Early and persistent high level of PS 100β is associated with increased poor neurological outcome in patients with SAH: is there a PS 100β threshold for SAH prognosis?. Issue 1 (December 2015)

• Record Type: Journal Article
• Authors: Quintard, Hervé; Leduc, Sébastien; Ferrari, Patricia; Petit, Isabelle; Ichai, Carole
• Is Part Of: Critical care. Volume 20:Issue 1(2016)
• Page Start: 1
• Page End: 9
• Publication Date: 2015-12
• Subjects: Surrogate marker -- Aneurysmal subarachnoid hemorrhage -- S100 protein -- Neuron specific enolase -- Outcome; Critical care medicine -- Periodicals; 616.02805
• DOI: 10.1186/s13054-016-1200-1
• Languages: English
• ISSNs: 1364-8535

Abstract

Abstract Background Protein S100β (PS100 β) and neuron specific enolase (NSE) have been described as biological markers of neuronal damage. The purpose of our study was to assess the prognosis thresholds of these biomarkers in subarachnoid aneurysmal hemorrhage (SAH). Methods Forty eight patients admitted following SAH were treated by endovascular coiling. Initial neurologic severity was assessed using the World Federation Neurologic Surgeons (WFNS), Fisher grades, initial Glasgow coma scale (GCS) and SAPS II. PS100β and NSE plasma concentration were measured daily within the first week. The primary endpoint of the study was the 6-month Glasgow Outcome Score (GOS) dichotomized as poor (GOS 1–3) or good (GOS 4–5). Results A poor outcome at 6-months was associated with significant higher levels of S100β value from day 1 to day 7, whereas NSE values were significantly higher from day 5 to day 7. Best threshold value, for prognosis, was obtained at day 5 for PS100β >0.13 μg/L (specificity 0.95 95 % confidence interval (CI) 0.74–1; sensitivity 0.83 95 % CI 0.65–0.93) and day 7 for NSE >14.5 μg/L (specificity 0.90 95 % CI 0.67–0.98); sensitivity (0.69 95 % CI 0.51–0.83)). After multivariate logistic analysis, only PS100β at day 5 and SAPS II enabled to predict neurological outcome at 6 months (p <0.05). Conclusion PS100β >0.13 μg/L at day 5 is an independent predicting factor of poor neurological outcome at 6 months following SAH. This result could support the use of this biomarker at the acute phase of SAH to help physician determine the prognosis.