S100B as an additional prognostic marker in subarachnoid aneurysmal hemorrhage
ABSTRACT Studies of new neuroprotective approaches in patients with subarachnoid aneurysmal hemorrhage and better family information would benefit from the development of laboratory markers of brain ischemia. The goal of this study was to evaluate mean 15-day S100B for predicting outcomes after subarachnoid aneurysmal hemorrhage.
Single center prospective cohort with consecutive inclusions.
Anesthesiology and Critical Care Neurosurgical Unit of a university hospital.
One hundred nine patients admitted within 48 hrs after subarachnoid aneurysmal hemorrhage onset and treated by surgical clipping or coiling within 48 hrs following admission.
We recorded initial World Federation of Neurologic Surgeons and Fisher grades; comorbidities; initial severity; aneurysm location; presence of acute hydrocephalus; presence of intraventricular hemorrhage; initial seizures and neurogenic lung edema; initial troponin values; treatment of aneurysm; and occurrence of vasospasm.
S100B was assayed daily over the first 15 days. Glasgow Outcome Scores were recorded at intensive care unit discharge and after 6 and 12 months. The main outcome criterion was the 12-month Glasgow Outcome Scale score dichotomized as poor (Glasgow Outcome Scale 1-3) or good (Glasgow Outcome Scale 4-5). Seventy percent of patients had good 12-month outcome. Poor outcome was associated with higher initial World Federation of Neurologic Surgeons and Fisher scores, neurogenic lung edema, high mean 15-day S100B but not initial, troponin initial value, intraventricular hemorrhage, angiographically documented vasospasm, all in an univariate manner. After multivariate analysis, only mean 15-day S100B value significantly predicted outcome (p < 0.0005). The best cutoff for the mean 15-day S100B value was 0.23 microg/L (specificity 0.90, 95% confidence interval [CI] 0.81-0.95; sensitivity 0.91, 95% CI 0.75-0.98; area under the curve 0.98, 95% CI 0.87-0.99).
S100B elevation over the first 15 days after subarachnoid aneurysmal hemorrhage is associated with poor outcome after subarachnoid aneurysmal hemorrhage. This result supports the use of S100B as a surrogate marker for brain ischemia in patients with subarachnoid aneurysmal hemorrhage.
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- "2006 S100B First 3 days after SAH TCD ↑ NE NE + ↑ NSE NE NE ↓ Weiss et al.  2006 S100B First 8 days after SAH TCD + arteriography − NE NE ++ No NSE detection (only CVS + S100B < 0.4 í µí¼g/L: no death) Sanchez-Pẽ na et al.  2008 S100B First 15 days after SAH TCD + arteriography ↑ in " ischemic vasospasm " patients ++ (↑) No NSE detection (only mean 15 day S100B value) Moritz et al.  2010 S100B Daily during ICU stay TCD − CT ++ ++ NSE − CT + + (only NSE peak value) "
ABSTRACT: Delayed cerebral vasospasm (CVS) and delayed cerebral ischemia (DCI) remain severe complications after subarachnoid hemorrhage (SAH). Although focal changes in cerebral metabolism indicating ischemia are detectable by microdialysis, routinely used biomarkers are missing. We therefore sought to evaluate a panel of possible global markers in serum and cerebrospinal fluid (CSF) of patients after SAH. CSF and serum of SAH patients were analyzed retrospectively. In CSF, levels of inhibitory, excitatory, and structural amino acids were detected by high-performance liquid chromatography (HPLC). In serum, neuron-specific enolase (NSE) and S100B level were measured and examined in conjunction with CVS and DCI. CVS was detected by arteriography, and ischemic lesions were assessed by computed tomography (CT) scans. All CSF amino acids were altered after SAH. CSF glutamate, glutamine, glycine, and histidine were significantly correlated with arteriographic CVS. CSF glutamate and serum S100B were significantly correlated with ischemic events after SAH; however, NSE did not correlate neither with ischemia nor with vasospasm. Glutamate, glutamine, glycine, and histidine might be used in CSF as markers for CVS. Glutamate also indicates ischemia. Serum S100B, but not NSE, is a suitable marker for ischemia. These results need to be validated in larger prospective cohorts.02/2013; 2013:560305. DOI:10.1155/2013/560305
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- "The present work adds to this consensus and suggests that levels of UCHL1 may also provide useful additional data in future studies. A recent study showed that S100b could be detected in the blood of recovering ASAH patients, and elevated average levels detected over the first 15 days post-AR were strongly predictive of poor patient outcome (Sanchez-Pena et al., 2008). Work is underway to examine UCHL1, pNF-H, and S100b in the blood of our growing cohort of recovering ASAH patients. "
ABSTRACT: By using two different approaches, ubiquitin C-terminal hydrolase 1 (UCHL1) was identified as a potential cerebrospinal fluid (CSF) biomarker of neuronal loss in aneurysmal subarachnoid hemorrhage (ASAH) and presumably other CNS damage and disease states. Appropriate antibodies and a sensitive ELISA were generated, and the release of UCHL1 into CSF was compared with that of pNF-H and S100beta in a cohort of 30 ASAH patients. Both UCHL1 and pNF-H showed persistent release into CSF in almost all patients in the second week postaneurysmal rupture (AR), and S100beta levels rapidly declined to baseline levels in 23 of 30 patients. Seven of thirty patients showed persistently elevated S100beta levels over the first 5 days post-AR and also had relatively higher levels of pNF-H and UCHL1 higher compared with the rest. These patients proved to have very poor outcomes, with 6 of 7 expiring. Patients who did reduce S100beta levels tended to have a better outcome if pNF-H and UCHL1 levels were also lower, and elevated UCHL1 levels in the second week post-AR were particularly predictive of poor outcome. Acute coordinated releases of large amounts of UCHL1, pNF-H, and S100beta in 16 of 30 patients were observed, suggesting sudden loss of brain tissues associated with secondary events. We conclude that measurement of the CSF levels of these proteins reveals details of ASAH progression and recovery and predicts patient outcome.Journal of Neuroscience Research 05/2010; 88(7):1475-84. DOI:10.1002/jnr.22323 · 2.73 Impact Factor
- Critical care medicine 09/2008; 36(8):2452-3. DOI:10.1097/CCM.0b013e3181810457 · 6.15 Impact Factor