A metabolomic analysis of thiol response for standard and modified N‐acetyl cysteine treatment regimens in patients with acetaminophen overdose
N‐acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol‐APAP)‐induced acute liver injury (ALI). The 3‐bag licensed 20.25 h standard regimen, and a 12 h modified regimen, are used to treat APAP overdose. This study evaluated the redox thiol response and APAP metabolites, in patien...
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| Vydáno v: | Clinical and translational science Ročník 14; číslo 4; s. 1476 - 1489 |
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| Jazyk: | angličtina |
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United States
John Wiley & Sons, Inc
01.07.2021
John Wiley and Sons Inc Wiley |
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| ISSN: | 1752-8054, 1752-8062, 1752-8062 |
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| Abstract | N‐acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol‐APAP)‐induced acute liver injury (ALI). The 3‐bag licensed 20.25 h standard regimen, and a 12 h modified regimen, are used to treat APAP overdose. This study evaluated the redox thiol response and APAP metabolites, in patients with a single APAP overdose treated with either the 20.25 h standard or 12 h modified regimen. We used liquid chromatography tandem mass spectrometry to quantify clinically important oxidative stress biomarkers and APAP metabolites in plasma samples from 45 patients who participated in a randomized controlled trial (SNAP trial). We investigated the time course response of plasma metabolites at predose, 12 h, and 20.25 h post‐start of NAC infusion. The results showed that the 12 h modified regimen resulted in a significant elevation of plasma NAC and cysteine concentrations at 12 h post‐infusion. We found no significant alteration in the metabolism of APAP, mitochondrial, amino acids, and other thiol biomarkers with the two regimens. We examined APAP and purine metabolism in overdose patients who developed ALI. We showed the major APAP‐metabolites and xanthine were significantly higher in patients with ALI. These biomarkers correlated well with alanine aminotransferase activity at admission. Receiver operating characteristic analysis showed that at admission, plasma APAP‐metabolites and xanthine concentrations were predictive for ALI. In conclusion, a significantly higher redox thiol response with the modified NAC regimen at 12 h postdose suggests this regimen may produce greater antioxidant efficacy. At baseline, plasma APAP and purine metabolites may be useful biomarkers for early prediction of APAP‐induced ALI. |
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| AbstractList | N-acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol-APAP)-induced acute liver injury (ALI). The 3-bag licensed 20.25 h standard regimen, and a 12 h modified regimen, are used to treat APAP overdose. This study evaluated the redox thiol response and APAP metabolites, in patients with a single APAP overdose treated with either the 20.25 h standard or 12 h modified regimen. We used liquid chromatography tandem mass spectrometry to quantify clinically important oxidative stress biomarkers and APAP metabolites in plasma samples from 45 patients who participated in a randomized controlled trial (SNAP trial). We investigated the time course response of plasma metabolites at predose, 12 h, and 20.25 h post-start of NAC infusion. The results showed that the 12 h modified regimen resulted in a significant elevation of plasma NAC and cysteine concentrations at 12 h post-infusion. We found no significant alteration in the metabolism of APAP, mitochondrial, amino acids, and other thiol biomarkers with the two regimens. We examined APAP and purine metabolism in overdose patients who developed ALI. We showed the major APAP-metabolites and xanthine were significantly higher in patients with ALI. These biomarkers correlated well with alanine aminotransferase activity at admission. Receiver operating characteristic analysis showed that at admission, plasma APAP-metabolites and xanthine concentrations were predictive for ALI. In conclusion, a significantly higher redox thiol response with the modified NAC regimen at 12 h postdose suggests this regimen may produce greater antioxidant efficacy. At baseline, plasma APAP and purine metabolites may be useful biomarkers for early prediction of APAP-induced ALI. N‐acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol‐APAP)‐induced acute liver injury (ALI). The 3‐bag licensed 20.25 h standard regimen, and a 12 h modified regimen, are used to treat APAP overdose. This study evaluated the redox thiol response and APAP metabolites, in patients with a single APAP overdose treated with either the 20.25 h standard or 12 h modified regimen. We used liquid chromatography tandem mass spectrometry to quantify clinically important oxidative stress biomarkers and APAP metabolites in plasma samples from 45 patients who participated in a randomized controlled trial (SNAP trial). We investigated the time course response of plasma metabolites at predose, 12 h, and 20.25 h post‐start of NAC infusion. The results showed that the 12 h modified regimen resulted in a significant elevation of plasma NAC and cysteine concentrations at 12 h post‐infusion. We found no significant alteration in the metabolism of APAP, mitochondrial, amino acids, and other thiol biomarkers with the two regimens. We examined APAP and purine metabolism in overdose patients who developed ALI. We showed the major APAP‐metabolites and xanthine were significantly higher in patients with ALI. These biomarkers correlated well with alanine aminotransferase activity at admission. Receiver operating characteristic analysis showed that at admission, plasma APAP‐metabolites and xanthine concentrations were predictive for ALI. In conclusion, a significantly higher redox thiol response with the modified NAC regimen at 12 h postdose suggests this regimen may produce greater antioxidant efficacy. At baseline, plasma APAP and purine metabolites may be useful biomarkers for early prediction of APAP‐induced ALI. N ‐acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol‐APAP)‐induced acute liver injury (ALI). The 3‐bag licensed 20.25 h standard regimen, and a 12 h modified regimen, are used to treat APAP overdose. This study evaluated the redox thiol response and APAP metabolites, in patients with a single APAP overdose treated with either the 20.25 h standard or 12 h modified regimen. We used liquid chromatography tandem mass spectrometry to quantify clinically important oxidative stress biomarkers and APAP metabolites in plasma samples from 45 patients who participated in a randomized controlled trial (SNAP trial). We investigated the time course response of plasma metabolites at predose, 12 h, and 20.25 h post‐start of NAC infusion. The results showed that the 12 h modified regimen resulted in a significant elevation of plasma NAC and cysteine concentrations at 12 h post‐infusion. We found no significant alteration in the metabolism of APAP, mitochondrial, amino acids, and other thiol biomarkers with the two regimens. We examined APAP and purine metabolism in overdose patients who developed ALI. We showed the major APAP‐metabolites and xanthine were significantly higher in patients with ALI. These biomarkers correlated well with alanine aminotransferase activity at admission. Receiver operating characteristic analysis showed that at admission, plasma APAP‐metabolites and xanthine concentrations were predictive for ALI. In conclusion, a significantly higher redox thiol response with the modified NAC regimen at 12 h postdose suggests this regimen may produce greater antioxidant efficacy. At baseline, plasma APAP and purine metabolites may be useful biomarkers for early prediction of APAP‐induced ALI. N-acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol-APAP)-induced acute liver injury (ALI). The 3-bag licensed 20.25 h standard regimen, and a 12 h modified regimen, are used to treat APAP overdose. This study evaluated the redox thiol response and APAP metabolites, in patients with a single APAP overdose treated with either the 20.25 h standard or 12 h modified regimen. We used liquid chromatography tandem mass spectrometry to quantify clinically important oxidative stress biomarkers and APAP metabolites in plasma samples from 45 patients who participated in a randomized controlled trial (SNAP trial). We investigated the time course response of plasma metabolites at predose, 12 h, and 20.25 h post-start of NAC infusion. The results showed that the 12 h modified regimen resulted in a significant elevation of plasma NAC and cysteine concentrations at 12 h post-infusion. We found no significant alteration in the metabolism of APAP, mitochondrial, amino acids, and other thiol biomarkers with the two regimens. We examined APAP and purine metabolism in overdose patients who developed ALI. We showed the major APAP-metabolites and xanthine were significantly higher in patients with ALI. These biomarkers correlated well with alanine aminotransferase activity at admission. Receiver operating characteristic analysis showed that at admission, plasma APAP-metabolites and xanthine concentrations were predictive for ALI. In conclusion, a significantly higher redox thiol response with the modified NAC regimen at 12 h postdose suggests this regimen may produce greater antioxidant efficacy. At baseline, plasma APAP and purine metabolites may be useful biomarkers for early prediction of APAP-induced ALI.N-acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol-APAP)-induced acute liver injury (ALI). The 3-bag licensed 20.25 h standard regimen, and a 12 h modified regimen, are used to treat APAP overdose. This study evaluated the redox thiol response and APAP metabolites, in patients with a single APAP overdose treated with either the 20.25 h standard or 12 h modified regimen. We used liquid chromatography tandem mass spectrometry to quantify clinically important oxidative stress biomarkers and APAP metabolites in plasma samples from 45 patients who participated in a randomized controlled trial (SNAP trial). We investigated the time course response of plasma metabolites at predose, 12 h, and 20.25 h post-start of NAC infusion. The results showed that the 12 h modified regimen resulted in a significant elevation of plasma NAC and cysteine concentrations at 12 h post-infusion. We found no significant alteration in the metabolism of APAP, mitochondrial, amino acids, and other thiol biomarkers with the two regimens. We examined APAP and purine metabolism in overdose patients who developed ALI. We showed the major APAP-metabolites and xanthine were significantly higher in patients with ALI. These biomarkers correlated well with alanine aminotransferase activity at admission. Receiver operating characteristic analysis showed that at admission, plasma APAP-metabolites and xanthine concentrations were predictive for ALI. In conclusion, a significantly higher redox thiol response with the modified NAC regimen at 12 h postdose suggests this regimen may produce greater antioxidant efficacy. At baseline, plasma APAP and purine metabolites may be useful biomarkers for early prediction of APAP-induced ALI. Abstract N‐acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol‐APAP)‐induced acute liver injury (ALI). The 3‐bag licensed 20.25 h standard regimen, and a 12 h modified regimen, are used to treat APAP overdose. This study evaluated the redox thiol response and APAP metabolites, in patients with a single APAP overdose treated with either the 20.25 h standard or 12 h modified regimen. We used liquid chromatography tandem mass spectrometry to quantify clinically important oxidative stress biomarkers and APAP metabolites in plasma samples from 45 patients who participated in a randomized controlled trial (SNAP trial). We investigated the time course response of plasma metabolites at predose, 12 h, and 20.25 h post‐start of NAC infusion. The results showed that the 12 h modified regimen resulted in a significant elevation of plasma NAC and cysteine concentrations at 12 h post‐infusion. We found no significant alteration in the metabolism of APAP, mitochondrial, amino acids, and other thiol biomarkers with the two regimens. We examined APAP and purine metabolism in overdose patients who developed ALI. We showed the major APAP‐metabolites and xanthine were significantly higher in patients with ALI. These biomarkers correlated well with alanine aminotransferase activity at admission. Receiver operating characteristic analysis showed that at admission, plasma APAP‐metabolites and xanthine concentrations were predictive for ALI. In conclusion, a significantly higher redox thiol response with the modified NAC regimen at 12 h postdose suggests this regimen may produce greater antioxidant efficacy. At baseline, plasma APAP and purine metabolites may be useful biomarkers for early prediction of APAP‐induced ALI. |
| Author | Ng, Mei Li Leroy Sivappiragasam, Pakkiri Bateman, D. Nicholas Ibrahim, Baharudin Khoo, Benjamin Bing Jie Choi, Hyungwon Dear, James W Drum, Chester Lee |
| AuthorAffiliation | 3 Department of Medicine Yong Loo Lin School of Medicine National University of Singapore Singapore City Singapore 6 School of Pharmaceutical Sciences Universiti Sains Malaysia Kepala Batas Malaysia 1 Pharmacology, Toxicology, and Therapeutics Centre for Cardiovascular Science University of Edinburgh Edinburgh UK 5 Institute of Molecular and Cell Biology Agency for Science, Technology, and Research Singapore City Singapore 2 Cardiovascular Research Institute National University Health System Singapore City Singapore 7 Department of Surgery Yong Loo Lin School of Medicine National University of Singapore Singapore City Singapore 8 Department of Biochemistry Yong Loo Lin School of Medicine National University of Singapore Singapore City Singapore 4 Advanced Medical and Dental Institute Universiti Sains Malaysia Kepala Batas Malaysia |
| AuthorAffiliation_xml | – name: 2 Cardiovascular Research Institute National University Health System Singapore City Singapore – name: 4 Advanced Medical and Dental Institute Universiti Sains Malaysia Kepala Batas Malaysia – name: 7 Department of Surgery Yong Loo Lin School of Medicine National University of Singapore Singapore City Singapore – name: 1 Pharmacology, Toxicology, and Therapeutics Centre for Cardiovascular Science University of Edinburgh Edinburgh UK – name: 3 Department of Medicine Yong Loo Lin School of Medicine National University of Singapore Singapore City Singapore – name: 5 Institute of Molecular and Cell Biology Agency for Science, Technology, and Research Singapore City Singapore – name: 8 Department of Biochemistry Yong Loo Lin School of Medicine National University of Singapore Singapore City Singapore – name: 6 School of Pharmaceutical Sciences Universiti Sains Malaysia Kepala Batas Malaysia |
| Author_xml | – sequence: 1 givenname: James W surname: Dear fullname: Dear, James W organization: University of Edinburgh – sequence: 2 givenname: Mei Li surname: Ng fullname: Ng, Mei Li organization: Universiti Sains Malaysia – sequence: 3 givenname: D. Nicholas surname: Bateman fullname: Bateman, D. Nicholas organization: University of Edinburgh – sequence: 4 givenname: Pakkiri surname: Leroy Sivappiragasam fullname: Leroy Sivappiragasam, Pakkiri organization: National University Health System – sequence: 5 givenname: Hyungwon surname: Choi fullname: Choi, Hyungwon organization: Agency for Science, Technology, and Research – sequence: 6 givenname: Benjamin Bing Jie surname: Khoo fullname: Khoo, Benjamin Bing Jie organization: National University of Singapore – sequence: 7 givenname: Baharudin surname: Ibrahim fullname: Ibrahim, Baharudin organization: Universiti Sains Malaysia – sequence: 8 givenname: Chester Lee surname: Drum fullname: Drum, Chester Lee email: mdccld@nus.edu.sg organization: National University of Singapore |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33742775$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1038_s41392_024_02072_z crossref_primary_10_1002_iub_2625 crossref_primary_10_1016_j_jaci_2022_07_025 crossref_primary_10_1016_j_ecoenv_2022_113773 crossref_primary_10_1124_dmd_121_000455 crossref_primary_10_1080_17425255_2023_2259787 crossref_primary_10_1016_j_dsx_2024_103068 crossref_primary_10_1039_D3SC00224A |
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| Notes | Funding information James W. Dear and Mei Li Ng contributed equally to this work. This study was generously supported by the Clinician Scientist Award (CSA) grant, National Medical Research Council of the Singapore Ministry of Health [CSAINV17nov12], and National Research Foundation, under its artificial intelligence (AI) Singapore Programme (AISG Award No: AISG‐GC‐2019‐002). Correction added on 20 April, 2021, after first online publication: The author name Bing Jie Khoo has been corrected as Benjamin Bing Jie Khoo in the author byline. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Article-2 ObjectType-Feature-1 content type line 23 ObjectType-Undefined-3 |
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| Snippet | N‐acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol‐APAP)‐induced acute liver injury (ALI). The 3‐bag licensed 20.25 h standard... N ‐acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol‐APAP)‐induced acute liver injury (ALI). The 3‐bag licensed 20.25 h standard... N-acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol-APAP)-induced acute liver injury (ALI). The 3-bag licensed 20.25 h standard... N‐acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol‐APAP)‐induced acute liver injury (ALI). The 3‐bag licensed 20.25 h standard... N-acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol-APAP)-induced acute liver injury (ALI). The 3-bag licensed 20.25 h standard... Abstract N‐acetylcysteine (NAC) is an antidote to prevent acetaminophen (paracetamol‐APAP)‐induced acute liver injury (ALI). The 3‐bag licensed 20.25 h... |
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| SubjectTerms | Acetaminophen Acetaminophen - pharmacokinetics Acetaminophen - poisoning Acetylcysteine Acetylcysteine - administration & dosage Adult Alanine Alanine transaminase Analgesics Antidotes - administration & dosage Antioxidants Biomarkers Biomarkers - blood Biomarkers - metabolism Chemical and Drug Induced Liver Injury - blood Chemical and Drug Induced Liver Injury - diagnosis Chemical and Drug Induced Liver Injury - etiology Chemical and Drug Induced Liver Injury - prevention & control Clinical trials Cysteine Drug Administration Schedule Drug Monitoring - methods Drug Overdose - blood Drug Overdose - drug therapy Drug Overdose - etiology Female Humans Infusions, Intravenous Liquid chromatography Liver Male Mass spectroscopy Metabolism Metabolites Metabolomics Middle Aged Mitochondria Nonsteroidal anti-inflammatory drugs Overdose Oxidation-Reduction - drug effects Oxidative stress Paracetamol Patients Plasma Regulatory agencies ROC Curve Sulfhydryl Compounds - blood Sulfhydryl Compounds - metabolism |
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| Title | A metabolomic analysis of thiol response for standard and modified N‐acetyl cysteine treatment regimens in patients with acetaminophen overdose |
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