- Aim for biomarkers
- Guide treatment
- Grade severity
- Prognostication
- Classify tissues injury
- Research
- Development of new treatment
- Warn deterioration
- Ideal biomarker
- Fast
- Accurate
- Reliable
- Easy to use
- Cheap
- Add values
- Likely to be used for head injury without positive CT findings
- S100B
- General
- Promising biomedical marker for the diagnosis, monitoring, and prognosis of TBI severity.
- Preoperative estimation of serum S100β in patients with TBI could be used
- As a prognostic predictor for postoperative survival and neurological outcome
- Being responsive to secondary insults.
- Measuring levels of S100β is useful in evaluating the severity of TBI and in the determination of long- term prognosis in patients presenting with moderate and severe injury
- S100B is a protein belonging to a multigenic family of low molecular-weight calcium-binding S100 proteins abundant in astrocytes.
- After traumatic brain injury, S100B protein is released by astrocytes; this protein may be neuroprotective and/or neurotrophic
- Half life of S100-B protein is 2hrs
- Testing must be done within 6 hrs of injury
- Have been used clinically
- Screen mild TBI patients → ?? Need to do CT scan
- Stats: (if taken within 6hrs of injury)
- NPV: 99% (better than d-dimer and TropT)
- Sensitivity: 97%
- If S100B < 0.1microgram/l can avoid doing CT → Scandinavian
- At the moment no cut off value for children as the cut of will change based on age
- Predict outcome of moderate to severe TBI
- Serum levels between 2.16 μg/l and 14.0 μg/l predicted an unfavorable outcome, defined as a Glasgow Outcome Score (GOS) of 1 (death), 2 (vegetative state) or 3 (severe disability
- But very wide range hence not useful
- Detect secondary injury development in brain injured patients
- Evaluate treatment efficacy
- Physiological function
- Unregulated Receptor for Advanced Glycation End-products (RAGE) → pro-inflammatory gene activation
- [S100B] 100x higher in CSF.
- Brain injury → leaky BBB → rise in [S100B] in serum
- S100B is also release from CSF into serum thru glymphatic system (Connection between glial cells and aquaporin-4-dependent paravascular pathways (mimicking a lymphatic drainage from the brain → drain S100B directly into the venous system)
- Extracranial sources of S100B
- Langerhan’s cells
- Adipocytes
- Epithelial cells
- Cardiac and skeletal muscle
- Melanocytes: darker skin people will have higher melanocytes metabolic rate hence higher S100B
- Chondrocystes
- Extracranial trauma causes a raise in S100B
Schematic overview of S100B release to serum. Schematic overview of the S100B release following severe TBI. Initially, there will be a great release of S100B from extracranial tissue to the serum (dotted, gray line), which will have a rapid wash-out the first hours after injury. While the cerebral release is more prolonged and shaped as a gamma function, as suggested by Ercole et al. 2016 (black line), it will initially be “masked” by these extracranial contributions. Our black line illustrates an “uneventful” release of S100B in a patient suffering from severe TBI; however, patients may suffer from subsequent injuries resulting in “secondary peaks” of S100B (dashed, gray line).
- ApoE4
- A current meta- analysis indicated that the ApoE4 allele might be associated with a poor prognosis in patients with severe TBI, but it may be used as a biomarker in predicting the prognosis of patients with TBI
- APoE4 allele presence influences recovery rate from severe TBI independent of other covariates and may also relate to the risk of subsequent cognitive decline.
- GFAP
Made with Bullet