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BioMed Research International
Volume 2017 (2017), Article ID 7931534, 7 pages
Research Article

Increase of Soluble RAGE in Cerebrospinal Fluid following Subarachnoid Haemorrhage

1Department of Neurosurgery, Poznan University of Medical Sciences, Poznan, Poland
2Department of Biochemistry and Molecular Biology, Poznan University of Medical Sciences, Poznan, Poland
3Department of Anaesthesiology and Intensive Therapy, Poznan University of Medical Sciences, Poznan, Poland
4Department of General and Interventional Radiology, Poznan University of Medical Sciences, Poznan, Poland

Correspondence should be addressed to Bartosz Sokół; moc.liamg@lokos.zsotrab

Received 15 February 2017; Revised 4 April 2017; Accepted 4 May 2017; Published 29 May 2017

Academic Editor: Sheng Chen

Copyright © 2017 Bartosz Sokół et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Receptors for advanced glycation end-products (RAGE) mediate the inflammatory reaction that follows aneurysmal subarachnoid haemorrhage. Soluble RAGE (sRAGE) may function as a decoy receptor. The significance of this endogenous anti-inflammatory mechanism in subarachnoid haemorrhage (SAH) remains unknown. The present study aims to analyse sRAGE levels in the cerebrospinal fluid (CSF) of SAH patients. sRAGE levels were assayed by ELISA kit in 47 CSF samples collected on post-SAH days 0–3, 5–7, and 10–14 from 27 SAH patients with acute hydrocephalus. CSF levels of sRAGE were compared with a control group and correlated with other monitored parameters. In the control group, the CSF contained only a trace amount of sRAGE. By contrast, the CSF of 20 SAH patients collected on post-SAH days 0–3 was found to contain statistically significant higher levels of sRAGE (mean concentration 3.91 pg/mL, ). The most pronounced difference in CSF sRAGE levels between good and poor outcome patients was found on days 0–3 post-SAH but did not reach the significance threshold (). CSF sRAGE levels did not change significantly during hospitalisation () and correlated poorly with treatment outcome, systemic inflammatory markers, and other monitored parameters. Our study revealed an early and constant increase of sRAGE level in the CSF of SAH patients.