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Stroke. 2003;34:637-642
Published online before print February 13, 2003, doi: 10.1161/01.STR.0000057579.25430.16
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(Stroke. 2003;34:637.)
© 2003 American Heart Association, Inc.


Original Contributions

Decreased Cerebrospinal Fluid Apolipoprotein E After Subarachnoid Hemorrhage

Correlation With Injury Severity and Clinical Outcome

Andrew Kay, MB; Axel Petzold, MD; Mary Kerr, PhD; Geoff Keir, PhD; Ed Thompson, DSc James Nicoll, MD

From the Department of Neurosurgery (A.K.), University of Glasgow, Institute of Neurological Sciences, Southern General Hospital, Glasgow, UK; the Department of Neuroimmunology (A.P., G.K., E.T.), University of London, Institute of Neurology and Neurosurgery, Queen Square, London, UK; Center for Nursing Research, University of Pittsburgh (M.K.), Pittsburgh, Pa; and the Division of Clinical Neurosciences (J.N.), University of Southampton, Southampton General Hospital, Southampton, UK.

Correspondence to Andrew Kay, University of Glasgow, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF, UK. E-mail adk4z{at}clinmed.gla.ac.uk

Background and Purpose— The apolipoprotein E (APOE) {epsilon}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.


Key Words: apolipoproteins • cerebrospinal fluid • outcome • subarachnoid hemorrhage




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