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Hyperfibrinolysis and fibrinolysis shutdown in patients with traumatic brain injury

Traumatic brain injury (TBI) is associated with coagulation/fibrinolysis disorders. We retrospectively evaluated 61 TBI cases transported to hospital within 1 h post-injury. Levels of thrombin-antithrombin III complex (TAT), D-dimer, and plasminogen activator inhibitor-1 (PAI-1) were measured on arr...

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Autores principales: Nakae, Ryuta, Murai, Yasuo, Wada, Takeshi, Fujiki, Yu, Kanaya, Takahiro, Takayama, Yasuhiro, Suzuki, Go, Naoe, Yasutaka, Yokota, Hiroyuki, Yokobori, Shoji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9646769/
https://www.ncbi.nlm.nih.gov/pubmed/36352256
http://dx.doi.org/10.1038/s41598-022-23912-4
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author Nakae, Ryuta
Murai, Yasuo
Wada, Takeshi
Fujiki, Yu
Kanaya, Takahiro
Takayama, Yasuhiro
Suzuki, Go
Naoe, Yasutaka
Yokota, Hiroyuki
Yokobori, Shoji
author_facet Nakae, Ryuta
Murai, Yasuo
Wada, Takeshi
Fujiki, Yu
Kanaya, Takahiro
Takayama, Yasuhiro
Suzuki, Go
Naoe, Yasutaka
Yokota, Hiroyuki
Yokobori, Shoji
author_sort Nakae, Ryuta
collection PubMed
description Traumatic brain injury (TBI) is associated with coagulation/fibrinolysis disorders. We retrospectively evaluated 61 TBI cases transported to hospital within 1 h post-injury. Levels of thrombin-antithrombin III complex (TAT), D-dimer, and plasminogen activator inhibitor-1 (PAI-1) were measured on arrival and 3 h, 6 h, 12 h, 1 day, 3 days and 7 days after injury. Multivariate logistic regression analysis was performed to identify prognostic factors for coagulation and fibrinolysis. Plasma TAT levels peaked at admission and decreased until 1 day after injury. Plasma D-dimer levels increased, peaking up to 3 h after injury, and decreasing up to 3 days after injury. Plasma PAI-1 levels increased up to 3 h after injury, the upward trend continuing until 6 h after injury, followed by a decrease until 3 days after injury. TAT, D-dimer, and PAI-1 were elevated in the acute phase of TBI in cases with poor outcome. Multivariate logistic regression analysis showed that D-dimer elevation from admission to 3 h after injury and PAI-1 elevation from 6 h to 1 day after injury were significant negative prognostic indicators. Post-TBI hypercoagulation, fibrinolysis, and fibrinolysis shutdown were activated consecutively. Hyperfibrinolysis immediately after injury and subsequent fibrinolysis shutdown were associated with poor outcome.
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spelling pubmed-96467692022-11-15 Hyperfibrinolysis and fibrinolysis shutdown in patients with traumatic brain injury Nakae, Ryuta Murai, Yasuo Wada, Takeshi Fujiki, Yu Kanaya, Takahiro Takayama, Yasuhiro Suzuki, Go Naoe, Yasutaka Yokota, Hiroyuki Yokobori, Shoji Sci Rep Article Traumatic brain injury (TBI) is associated with coagulation/fibrinolysis disorders. We retrospectively evaluated 61 TBI cases transported to hospital within 1 h post-injury. Levels of thrombin-antithrombin III complex (TAT), D-dimer, and plasminogen activator inhibitor-1 (PAI-1) were measured on arrival and 3 h, 6 h, 12 h, 1 day, 3 days and 7 days after injury. Multivariate logistic regression analysis was performed to identify prognostic factors for coagulation and fibrinolysis. Plasma TAT levels peaked at admission and decreased until 1 day after injury. Plasma D-dimer levels increased, peaking up to 3 h after injury, and decreasing up to 3 days after injury. Plasma PAI-1 levels increased up to 3 h after injury, the upward trend continuing until 6 h after injury, followed by a decrease until 3 days after injury. TAT, D-dimer, and PAI-1 were elevated in the acute phase of TBI in cases with poor outcome. Multivariate logistic regression analysis showed that D-dimer elevation from admission to 3 h after injury and PAI-1 elevation from 6 h to 1 day after injury were significant negative prognostic indicators. Post-TBI hypercoagulation, fibrinolysis, and fibrinolysis shutdown were activated consecutively. Hyperfibrinolysis immediately after injury and subsequent fibrinolysis shutdown were associated with poor outcome. Nature Publishing Group UK 2022-11-09 /pmc/articles/PMC9646769/ /pubmed/36352256 http://dx.doi.org/10.1038/s41598-022-23912-4 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Nakae, Ryuta
Murai, Yasuo
Wada, Takeshi
Fujiki, Yu
Kanaya, Takahiro
Takayama, Yasuhiro
Suzuki, Go
Naoe, Yasutaka
Yokota, Hiroyuki
Yokobori, Shoji
Hyperfibrinolysis and fibrinolysis shutdown in patients with traumatic brain injury
title Hyperfibrinolysis and fibrinolysis shutdown in patients with traumatic brain injury
title_full Hyperfibrinolysis and fibrinolysis shutdown in patients with traumatic brain injury
title_fullStr Hyperfibrinolysis and fibrinolysis shutdown in patients with traumatic brain injury
title_full_unstemmed Hyperfibrinolysis and fibrinolysis shutdown in patients with traumatic brain injury
title_short Hyperfibrinolysis and fibrinolysis shutdown in patients with traumatic brain injury
title_sort hyperfibrinolysis and fibrinolysis shutdown in patients with traumatic brain injury
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9646769/
https://www.ncbi.nlm.nih.gov/pubmed/36352256
http://dx.doi.org/10.1038/s41598-022-23912-4
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