Traumatic brain injury is associated with increased syndecan-1 shedding in severely injured patients
Abstract Introduction Head injury and exsanguination are the leading causes of death in trauma patients. Hemorrhagic shock triggers systemic endothelial glycocalyx breakdown, potentially leading to traumatic endotheliopathy (EoT). Levels of syndecan-1, a main glycocalyx component, have been used to...
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doaj-a8978f3172154ca6a6dd3474dad7e7942020-11-25T02:09:20ZengBMCScandinavian Journal of Trauma, Resuscitation and Emergency Medicine1757-72412018-11-0126111010.1186/s13049-018-0565-3Traumatic brain injury is associated with increased syndecan-1 shedding in severely injured patientsErika Gonzalez Rodriguez0Jessica C. Cardenas1Charles S. Cox2Ryan S. Kitagawa3Jakob Stensballe4John B. Holcomb5Pär I. Johansson6Charles E. Wade7Center for Translational Injury Research (CeTIR), Department of Surgery, McGovern Medical School, University of Texas Health Science CenterCenter for Translational Injury Research (CeTIR), Department of Surgery, McGovern Medical School, University of Texas Health Science CenterDepartment of Pediatric Surgery, McGovern Medical School at The University of Texas Health Science CenterDepartment of Neurosurgery, Mischer Neuroscience Institute, McGovern Medical School at The University of Texas Health Science CenterSection for Transfusion Medicine, Capital Region Blood Bank, Copenhagen University Hospital, RigshospitaletCenter for Translational Injury Research (CeTIR), Department of Surgery, McGovern Medical School, University of Texas Health Science CenterCenter for Translational Injury Research (CeTIR), Department of Surgery, McGovern Medical School, University of Texas Health Science CenterCenter for Translational Injury Research (CeTIR), Department of Surgery, McGovern Medical School, University of Texas Health Science CenterAbstract Introduction Head injury and exsanguination are the leading causes of death in trauma patients. Hemorrhagic shock triggers systemic endothelial glycocalyx breakdown, potentially leading to traumatic endotheliopathy (EoT). Levels of syndecan-1, a main glycocalyx component, have been used to assess the integrity of the glycocalyx. In TBI patients, it remains unclear whether syndecan-1 shedding occurs and its correlation with outcomes. We aimed to determine the frequency of EoT+, defined as a syndecan-1 level of 40 ng/ml or higher, after TBI in isolated and polytraumatic injury. We also investigated how the presence of EoT+ affected outcomes in TBI patients. Methods Severely injured trauma patients were enrolled. From blood samples collected upon patients’ arrival to the hospital, we measured syndecan-1 (main biomarker of EoT+), soluble thrombomodulin (sTM, endothelial activation) adrenaline and noradrenaline (sympathoadrenal activation), and assessed TBI patients’ coagulation capacity. Results Of the enrolled patients (n = 331), those with TBI and polytrauma (n = 68) had the highest rate of EoT+ compared to isolated TBI (n = 58) and Non-TBI patients (n = 205) (Polytrauma-TBI 55.9% vs. Isolated-TBI 20.0% vs. non-TBI polytrauma 40.0%; p = 0.001). TBI patients with EoT+ exhibited marked increases in sTM, adrenaline and noradrenaline levels, and physiological and coagulation derangements. In isolated TBI patients, increasing syndecan-1 levels (β for every 10 ng/ml increase: 0.14; 95% CI: 0.02, 0.26) and hypocoagulability were negatively associated with survival. Conclusions This study provides evidence of syndecan-1 shedding after TBI supporting the notion that breakdown of the glycocalyx contributes to the physiological derangements after TBI.http://link.springer.com/article/10.1186/s13049-018-0565-3EndotheliumSyndecan-1Traumatic endotheliopathySympathoadrenal activation |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Erika Gonzalez Rodriguez Jessica C. Cardenas Charles S. Cox Ryan S. Kitagawa Jakob Stensballe John B. Holcomb Pär I. Johansson Charles E. Wade |
spellingShingle |
Erika Gonzalez Rodriguez Jessica C. Cardenas Charles S. Cox Ryan S. Kitagawa Jakob Stensballe John B. Holcomb Pär I. Johansson Charles E. Wade Traumatic brain injury is associated with increased syndecan-1 shedding in severely injured patients Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine Endothelium Syndecan-1 Traumatic endotheliopathy Sympathoadrenal activation |
author_facet |
Erika Gonzalez Rodriguez Jessica C. Cardenas Charles S. Cox Ryan S. Kitagawa Jakob Stensballe John B. Holcomb Pär I. Johansson Charles E. Wade |
author_sort |
Erika Gonzalez Rodriguez |
title |
Traumatic brain injury is associated with increased syndecan-1 shedding in severely injured patients |
title_short |
Traumatic brain injury is associated with increased syndecan-1 shedding in severely injured patients |
title_full |
Traumatic brain injury is associated with increased syndecan-1 shedding in severely injured patients |
title_fullStr |
Traumatic brain injury is associated with increased syndecan-1 shedding in severely injured patients |
title_full_unstemmed |
Traumatic brain injury is associated with increased syndecan-1 shedding in severely injured patients |
title_sort |
traumatic brain injury is associated with increased syndecan-1 shedding in severely injured patients |
publisher |
BMC |
series |
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine |
issn |
1757-7241 |
publishDate |
2018-11-01 |
description |
Abstract Introduction Head injury and exsanguination are the leading causes of death in trauma patients. Hemorrhagic shock triggers systemic endothelial glycocalyx breakdown, potentially leading to traumatic endotheliopathy (EoT). Levels of syndecan-1, a main glycocalyx component, have been used to assess the integrity of the glycocalyx. In TBI patients, it remains unclear whether syndecan-1 shedding occurs and its correlation with outcomes. We aimed to determine the frequency of EoT+, defined as a syndecan-1 level of 40 ng/ml or higher, after TBI in isolated and polytraumatic injury. We also investigated how the presence of EoT+ affected outcomes in TBI patients. Methods Severely injured trauma patients were enrolled. From blood samples collected upon patients’ arrival to the hospital, we measured syndecan-1 (main biomarker of EoT+), soluble thrombomodulin (sTM, endothelial activation) adrenaline and noradrenaline (sympathoadrenal activation), and assessed TBI patients’ coagulation capacity. Results Of the enrolled patients (n = 331), those with TBI and polytrauma (n = 68) had the highest rate of EoT+ compared to isolated TBI (n = 58) and Non-TBI patients (n = 205) (Polytrauma-TBI 55.9% vs. Isolated-TBI 20.0% vs. non-TBI polytrauma 40.0%; p = 0.001). TBI patients with EoT+ exhibited marked increases in sTM, adrenaline and noradrenaline levels, and physiological and coagulation derangements. In isolated TBI patients, increasing syndecan-1 levels (β for every 10 ng/ml increase: 0.14; 95% CI: 0.02, 0.26) and hypocoagulability were negatively associated with survival. Conclusions This study provides evidence of syndecan-1 shedding after TBI supporting the notion that breakdown of the glycocalyx contributes to the physiological derangements after TBI. |
topic |
Endothelium Syndecan-1 Traumatic endotheliopathy Sympathoadrenal activation |
url |
http://link.springer.com/article/10.1186/s13049-018-0565-3 |
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