Observational studyScandinavian journal of trauma, resuscitation and emergency medicine2018
Traumatic brain injury is associated with increased syndecan-1 shedding in severely injured patients.
Observational study in Scandinavian journal of trauma, resuscitation and emergency medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Resuscitation-associated endotheliopathy (RAsE): a conceptual framework based on a systematic review and meta-analysis.Systematic reviews · 2023Pooled it
- Brain Hypoxia Is Associated With Neuroglial Injury in Humans Post-Cardiac Arrest.Circulation research · 2021Trial
- Association of Prehospital Plasma With Survival in Patients With Traumatic Brain Injury: A Secondary Analysis of the PAMPer Cluster Randomized Clinical Trial.JAMA network open · 2020Trial
- Inflammatory Cytokines Outperform Endotheliopathy Markers as Early Predictors of Mortality in Trauma.The Journal of surgical research · 2025Article
- Mechanobiology of the blood-brain barrier during development, disease and ageing.Nature communications · 2025Review
- Tranexamic acid did not attenuate the acute rise in plasma syndecan-1 in a severely injured cohort: a laboratory analysis of the PATCH clinical trial.Intensive care medicine experimental · 2025Article
- Repetitive Low-Level Blast Exposure Alters Circulating Myeloperoxidase, Matrix Metalloproteinases, and Neurovascular Endothelial Molecules in Experienced Military Breachers.International journal of molecular sciences · 2025Article
- Systemic endothelial glycocalyx shedding mediates vascular hyperpermeability after traumatic brain injury.Frontiers in neurology · 2025Article
- Concomitant Traumatic Brain Injury Exacerbates Endotheliopathy in Patients with Spinal Cord Injury.Neurotrauma reports · 2025Article
- Implications and pathophysiology of neuroinflammation in pediatric patients with traumatic brain injury: an updated review.Frontiers in neuroscience · 2025Review
- Traumatic Brain Injury and Alzheimer's Disease: A Shared Neurovascular Hypothesis.Neuroscience insights · 2025Review
- The Neuroprotection of 1,2,4-Triazole Derivative by Inhibiting Inflammation and Protecting BBB Integrity in Acute Ischemic Stroke.CNS neuroscience & therapeutics · 2024Article
- Dose-Dependent Tranexamic Acid Blunting of Penumbral Leukocyte Mobilization and Blood-Brain Barrier Permeability Following Traumatic Brain Injury: An In Vivo Murine Study.Neurocritical care · 2024Article
- Exploring Heparan Sulfate Proteoglycans as Mediators of Human Mesenchymal Stem Cell Neurogenesis.Cellular and molecular neurobiology · 2024Review
- Temporal Alterations in Cerebrovascular Glycocalyx and Cerebral Blood Flow after Exposure to a High-Intensity Blast in Rats.International journal of molecular sciences · 2024Article
- A role for decorin in improving motor deficits after traumatic brain injury.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- Unraveling neurovascular mysteries: the role of endothelial glycocalyx dysfunction in Alzheimer's disease pathogenesis.Frontiers in physiology · 2024Review
- ADAMTS13 and Non-ADAMTS13 Biomarkers in Immune-Mediated Thrombotic Thrombocytopenic Purpura.Journal of clinical medicine · 2023Review
- Resuscitating the Endothelial Glycocalyx in Trauma and Hemorrhagic Shock.Annals of surgery open : perspectives of surgical history, education, and clinical approaches · 2023Review
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionHead 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.
methodsSeverely 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.
resultsOf 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.
conclusionsThis study provides evidence of syndecan-1 shedding after TBI supporting the notion that breakdown of the glycocalyx contributes to the physiological derangements after TBI.
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