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Author Małkiewicz, Tomasz ♦ Hołysz, Marcin ♦ Wąsik, Norbert ♦ Mańko, Witold ♦ Sokół, Bartosz ♦ Jankowski, Roman ♦ Jagodziński, Paweł P. ♦ Juszkat, Robert
Source Directory of Open Access Journals (DOAJ)
Content type Text
Publisher Hindawi Limited
File Format HTM / HTML
Date Created 2017-06-14
Copyright Year ©2017
Language English
Subject Domain (in LCC) R
Subject Keyword Medicine
Abstract 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.
ISSN 23146133
Age Range 18 to 22 years ♦ above 22 year
Educational Use Research
Education Level UG and PG ♦ Career/Technical Study
Learning Resource Type Article
Publisher Date 2017-01-01
e-ISSN 23146133
Journal BioMed Research International
Volume Number 2017

Source: Directory of Open Access Journals (DOAJ)