ArticleToxicological sciences : an official journal of the Society of Toxicology2014
Glycodeoxycholic acid levels as prognostic biomarker in acetaminophen-induced acute liver failure patients.
Registry-linked trialOpen access · bronzeAbstract read
In one paragraph
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00518440 (A Multi-Center Trial to Study Acute Liver Failure in Adults), which is not on this map. Cited by 47 papers.
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47citing papers in PubMed
9.0field-weighted citation impact, top 2% of its field
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Multi-Center Trial to Study Acute Liver Failure in Adults
Who cites it
47 citing papers in PubMed, 85 citations in OpenAlex.
- Molecular adsorbent recirculating system and single-pass albumin dialysis in liver failure--a prospective, randomised crossover study.Critical care (London, England) · 2016Trial
- Extract from Eucommia ulmoides Oliv. Leaves alleviates APAP-induced acute liver injury via reshaping gut microbiota and attenuating microbial bile acids metabolism disorder.Chinese medicine · 2026Article
- Application of metabolomics in drug-induced liver injury: A systematic review.Journal of translational internal medicine · 2026Article
- The gut-liver axis in drug-induced liver injury (DILI): Interplay between gut microbiota, intestinal barrier, and immune system.Acta pharmaceutica Sinica. B · 2026Review
- Usefulness of plasma bile acid profile as a prognostic biomarker for drug-induced liver injury.EBioMedicine · 2026Article
- Comparative urinary metabolomics reveals unique and shared pathways in COVID-19 and liver diseases.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Comparison of LDH activity and LDH-M to predict death in patients with acetaminophen-induced acute liver failure.EXCLI journal · 2026Article
- Multiomics analysis elucidated the role of inflammatory response and bile acid metabolism disturbance in electric shock-induced liver injury in mice.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026Article
- Applications of Metabolomics in the Development of Biomedicine and Biotechnology.Advances in experimental medicine and biology · 2026Review
- Dysfunctional digestive tract highlights the metabolic hallmarks of nanoplastic-exacerbated Parkinson's pathology.NPJ Parkinson's disease · 2025Article
- Biological functions and pharmacological behaviors of bile acids in metabolic diseases.Journal of advanced research · 2025Review
- From fructose to the future: liver disease biomarkers and their prognostic value in acute liver failure.Critical reviews in clinical laboratory sciences · 2025Review
- Advances in drug-induced liver injury research: in vitro models, mechanisms, omics and gene modulation techniques.Cell & bioscience · 2024Review
- Functional metabolomics characterizes the contribution of farnesoid X receptor in pyrrolizidine alkaloid-induced hepatic sinusoidal obstruction syndrome.Archives of toxicology · 2024Article
- The Role of Mechanistic Biomarkers in Understanding Acetaminophen Hepatotoxicity in Humans.Drug metabolism and disposition: the biological fate of chemicals · 2024Review
- Gut-Liver Axis as a Therapeutic Target for Drug-Induced Liver Injury.Current issues in molecular biology · 2024Review
- Safety and efficacy of Single-Pass Albumin Dialysis (SPAD), Prometheus, and Molecular Adsorbent Recycling System (MARS) liver haemodialysis vs. Standard Medical Therapy (SMT): meta-analysis and systematic review.Przeglad gastroenterologiczny · 2024Review
- Article
- Study design for development of novel safety biomarkers of drug-induced liver injury by the translational safety biomarker pipeline (TransBioLine) consortium: a study protocol for a nested case-control study.Diagnostic and prognostic research · 2023Article
- Semi-Targeted Profiling of Bile Acids by High-Resolution Mass Spectrometry in a Rat Model of Drug-Induced Liver Injury.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Benjamin L Woolbright*Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medicine, and Center for Toxicology and Pharmacology Education and Research, University of Arizona College of Medicine, Phoenix, Arizona 85006 and Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
Mitchell R McGill*Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medicine, and Center for Toxicology and Pharmacology Education and Research, University of Arizona College of Medicine, Phoenix, Arizona 85006 and Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
Vincent S Staggs*Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medicine, and Center for Toxicology and Pharmacology Education and Research, University of Arizona College of Medicine, Phoenix, Arizona 85006 and Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
Robert D Winefield*Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medicine, and Center for Toxicology and Pharmacology Education and Research, University of Arizona College of Medicine, Phoenix, Arizona 85006 and Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
Parviz Gholami*Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medicine, and Center for Toxicology and Pharmacology Education and Research, University of Arizona College of Medicine, Phoenix, Arizona 85006 and Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
Mojtaba Olyaee*Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medicine, and Center for Toxicology and Pharmacology Education and Research, University of Arizona College of Medicine, Phoenix, Arizona 85006 and Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
Matthew R Sharpe*Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medicine, and Center for Toxicology and Pharmacology Education and Research, University of Arizona College of Medicine, Phoenix, Arizona 85006 and Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
Steven C Curry*Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medicine, and Center for Toxicology and Pharmacology Education and Research, University of Arizona College of Medicine, Phoenix, Arizona 85006 and Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390 *Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medicine, and Center for Toxicology and Pharmacology Education and Research, University of Arizona College of Medicine, Phoenix, Arizona 85006 and Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
William M Lee*Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medicine, and Center for Toxicology and Pharmacology Education and Research, University of Arizona College of Medicine, Phoenix, Arizona 85006 and Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390 *Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medicine, and Center for Toxicology and Pharmacology Education and Research, University of Arizona College of Medicine, Phoenix, Arizona 85006 and Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
Hartmut Jaeschke*Department of Pharmacology, Toxicology and Therapeutics, Department of Biostatistics, Department of Internal Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, Arizona 85006, Department of Medicine, and Center for Toxicology and Pharmacology Education and Research, University of Arizona College of Medicine, Phoenix, Arizona 85006 and Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390 hjaeschke@kumc.edu.
Acute Liver Failure Study Group
The University of Texas Southwestern Medical Center · USUniversity of Arizona · USUniversity of Kansas Medical Center · USGood Samaritan Medical Center · US
Funding
Heartland Institute for Clinical and Translational ResearchUL1TR000001 · NCATS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BAROHN, RICHARD J. · 2012 to 2015
$13.0MTHE ROLE OF HUMAN PXR IN ANTI-TUBERCULOSIS DRUG-INDUCED LIVER INJURYP20RR021940 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI COPPLE, BRYAN L · 2006 to 2011
$12.1MNuclear Receptors in Liver Health and DiseaseP20GM103549 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2012 to 2015
$8.1MTRAINING PROGRAM IN ENVIRONMENTAL TOXICOLOGYT32ES007079 · NIEHS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI HAGENBUCH, BRUNO · 1985 to 2015
$4.1MHEARTLAND INSTITUTE FOR CLINICAL AND TRANSLATIONAL RESEARCHUL1RR033179 · NCRR · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BAROHN, RICHARD J. · 2011 to 2011
$3.2MNEUTROPHIL-INDUCED LIVER INJURY TOXICITYR01AA012916 · NIAAA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2001 to 2012
$2.9MMitochondrial Dysfunction and Drug HepatotoxicityR01DK070195 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2005 to 2010
$1.8MNCATS NIH HHS UL1TR000001NCRR NIH HHS 5P20RR021940-07NCRR NIH HHS UL1RR033179NIAAA NIH HHS R01 AA12916NIDDK NIH HHS R01 DK070195NIEHS NIH HHS T32 ES007079-26A2NIGMS NIH HHS 8 P20 GM103549-07NIGMS NIH HHS P20 GM103549PHS HHS U-01-58369
Abstract
Acetaminophen (APAP)-induced acute liver failure (ALF) remains a major clinical problem. Although a majority of patients recovers after severe liver injury, a subpopulation of patients proceeds to ALF. Bile acids are generated in the liver and accumulate in blood during liver injury, and as such, have been proposed as biomarkers for liver injury and dysfunction. The goal of this study was to determine whether individual bile acid levels could determine outcome in patients with APAP-induced ALF (AALF). Serum bile acid levels were measured in AALF patients using mass spectrometry. Bile acid levels were elevated 5-80-fold above control values in injured patients on day 1 after the overdose and decreased over the course of hospital stay. Interestingly, glycodeoxycholic acid (GDCA) was significantly increased in non-surviving AALF patients compared with survivors. GDCA values obtained at peak alanine aminotransferase (ALT) and from day 1 of admission indicated GDCA could predict survival in these patients by receiver-operating characteristic analysis (AUC = 0.70 for day 1, AUC = 0.68 for peak ALT). Of note, AALF patients also had significantly higher levels of serum bile acids than patients with active cholestatic liver injury. These data suggest measurements of GDCA in this patient cohort modestly predicted outcome and may serve as a prognostic biomarker. Furthermore, accumulation of bile acids in serum or plasma may be a result of liver cell dysfunction and not cholestasis, suggesting elevation of circulating bile acid levels may be a consequence and not a cause of liver injury.
Indexed as
Drug OverdoseAcetaminophenAdultBiomarkersCase-Control StudiesChemical and Drug Induced Liver InjuryCholestasisFemaleGlycodeoxycholic AcidHumansLiver Function TestsMaleMiddle AgedPredictive Value of TestsYoung AdultAcetaminophenBiomarkersGlycodeoxycholic Acidacetaminophenacute liver failurebile acidcholestasishepatotoxicityserum biomarker
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Registered trials
NCT00518440ClinicalTrials.gov
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.