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Increase of Soluble RAGE in Cerebrospinal Fluid following Subarachnoid Haemorrhage

BioMed Research International. 2017;2017 DOI 10.1155/2017/7931534

 

Journal Homepage

Journal Title: BioMed Research International

ISSN: 2314-6133 (Print); 2314-6141 (Online)

Publisher: Hindawi Limited

LCC Subject Category: Medicine

Country of publisher: United Kingdom

Language of fulltext: English

Full-text formats available: PDF, HTML, ePUB, XML

 

AUTHORS


Bartosz Sokół (Department of Neurosurgery, Poznan University of Medical Sciences, Poznan, Poland)

Norbert Wąsik (Department of Neurosurgery, Poznan University of Medical Sciences, Poznan, Poland)

Roman Jankowski (Department of Neurosurgery, Poznan University of Medical Sciences, Poznan, Poland)

Marcin Hołysz (Department of Biochemistry and Molecular Biology, Poznan University of Medical Sciences, Poznan, Poland)

Witold Mańko (Department of Anaesthesiology and Intensive Therapy, Poznan University of Medical Sciences, Poznan, Poland)

Robert Juszkat (Department of Neurosurgery, Poznan University of Medical Sciences, Poznan, Poland)

Tomasz Małkiewicz (Department of Anaesthesiology and Intensive Therapy, Poznan University of Medical Sciences, Poznan, Poland)

Paweł P. Jagodziński (Department of Biochemistry and Molecular Biology, Poznan University of Medical Sciences, Poznan, Poland)

EDITORIAL INFORMATION

Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 19 weeks

 

Abstract | Full Text

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, p<0.001). 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 (p=0.234). CSF sRAGE levels did not change significantly during hospitalisation (p=0.868) 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.