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Plasma thioredoxin levels during post-cardiac arrest syndrome: relationship with severity and outcome
INTRODUCTION: Despite experimental evidence, clinical demonstration of acute state of oxidative stress and inflammation during post-cardiac arrest syndrome is lacking. Plasma level of thioredoxin (TRX), a redox-active protein induced under conditions of oxidative stress and inflammation, is increase...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4056807/ https://www.ncbi.nlm.nih.gov/pubmed/23356570 http://dx.doi.org/10.1186/cc12492 |
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author | Mongardon, Nicolas Lemiale, Virginie Borderie, Didier Burke-Gaffney, Anne Perbet, Sébastien Marin, Nathalie Charpentier, Julien Pène, Frédéric Chiche, Jean-Daniel Mira, Jean-Paul Cariou, Alain |
author_facet | Mongardon, Nicolas Lemiale, Virginie Borderie, Didier Burke-Gaffney, Anne Perbet, Sébastien Marin, Nathalie Charpentier, Julien Pène, Frédéric Chiche, Jean-Daniel Mira, Jean-Paul Cariou, Alain |
author_sort | Mongardon, Nicolas |
collection | PubMed |
description | INTRODUCTION: Despite experimental evidence, clinical demonstration of acute state of oxidative stress and inflammation during post-cardiac arrest syndrome is lacking. Plasma level of thioredoxin (TRX), a redox-active protein induced under conditions of oxidative stress and inflammation, is increased in various critical care conditions. We determined plasma TRX concentrations after cardiac arrest and assessed relationships with severity and outcome. METHODS: Retrospective study of consecutive patients admitted to a single academic intensive care unit (ICU) for out-of-hospital cardiac arrest (between July 2006 and March 2008). Plasma levels of TRX were measured at admission, day (D) 1, 2 and 3. RESULTS: Of 176 patients included, median TRX values measured in ICU survivors and non-survivors were, respectively: 22 ng/mL (7.8 to 77) vs. 72.4 (21.9 to 117.9) at admission (P < 0.001); 5.9 (3.5 to 25.5) vs. 23.2 (5.8 to 81.4) at D1 (P = 0.003); 10.8 (3.6 to 50.8) vs. 11.7 (4.5 to 66.4) at D2 (P = 0.22); and 16.7 (5.3 to 68.3) vs. 17 (4.3 to 62.9) at D3 (P = 0.96). Patients dying within 24 hours had significantly (P < 0.001) higher TRX levels (118.6 ng/mL (94.8 to 280)) than those who died after 24 hours or survived (50.8 (13.9 to 95.7) and 22 (7.8 to 77)). The area under the ROC curve to predict early death was 0.84 (0.76 to 0.91). TRX levels on admission were significantly correlated with 'low-flow' duration (P = 0.003), sequential organ failure assessment (SOFA) score (P < 0.001), and blood lactate concentration (P < 0.001), but not with 'no-flow' duration or simplified acute physiology score (SAPS) II score. TRX levels and admission arterial pO(2 )correlated negatively (r = -0.17, P = 0.03). Finally, cardiac arrest with cardiac etiology exhibited lower levels of TRX than in cases of extra-cardiac cause (46 ng/mL (11 to 104) vs. 68 (42 to 137), P = 0.01). CONCLUSIONS: Our data show for the first time that TRX levels were elevated early following cardiac arrest, suggestive of oxidative stress and inflammation occurring with this condition. Highest values were found in the most severe patients. TRX could be a useful tool for further exploration and comprehension of post-cardiac arrest syndrome. |
format | Online Article Text |
id | pubmed-4056807 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-40568072014-06-14 Plasma thioredoxin levels during post-cardiac arrest syndrome: relationship with severity and outcome Mongardon, Nicolas Lemiale, Virginie Borderie, Didier Burke-Gaffney, Anne Perbet, Sébastien Marin, Nathalie Charpentier, Julien Pène, Frédéric Chiche, Jean-Daniel Mira, Jean-Paul Cariou, Alain Crit Care Research INTRODUCTION: Despite experimental evidence, clinical demonstration of acute state of oxidative stress and inflammation during post-cardiac arrest syndrome is lacking. Plasma level of thioredoxin (TRX), a redox-active protein induced under conditions of oxidative stress and inflammation, is increased in various critical care conditions. We determined plasma TRX concentrations after cardiac arrest and assessed relationships with severity and outcome. METHODS: Retrospective study of consecutive patients admitted to a single academic intensive care unit (ICU) for out-of-hospital cardiac arrest (between July 2006 and March 2008). Plasma levels of TRX were measured at admission, day (D) 1, 2 and 3. RESULTS: Of 176 patients included, median TRX values measured in ICU survivors and non-survivors were, respectively: 22 ng/mL (7.8 to 77) vs. 72.4 (21.9 to 117.9) at admission (P < 0.001); 5.9 (3.5 to 25.5) vs. 23.2 (5.8 to 81.4) at D1 (P = 0.003); 10.8 (3.6 to 50.8) vs. 11.7 (4.5 to 66.4) at D2 (P = 0.22); and 16.7 (5.3 to 68.3) vs. 17 (4.3 to 62.9) at D3 (P = 0.96). Patients dying within 24 hours had significantly (P < 0.001) higher TRX levels (118.6 ng/mL (94.8 to 280)) than those who died after 24 hours or survived (50.8 (13.9 to 95.7) and 22 (7.8 to 77)). The area under the ROC curve to predict early death was 0.84 (0.76 to 0.91). TRX levels on admission were significantly correlated with 'low-flow' duration (P = 0.003), sequential organ failure assessment (SOFA) score (P < 0.001), and blood lactate concentration (P < 0.001), but not with 'no-flow' duration or simplified acute physiology score (SAPS) II score. TRX levels and admission arterial pO(2 )correlated negatively (r = -0.17, P = 0.03). Finally, cardiac arrest with cardiac etiology exhibited lower levels of TRX than in cases of extra-cardiac cause (46 ng/mL (11 to 104) vs. 68 (42 to 137), P = 0.01). CONCLUSIONS: Our data show for the first time that TRX levels were elevated early following cardiac arrest, suggestive of oxidative stress and inflammation occurring with this condition. Highest values were found in the most severe patients. TRX could be a useful tool for further exploration and comprehension of post-cardiac arrest syndrome. BioMed Central 2013 2013-01-29 /pmc/articles/PMC4056807/ /pubmed/23356570 http://dx.doi.org/10.1186/cc12492 Text en Copyright © 2013 Mongardon et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Mongardon, Nicolas Lemiale, Virginie Borderie, Didier Burke-Gaffney, Anne Perbet, Sébastien Marin, Nathalie Charpentier, Julien Pène, Frédéric Chiche, Jean-Daniel Mira, Jean-Paul Cariou, Alain Plasma thioredoxin levels during post-cardiac arrest syndrome: relationship with severity and outcome |
title | Plasma thioredoxin levels during post-cardiac arrest syndrome: relationship with severity and outcome |
title_full | Plasma thioredoxin levels during post-cardiac arrest syndrome: relationship with severity and outcome |
title_fullStr | Plasma thioredoxin levels during post-cardiac arrest syndrome: relationship with severity and outcome |
title_full_unstemmed | Plasma thioredoxin levels during post-cardiac arrest syndrome: relationship with severity and outcome |
title_short | Plasma thioredoxin levels during post-cardiac arrest syndrome: relationship with severity and outcome |
title_sort | plasma thioredoxin levels during post-cardiac arrest syndrome: relationship with severity and outcome |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4056807/ https://www.ncbi.nlm.nih.gov/pubmed/23356570 http://dx.doi.org/10.1186/cc12492 |
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