Mechanistic biomarkers provide early and sensitive detection of acetaminophen‐induced acute liver injury at first presentation to hospital
Acetaminophen overdose is a common reason for hospital admission and the most frequent cause of hepatotoxicity in the Western world. Early identification would facilitate patient‐individualized treatment strategies. We investigated the potential of a panel of novel biomarkers (with enhanced liver ex...
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| Veröffentlicht in: | Hepatology (Baltimore, Md.) Jg. 58; H. 2; S. 777 - 787 |
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| Hauptverfasser: | , , , , , , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
United States
Wolters Kluwer Health, Inc
01.08.2013
WILEY-VCH Verlag |
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| ISSN: | 0270-9139, 1527-3350, 1527-3350 |
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| Abstract | Acetaminophen overdose is a common reason for hospital admission and the most frequent cause of hepatotoxicity in the Western world. Early identification would facilitate patient‐individualized treatment strategies. We investigated the potential of a panel of novel biomarkers (with enhanced liver expression or linked to the mechanisms of toxicity) to identify patients with acetaminophen‐induced acute liver injury (ALI) at first presentation to the hospital when currently used markers are within the normal range. In the first hospital presentation plasma sample from patients (n = 129), we measured microRNA‐122 (miR‐122; high liver specificity), high mobility group box‐1 (HMGB1; marker of necrosis), full‐length and caspase‐cleaved keratin‐18 (K18; markers of necrosis and apoptosis), and glutamate dehydrogenase (GLDH; marker of mitochondrial dysfunction). Receiver operator characteristic curve analysis and positive/negative predictive values were used to compare sensitivity to report liver injury versus alanine transaminase (ALT) and International Normalized Ratio (INR). In all patients, biomarkers at first presentation significantly correlated with peak ALT or INR. In patients presenting with normal ALT or INR, miR‐122, HMGB1, and necrosis K18 identified the development of liver injury (n = 15) or not (n = 84) with a high degree of accuracy and significantly outperformed ALT, INR, and plasma acetaminophen concentration for the prediction of subsequent ALI (n = 11) compared with no ALI (n = 52) in patients presenting within 8 hours of overdose. Conclusion: Elevations in plasma miR‐122, HMGB1, and necrosis K18 identified subsequent ALI development in patients on admission to the hospital, soon after acetaminophen overdose, and in patients with ALTs in the normal range. The application of such a biomarker panel could improve the speed of clinical decision‐making, both in the treatment of ALI and the design/execution of patient‐individualized treatment strategies. (Hepatology 2013;58:777–787) |
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| AbstractList | Acetaminophen overdose is a common reason for hospital admission and the most frequent cause of hepatotoxicity in the Western world. Early identification would facilitate patient-individualized treatment strategies. We investigated the potential of a panel of novel biomarkers (with enhanced liver expression or linked to the mechanisms of toxicity) to identify patients with acetaminophen-induced acute liver injury (ALI) at first presentation to the hospital when currently used markers are within the normal range. In the first hospital presentation plasma sample from patients (n = 129), we measured microRNA-122 (miR-122; high liver specificity), high mobility group box-1 (HMGB1; marker of necrosis), full-length and caspase-cleaved keratin-18 (K18; markers of necrosis and apoptosis), and glutamate dehydrogenase (GLDH; marker of mitochondrial dysfunction). Receiver operator characteristic curve analysis and positive/negative predictive values were used to compare sensitivity to report liver injury versus alanine transaminase (ALT) and International Normalized Ratio (INR). In all patients, biomarkers at first presentation significantly correlated with peak ALT or INR. In patients presenting with normal ALT or INR, miR-122, HMGB1, and necrosis K18 identified the development of liver injury (n = 15) or not (n = 84) with a high degree of accuracy and significantly outperformed ALT, INR, and plasma acetaminophen concentration for the prediction of subsequent ALI (n = 11) compared with no ALI (n = 52) in patients presenting within 8 hours of overdose. Conclusion: Elevations in plasma miR-122, HMGB1, and necrosis K18 identified subsequent ALI development in patients on admission to the hospital, soon after acetaminophen overdose, and in patients with ALTs in the normal range. The application of such a biomarker panel could improve the speed of clinical decision-making, both in the treatment of ALI and the design/execution of patient-individualized treatment strategies. (Hepatology 2013;58:777-787) [PUBLICATION ABSTRACT] Acetaminophen overdose is a common reason for hospital admission and the most frequent cause of hepatotoxicity in the Western world. Early identification would facilitate patient‐individualized treatment strategies. We investigated the potential of a panel of novel biomarkers (with enhanced liver expression or linked to the mechanisms of toxicity) to identify patients with acetaminophen‐induced acute liver injury (ALI) at first presentation to the hospital when currently used markers are within the normal range. In the first hospital presentation plasma sample from patients (n = 129), we measured microRNA‐122 (miR‐122; high liver specificity), high mobility group box‐1 (HMGB1; marker of necrosis), full‐length and caspase‐cleaved keratin‐18 (K18; markers of necrosis and apoptosis), and glutamate dehydrogenase (GLDH; marker of mitochondrial dysfunction). Receiver operator characteristic curve analysis and positive/negative predictive values were used to compare sensitivity to report liver injury versus alanine transaminase (ALT) and International Normalized Ratio (INR). In all patients, biomarkers at first presentation significantly correlated with peak ALT or INR. In patients presenting with normal ALT or INR, miR‐122, HMGB1, and necrosis K18 identified the development of liver injury (n = 15) or not (n = 84) with a high degree of accuracy and significantly outperformed ALT, INR, and plasma acetaminophen concentration for the prediction of subsequent ALI (n = 11) compared with no ALI (n = 52) in patients presenting within 8 hours of overdose. Conclusion: Elevations in plasma miR‐122, HMGB1, and necrosis K18 identified subsequent ALI development in patients on admission to the hospital, soon after acetaminophen overdose, and in patients with ALTs in the normal range. The application of such a biomarker panel could improve the speed of clinical decision‐making, both in the treatment of ALI and the design/execution of patient‐individualized treatment strategies. (Hepatology 2013;58:777–787) Acetaminophen overdose is a common reason for hospital admission and the most frequent cause of hepatotoxicity in the Western world. Early identification would facilitate patient-individualized treatment strategies. We investigated the potential of a panel of novel biomarkers (with enhanced liver expression or linked to the mechanisms of toxicity) to identify patients with acetaminophen-induced acute liver injury (ALI) at first presentation to the hospital when currently used markers are within the normal range. In the first hospital presentation plasma sample from patients (n = 129), we measured microRNA-122 (miR-122; high liver specificity), high mobility group box-1 (HMGB1; marker of necrosis), full-length and caspase-cleaved keratin-18 (K18; markers of necrosis and apoptosis), and glutamate dehydrogenase (GLDH; marker of mitochondrial dysfunction). Receiver operator characteristic curve analysis and positive/negative predictive values were used to compare sensitivity to report liver injury versus alanine transaminase (ALT) and International Normalized Ratio (INR). In all patients, biomarkers at first presentation significantly correlated with peak ALT or INR. In patients presenting with normal ALT or INR, miR-122, HMGB1, and necrosis K18 identified the development of liver injury (n = 15) or not (n = 84) with a high degree of accuracy and significantly outperformed ALT, INR, and plasma acetaminophen concentration for the prediction of subsequent ALI (n = 11) compared with no ALI (n = 52) in patients presenting within 8 hours of overdose. Elevations in plasma miR-122, HMGB1, and necrosis K18 identified subsequent ALI development in patients on admission to the hospital, soon after acetaminophen overdose, and in patients with ALTs in the normal range. The application of such a biomarker panel could improve the speed of clinical decision-making, both in the treatment of ALI and the design/execution of patient-individualized treatment strategies. Acetaminophen overdose is a common reason for hospital admission and the most frequent cause of hepatotoxicity in the Western world. Early identification would facilitate patient-individualized treatment strategies. We investigated the potential of a panel of novel biomarkers (with enhanced liver expression or linked to the mechanisms of toxicity) to identify patients with acetaminophen-induced acute liver injury (ALI) at first presentation to the hospital when currently used markers are within the normal range. In the first hospital presentation plasma sample from patients (n = 129), we measured microRNA-122 (miR-122; high liver specificity), high mobility group box-1 (HMGB1; marker of necrosis), full-length and caspase-cleaved keratin-18 (K18; markers of necrosis and apoptosis), and glutamate dehydrogenase (GLDH; marker of mitochondrial dysfunction). Receiver operator characteristic curve analysis and positive/negative predictive values were used to compare sensitivity to report liver injury versus alanine transaminase (ALT) and International Normalized Ratio (INR). In all patients, biomarkers at first presentation significantly correlated with peak ALT or INR. In patients presenting with normal ALT or INR, miR-122, HMGB1, and necrosis K18 identified the development of liver injury (n = 15) or not (n = 84) with a high degree of accuracy and significantly outperformed ALT, INR, and plasma acetaminophen concentration for the prediction of subsequent ALI (n = 11) compared with no ALI (n = 52) in patients presenting within 8 hours of overdose. Conclusion: Elevations in plasma miR-122, HMGB1, and necrosis K18 identified subsequent ALI development in patients on admission to the hospital, soon after acetaminophen overdose, and in patients with ALTs in the normal range. The application of such a biomarker panel could improve the speed of clinical decision-making, both in the treatment of ALI and the design/execution of patient-individualized treatment strategies. Acetaminophen overdose is a common reason for hospital admission and the most frequent cause of hepatotoxicity in the Western world. Early identification would facilitate patient-individualized treatment strategies. We investigated the potential of a panel of novel biomarkers (with enhanced liver expression or linked to the mechanisms of toxicity) to identify patients with acetaminophen-induced acute liver injury (ALI) at first presentation to the hospital when currently used markers are within the normal range. In the first hospital presentation plasma sample from patients (n = 129), we measured microRNA-122 (miR-122; high liver specificity), high mobility group box-1 (HMGB1; marker of necrosis), full-length and caspase-cleaved keratin-18 (K18; markers of necrosis and apoptosis), and glutamate dehydrogenase (GLDH; marker of mitochondrial dysfunction). Receiver operator characteristic curve analysis and positive/negative predictive values were used to compare sensitivity to report liver injury versus alanine transaminase (ALT) and International Normalized Ratio (INR). In all patients, biomarkers at first presentation significantly correlated with peak ALT or INR. In patients presenting with normal ALT or INR, miR-122, HMGB1, and necrosis K18 identified the development of liver injury (n = 15) or not (n = 84) with a high degree of accuracy and significantly outperformed ALT, INR, and plasma acetaminophen concentration for the prediction of subsequent ALI (n = 11) compared with no ALI (n = 52) in patients presenting within 8 hours of overdose.UNLABELLEDAcetaminophen overdose is a common reason for hospital admission and the most frequent cause of hepatotoxicity in the Western world. Early identification would facilitate patient-individualized treatment strategies. We investigated the potential of a panel of novel biomarkers (with enhanced liver expression or linked to the mechanisms of toxicity) to identify patients with acetaminophen-induced acute liver injury (ALI) at first presentation to the hospital when currently used markers are within the normal range. In the first hospital presentation plasma sample from patients (n = 129), we measured microRNA-122 (miR-122; high liver specificity), high mobility group box-1 (HMGB1; marker of necrosis), full-length and caspase-cleaved keratin-18 (K18; markers of necrosis and apoptosis), and glutamate dehydrogenase (GLDH; marker of mitochondrial dysfunction). Receiver operator characteristic curve analysis and positive/negative predictive values were used to compare sensitivity to report liver injury versus alanine transaminase (ALT) and International Normalized Ratio (INR). In all patients, biomarkers at first presentation significantly correlated with peak ALT or INR. In patients presenting with normal ALT or INR, miR-122, HMGB1, and necrosis K18 identified the development of liver injury (n = 15) or not (n = 84) with a high degree of accuracy and significantly outperformed ALT, INR, and plasma acetaminophen concentration for the prediction of subsequent ALI (n = 11) compared with no ALI (n = 52) in patients presenting within 8 hours of overdose.Elevations in plasma miR-122, HMGB1, and necrosis K18 identified subsequent ALI development in patients on admission to the hospital, soon after acetaminophen overdose, and in patients with ALTs in the normal range. The application of such a biomarker panel could improve the speed of clinical decision-making, both in the treatment of ALI and the design/execution of patient-individualized treatment strategies.CONCLUSIONElevations in plasma miR-122, HMGB1, and necrosis K18 identified subsequent ALI development in patients on admission to the hospital, soon after acetaminophen overdose, and in patients with ALTs in the normal range. The application of such a biomarker panel could improve the speed of clinical decision-making, both in the treatment of ALI and the design/execution of patient-individualized treatment strategies. |
| Author | Coyle, Judy Masson, Moyra Platt, Vivien Park, B. Kevin Goldring, Christopher E. Antoine, Daniel J. Moggs, Jonathan G. Bateman, D. Nicholas Thanacoody, Ruben H. Webb, David J. Gray, Alasdair J. Dear, James W. Lewis, Philip Starkey |
| Author_xml | – sequence: 1 givenname: Daniel J. surname: Antoine fullname: Antoine, Daniel J. organization: University of Liverpool – sequence: 2 givenname: James W. surname: Dear fullname: Dear, James W. organization: University of Edinburgh/British Heart Foundation Centre for Cardiovascular Science – sequence: 3 givenname: Philip Starkey surname: Lewis fullname: Lewis, Philip Starkey organization: University of Liverpool – sequence: 4 givenname: Vivien surname: Platt fullname: Platt, Vivien organization: University of Liverpool – sequence: 5 givenname: Judy surname: Coyle fullname: Coyle, Judy organization: Royal Infirmary of Edinburgh – sequence: 6 givenname: Moyra surname: Masson fullname: Masson, Moyra organization: Royal Infirmary of Edinburgh – sequence: 7 givenname: Ruben H. surname: Thanacoody fullname: Thanacoody, Ruben H. organization: University of Newcastle – sequence: 8 givenname: Alasdair J. surname: Gray fullname: Gray, Alasdair J. organization: Royal Infirmary of Edinburgh – sequence: 9 givenname: David J. surname: Webb fullname: Webb, David J. organization: University of Edinburgh/British Heart Foundation Centre for Cardiovascular Science – sequence: 10 givenname: Jonathan G. surname: Moggs fullname: Moggs, Jonathan G. organization: Novartis Institutes for Biomedical Research (NIBR) – sequence: 11 givenname: D. Nicholas surname: Bateman fullname: Bateman, D. Nicholas organization: Royal Infirmary of Edinburgh – sequence: 12 givenname: Christopher E. surname: Goldring fullname: Goldring, Christopher E. organization: University of Liverpool – sequence: 13 givenname: B. Kevin surname: Park fullname: Park, B. Kevin organization: University of Liverpool |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23390034$$D View this record in MEDLINE/PubMed |
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| Notes | These authors contributed equally to this work. Supported by the Medical Research Council (via the Centre for Drug Safety Science, grant number G0700654), Chief Scientist's Office of Scotland, Mason Medical Research Foundation; D.J.A. received financial support from the Wellcome Trust; J.W.D. received a contribution from the British Heart Foundation Center of Research Excellence Award and financial support from the National Health Service (NHS) Research Scotland though NHS Lothian. Potential conflict of interest: The authors have no conflict of interest to declare. J.G.M. is a full‐time employee of, consults for, and advises Novartis therapeutic targets or biomarkers were investigated in this study. ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Undefined-1 ObjectType-Feature-3 content type line 23 |
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| References | 2012; 92 2010; 53 2009; 68 2012; 122 2011 1984; 289 2010; 376 2008; 28 2007; 8 2009; 112 2008; 7 2008; 46 2011; 54 2007; 5 2012; 56 2012; 44 2005; 45 2003; 22 2009; 39 2009; 106 2012; 73 Craig (RU18-34-20241201) 2012; 73 Jaeschke (R21-34-20241201) 2012; 44 Waring (R3-34-20241201) 2008; 46 Liang (R14-34-20241201) 2007; 8 Kerr (R2-34-20241201) 2005; 45 McGill (R8-34-20241201) 2012; 122 Mant (R4-34-20241201) 1984; 289 Antoine (R6-34-20241201) 2009; 112 Prescott (R22-34-20241201) 2009; 68 Adebayo (R12-34-20241201) 2012; 56 Wang (R7-34-20241201) 2009; 106 Bechmann (R19-34-20241201) 2008; 28 Antoine (R9-34-20241201) 2012; 56 Antoine (R5-34-20241201) 2009; 39 McPhail (RU17-34-20241201) 2010; 53 Bonaldi (R11-34-20241201) 2003; 22 Starkey Lewis (R10-34-20241201) 2011; 54 Cummings (R13-34-20241201) 2008; 7 Harrill (R15-34-20241201) 2012; 92 Bernal (R16-34-20241201) 2010; 376 Rutherford (R20-34-20241201) 2007; 5 23984999 - Expert Rev Gastroenterol Hepatol. 2013 Aug;7(6):509-12. doi: 10.1586/17474124.2013.814901. |
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| SubjectTerms | Acetaminophen - adverse effects Adult Alanine Transaminase - metabolism Biomarkers Biomarkers - blood Chemical and Drug Induced Liver Injury - blood Chemical and Drug Induced Liver Injury - diagnosis Disease Management Female Glutamate Dehydrogenase - metabolism Hepatology HMGB1 Protein - blood Hospitalization Humans Keratin-18 - blood Liver Liver - metabolism Liver Injury/Regeneration Male MicroRNAs - blood Middle Aged Patients Sensitivity and Specificity Time Factors |
| Title | Mechanistic biomarkers provide early and sensitive detection of acetaminophen‐induced acute liver injury at first presentation to hospital |
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