HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER		Author Keyword(s) Vol Page [Advanced]

This Article Full Text Full Text (PDF) All Versions of this Article: jnnp.2005.081539v1 77/7/863    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Frijns, C J M Articles by Rinkel, G J E Search for Related Content PubMed PubMed Citation Articles by Frijns, C J M Articles by Rinkel, G J E

Endothelial cell activation markers and delayed cerebral ischaemia in patients with subarachnoid haemorrhage

¹ Department of Neurology, University Medical Centre Utrecht, Utrecht, The Netherlands
² Department of Haematology, Research Laboratory, University Medical Centre Utrecht
³ Julius Centre for Health Sciences and Primary Care, University Medical Centre Utrecht

Correspondence to:
Correspondence to:
Dr C J M Frijns
Department of Neurology, G03.228, University Medical Centre Utrecht, PO Box 85500, 3508 GA Utrecht, The Netherlands; C.J.M.Frijns{at}umcutrecht.nl

Background: Endothelial cell activation may be connected with the pathogenesis of delayed cerebral ischaemia (DCI) after subarachnoid haemorrhage (SAH).

Aim: To assess the relationship between serial concentrations of circulating markers of endothelial cell activation (soluble intercellular adhesion molecule-1, soluble platelet selectin (sP-selectin), soluble endothelial selectin, ED1-fibronectin, Von Willebrand Factor (VWF) and VWF propeptide) and development of DCI.

Methods: 687 blood samples were collected from 106 consecutive patients admitted within 72 h after onset of SAH. Changes in levels were analysed in the last sample before and in the first sample after the onset of DCI (n = 30), and in subgroups with DCI occurring within 24 h after treatment of the aneurysm (n = 12) or unrelated to treatment of the aneurysm (n = 18). Patients without DCI (n = 56) served as controls.

Results: Concentrations of sP-selectin, but not of the other markers, were found to increase considerably after DCI unrelated to treatment of the aneurysm (increase 25 ng/ml, 95% CI 8 to 43), whereas they tended to decrease in the control patients without DCI (decrease 13 ng/ml, 95% CI –28 to 2.4). Surgery was found to profoundly influence the levels of the markers irrespective of the occurrence of DCI.

Conclusion: The rise in sP-selectin level during DCI is suggested to be the result of platelet activation, as levels of the other markers of endothelial cell activation were not increased after DCI unrelated to treatment. Whether a causal role of platelet activation is implicated in the development of DCI should be determined in further studies in which the relationship between concentrations of markers and treatment is taken into account.

Abbreviations: DCI, delayed cerebral ischaemia; ED1-fn, ED1-fibronectin; GCS, Glasgow Coma Scale; ICAM, intercellular adhesion molecule; SAH, subarachnoid haemorrhage; sE-selectin, soluble endothelial selectin; sICAM, soluble intercellular adhesion molecule; sP-selectin, soluble platelet selectin; VWF, Von Willebrand Factor