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Decreased cerebrospinal fluid apolipoprotein E after subarachnoid hemorrhage: correlation with injury severity and clinical outcome

Decreased cerebrospinal fluid apolipoprotein E after subarachnoid hemorrhage: correlation with injury severity and clinical outcome
Decreased cerebrospinal fluid apolipoprotein E after subarachnoid hemorrhage: correlation with injury severity and clinical outcome
Background and Purpose— The apolipoprotein E (APOE) 4 allele has been associated with unfavorable outcome after subarachnoid hemorrhage (SAH), suggesting that apoE plays an important role in the response of the brain to SAH. We determined the concentration of apoE in the cerebrospinal fluid (CSF) of patients with SAH and a control group to test the hypothesis that alterations in CSF apoE reflect the response of the brain to SAH and are correlated with the severity of injury and outcome.
Methods— ApoE and S100B (a marker of brain injury) were measured by ELISA in CSF from a non–brain-injured control group and patients with SAH. The severity of SAH was determined from the Glasgow Coma Scale, and the clinical outcome was determined from the Glasgow Outcome Scale.
Results— In contrast to increased CSF concentration of S100B, CSF apoE concentration was significantly lower in patients after SAH than in control subjects (Mann-Whitney test, P<0.0001). SAH patients with more severe injury and less favorable outcome had lower CSF apoE concentration than did patients with milder injury and better clinical outcome (Fisher exact test, P=0.02).
Conclusions— The concentration of apoE in the CSF decreases after SAH, despite the likely leakage of plasma apoE into the CSF. We speculate that apoE is retained within the parenchyma of the central nervous system in response to injury, where, in view of previous data, it may have a protective role.
0039-2499
637-642
Kay, A.
9652622a-63d6-4c17-83fa-9cb0baf5b29d
Petzold, A.
3142ddf4-b2e1-4f9f-bfad-ba869e3b190f
Kerr, M.
86f31459-0cab-493f-a861-b93d7a396863
Keir, G.
fbca9e6b-cb9c-4c91-a2f7-0fbebc44308b
Thompson, E.
fee77a63-09fc-4dca-b1d3-777f368ebe3e
Nicoll, J.
88c0685f-000e-4eb7-8f72-f36b4985e8ed
Kay, A.
9652622a-63d6-4c17-83fa-9cb0baf5b29d
Petzold, A.
3142ddf4-b2e1-4f9f-bfad-ba869e3b190f
Kerr, M.
86f31459-0cab-493f-a861-b93d7a396863
Keir, G.
fbca9e6b-cb9c-4c91-a2f7-0fbebc44308b
Thompson, E.
fee77a63-09fc-4dca-b1d3-777f368ebe3e
Nicoll, J.
88c0685f-000e-4eb7-8f72-f36b4985e8ed

Kay, A., Petzold, A., Kerr, M., Keir, G., Thompson, E. and Nicoll, J. (2003) Decreased cerebrospinal fluid apolipoprotein E after subarachnoid hemorrhage: correlation with injury severity and clinical outcome. Stroke, 34 (3), 637-642. (doi:10.1161/01.STR.0000057579.25430.16).

Record type: Article

Abstract

Background and Purpose— The apolipoprotein E (APOE) 4 allele has been associated with unfavorable outcome after subarachnoid hemorrhage (SAH), suggesting that apoE plays an important role in the response of the brain to SAH. We determined the concentration of apoE in the cerebrospinal fluid (CSF) of patients with SAH and a control group to test the hypothesis that alterations in CSF apoE reflect the response of the brain to SAH and are correlated with the severity of injury and outcome.
Methods— ApoE and S100B (a marker of brain injury) were measured by ELISA in CSF from a non–brain-injured control group and patients with SAH. The severity of SAH was determined from the Glasgow Coma Scale, and the clinical outcome was determined from the Glasgow Outcome Scale.
Results— In contrast to increased CSF concentration of S100B, CSF apoE concentration was significantly lower in patients after SAH than in control subjects (Mann-Whitney test, P<0.0001). SAH patients with more severe injury and less favorable outcome had lower CSF apoE concentration than did patients with milder injury and better clinical outcome (Fisher exact test, P=0.02).
Conclusions— The concentration of apoE in the CSF decreases after SAH, despite the likely leakage of plasma apoE into the CSF. We speculate that apoE is retained within the parenchyma of the central nervous system in response to injury, where, in view of previous data, it may have a protective role.

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Published date: March 2003

Identifiers

Local EPrints ID: 27611
URI: http://eprints.soton.ac.uk/id/eprint/27611
ISSN: 0039-2499
PURE UUID: feac202d-28e6-4846-ab08-93cdb2b066c3
ORCID for J. Nicoll: ORCID iD orcid.org/0000-0002-9444-7246

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Date deposited: 27 Apr 2006
Last modified: 16 Mar 2024 03:26

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Contributors

Author: A. Kay
Author: A. Petzold
Author: M. Kerr
Author: G. Keir
Author: E. Thompson
Author: J. Nicoll ORCID iD

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