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Syndecan-1 Levels in Trauma and Burn Patients Remain Elevated During Resuscitation and Correlate With Coagulopathy
Grace Bonson1, Peter Callas2, Maria-Cristina Bravo3
1Department of Emergency Medicine, University of Vermont, Burlington, Vermont, USA.
Insights
Elevated levels of syndecan-1 (SDC-1) in severe trauma patients peak early and persist, indicating a higher risk of coagulopathy. This finding highlights SDC-1 as a potential biomarker for trauma-induced coagulopathy.
Area of Science:
- Biochemistry
- Trauma Medicine
- Hematology
Background:
- Syndecan-1 (SDC-1) shedding from vascular endothelium into circulation in severe trauma is linked to mortality.
- The temporal profile of SDC-1 elevation in trauma patients remains underexplored.
Purpose of the Study:
- To characterize the longitudinal pattern of SDC-1 elevation in trauma patients within 120 hours of resuscitation.
- To investigate the association between elevated SDC-1 levels (endotheliopathy) and trauma-induced coagulopathy (INR ≥ 1.4).
Main Methods:
- Prospective observational study of 301 severely injured adults across 3 trauma centers.
- Blood samples collected at multiple time points (0-120 hours); SDC-1 quantified by ELISA (≥40 ng/mL considered elevated).
- Coagulopathy defined as INR ≥ 1.4; association analyzed using logistic regression, adjusting for covariates.
Main Results:
- SDC-1 levels were significantly higher in patients with coagulopathy.
- Elevated SDC-1 (≥40 ng/mL) strongly predicted coagulopathy (adjusted OR 17.88, P < .05).
- High SDC-1 levels were most prominent at initial presentation and tended to remain elevated.
Conclusions:
- Plasma SDC-1 levels peak early and remain elevated throughout the initial 120 hours in most trauma patients with mechanical and/or burn injuries.
- Elevated SDC-1 is independently associated with an increased risk of coagulopathy, regardless of injury severity.
Objectives:
Shedding of the proteoglycan syndecan-1 (SDC-1) from the vascular endothelial surface into the circulation in severe trauma predicts mortality in trauma patients. However, the timing and duration of SDC-1 elevation in trauma patients have not been defined. The primary aim of this study was to describe the longitudinal pattern of SDC-1 elevation in trauma patients with either mechanical and/or burn injury during the first 120 hours of resuscitation and initial stabilization. Our secondary objective was to determine the association of endotheliopathy, as defined by elevated SDC-1 levels, with trauma-induced coagulopathy (international normalized ratio [INR] ≥ 1.4).
Methods:
This prospective observational study enrolled adults meeting trauma activation criteria at 1 of 3 trauma centers. The blood was collected at presentation in the emergency department (time 0) and again at 2, 4, 6, 12, 24, 72, 96, and 120 hours. SDC-1 was quantified by ELISA, and elevated levels were defined as ≥40 ng/mL. The primary outcome of coagulopathy was defined as a clinical laboratory report of INR ≥ 1.4 during this timeframe. We determined the association between elevated SDC-1 and coagulopathy using logistic regression and adjusted for age, sex, burn status, and injury severity.
Results:
We studied 301 severely injured individuals, including those with mechanical and burn injuries. Among these individuals, 96 (31.9%) had coagulopathy, 122 (40.5%) required transfusions, and 42 (14%) died. SDC-1 plasma levels were significantly greater in subjects with coagulopathy relative to noncoagulopathic patients. Plasma levels of SDC-1 ≥ 40 ng/mL conferred significantly increased odds of presenting with INR ≥ 1.4, with an adjusted odds ratio of 17.88 (95% CI, 5.14-62.24), P < .05. High SDC-1 levels (≥40 ng/mL) were most often evident at the initial blood draw and tended to remain elevated.
Conclusion:
Plasma SDC-1 peaks early and remains elevated across time in most individuals with mechanical and/or burn injury. Individuals with elevated SDC-1 levels have an increased risk of coagulopathy independent of injury severity.
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