. RESULTS: In total, 622 eligible patients were identified in the database, including 287 (46{\%}) with APAP-induced ALF; 76 (12{\%}) patients met the criteria for HA. Among patients with HA, 7 (9{\%}) had documented clinical pancreatitis. The incidence of HA was similar among APAP (13{\%}) and non-APAP (12{\%}) patients. Although HA was associated with renal failure and greater Model for End-stage Liver Disease scores for both groups, HA was not an independent predictor of mortality in multivariate analysis. CONCLUSIONS: Although not an independent predictor of mortality, HA in ALF was present in all etiologies and was associated with diminished overall survival. HA appeared to be related to renal dysfunction in both groups and multiorgan failure in non-APAP ALF.",
author = "Cot{\'e}, {Gregory A.} and Gottstein, {Jeanne H.} and Amna Daud and Lee, {William M.} and Blei, {Andres T.} and Julie Polson and Carla Pezzia and Ezmina Lalani and Corron Sanders and Hynan, {Linda S.} and Reisch, {Joan S.} and Larson, {Anne M.} and Hao Do and Crippin, {Jeffrey S.} and Laura Gerstle and Davern, {Timothy J.} and Kristine Partovi and Sukru Emre and McCashland, {Timothy M.} and Tamara Bernard and Hay, {J. Eileen} and Cindy Groettum and Natalie Murray and Sonnya Coultrup and Shakil, {A. Obaid} and Diane Morton and Jeanne Gottstein and Atif Zaman and Schwartz, {Jonathan M.} and Ken Ingram and Steven Han and Val Peacock and Fontana, {Robert J.} and Suzanne Welch and Brendan McGuire and Linda Avant and Raymond Chung and Deborah Casson and Robert Brown and Michael Schilsky and Lauren Senkbeil and Harrison, {M. Edwyn} and Rebecca Rush and Adrian Reuben and Nancy Huntley and Santiago Munoz and Chandra Misra and Todd Stravitz and Jennifer Salvatori and Lorenzo Rossaro and Colette Prosser and Raj Satyanarayana and Wendy Taylor and Raj Reddy and Mical Campbell and Tarek Hassanein and Fatma Barakat and Alistair Smith",
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TY - JOUR

T1 - The role of etiology in the hyperamylasemia of acute liver failure

AU - Coté, Gregory A.

AU - Gottstein, Jeanne H.

AU - Daud, Amna

AU - Lee, William M.

AU - Blei, Andres T.

AU - Polson, Julie

AU - Pezzia, Carla

AU - Lalani, Ezmina

AU - Sanders, Corron

AU - Hynan, Linda S.

AU - Reisch, Joan S.

AU - Larson, Anne M.

AU - Do, Hao

AU - Crippin, Jeffrey S.

AU - Gerstle, Laura

AU - Davern, Timothy J.

AU - Partovi, Kristine

AU - Emre, Sukru

AU - McCashland, Timothy M.

AU - Bernard, Tamara

AU - Hay, J. Eileen

AU - Groettum, Cindy

AU - Murray, Natalie

AU - Coultrup, Sonnya

AU - Shakil, A. Obaid

AU - Morton, Diane

AU - Gottstein, Jeanne

AU - Zaman, Atif

AU - Schwartz, Jonathan M.

AU - Ingram, Ken

AU - Han, Steven

AU - Peacock, Val

AU - Fontana, Robert J.

AU - Welch, Suzanne

AU - McGuire, Brendan

AU - Avant, Linda

AU - Chung, Raymond

AU - Casson, Deborah

AU - Brown, Robert

AU - Schilsky, Michael

AU - Senkbeil, Lauren

AU - Harrison, M. Edwyn

AU - Rush, Rebecca

AU - Reuben, Adrian

AU - Huntley, Nancy

AU - Munoz, Santiago

AU - Misra, Chandra

AU - Stravitz, Todd

AU - Salvatori, Jennifer

AU - Rossaro, Lorenzo

AU - Prosser, Colette

AU - Satyanarayana, Raj

AU - Taylor, Wendy

AU - Reddy, Raj

AU - Campbell, Mical

AU - Hassanein, Tarek

AU - Barakat, Fatma

AU - Smith, Alistair

PY - 2009/3

Y1 - 2009/3

N2 - OBJECTIVES: 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. METHODS: Patients enrolled in the Acute Liver Failure Study Group registry with an admission amylase value available were included. For the purpose of this analysis, HA was defined as ≥3x upper limits of normal. Patients were classified as having acetaminophen (APAP)- or non-APAP-induced ALF, and by amylase group: normal (<115), mildly elevated (115-345), or HA (>345). Significant variables identified by univariate analysis were added to a multiple linear regression model. The primary outcome was overall survival. RESULTS: In total, 622 eligible patients were identified in the database, including 287 (46%) with APAP-induced ALF; 76 (12%) patients met the criteria for HA. Among patients with HA, 7 (9%) had documented clinical pancreatitis. The incidence of HA was similar among APAP (13%) and non-APAP (12%) patients. Although HA was associated with renal failure and greater Model for End-stage Liver Disease scores for both groups, HA was not an independent predictor of mortality in multivariate analysis. CONCLUSIONS: Although not an independent predictor of mortality, HA in ALF was present in all etiologies and was associated with diminished overall survival. HA appeared to be related to renal dysfunction in both groups and multiorgan failure in non-APAP ALF.

AB - OBJECTIVES: 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. METHODS: Patients enrolled in the Acute Liver Failure Study Group registry with an admission amylase value available were included. For the purpose of this analysis, HA was defined as ≥3x upper limits of normal. Patients were classified as having acetaminophen (APAP)- or non-APAP-induced ALF, and by amylase group: normal (<115), mildly elevated (115-345), or HA (>345). Significant variables identified by univariate analysis were added to a multiple linear regression model. The primary outcome was overall survival. RESULTS: In total, 622 eligible patients were identified in the database, including 287 (46%) with APAP-induced ALF; 76 (12%) patients met the criteria for HA. Among patients with HA, 7 (9%) had documented clinical pancreatitis. The incidence of HA was similar among APAP (13%) and non-APAP (12%) patients. Although HA was associated with renal failure and greater Model for End-stage Liver Disease scores for both groups, HA was not an independent predictor of mortality in multivariate analysis. CONCLUSIONS: Although not an independent predictor of mortality, HA in ALF was present in all etiologies and was associated with diminished overall survival. HA appeared to be related to renal dysfunction in both groups and multiorgan failure in non-APAP ALF.

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DO - 10.1038/ajg.2008.84

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