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Infection and IL-6 are independent risk factors for a poor functional outcome from ischemic stroke

Infection and IL-6 are independent risk factors for a poor functional outcome from ischemic stroke
Infection and IL-6 are independent risk factors for a poor functional outcome from ischemic stroke
Background: Infections cause an inflammatory response that may activate the endothelial cells lining blood vessels. Infections affect stroke outcome but the mechanisms have not been elucidated. Our hypothesis is that inflammation due to infections may increase endothelial cell activation, causing prothrombotic changes in coagulation, thereby causing more severe strokes. Methods: People suffering an ischemic stroke in the last 72 hours (n=85) were recruited. Information on infections was collected from patient notes. ELISAs were used to measure plasma markers of endothelial cell activation, inflammation and coagulation. Results: 32% of people with an acute stroke had an infection in the 7 days post stroke. There were no differences in characteristics of the groups, except that 77% of people without an infection took aspirin compared with 46% of people with an infection (p=0.005). Infection, in particular pneumonia, was related to the subclass of stroke (OCSP) (p=0.036, with more TACS and fewer LACS in the infection group). There was a trend for those with an infection to have a larger infarct volume. Stroke functional outcome was worse in those people with an infection (p<0.001 for Rankin’s, Barthel and NIHSS scores). Infection was also related to destination on discharge. People with infections had increased inflammation (IL-6: p<0.001), increased coagulation (F1+2, p=0.048) and a trend for increased endothelial activation (vWF, p=0.125). IL-6 was correlated with vWF (R=0.371, p<0.001) and F1+2 (0.210, p=0.079). 41% of the variation in functional outcome was explained by linear regression models containing infection + IL-6 + stroke subtype, or 28% by infection + IL-6 + infarct volume. Discussion: These data are consistent with our hypothesis that infection increases inflammation, resulting in a poorer functional outcome. We suggest that IL-6 is associated with endothelial cell activation and coagulation, and that infection and IL-6 are independent risk factors for a poor functional outcome.
stroke, risk factors, risk
9783805583084
p.64
Karger
Englyst, N.A.
f84399af-7265-4224-b556-102c3aa272b0
Kwan, J.
2f6e316b-60bc-48a4-8b96-464b965ea6a5
Horsfield, G.
19927dea-2701-42f0-8341-87445138b630
Bryant, T.
1370b997-cead-4229-83a7-53301ed2a43c
Gawne-Cain, M.
965db1c3-79ca-455a-82e0-1cdc9b8042c4
Englyst, N.A.
f84399af-7265-4224-b556-102c3aa272b0
Kwan, J.
2f6e316b-60bc-48a4-8b96-464b965ea6a5
Horsfield, G.
19927dea-2701-42f0-8341-87445138b630
Bryant, T.
1370b997-cead-4229-83a7-53301ed2a43c
Gawne-Cain, M.
965db1c3-79ca-455a-82e0-1cdc9b8042c4

Englyst, N.A., Kwan, J., Horsfield, G., Bryant, T. and Gawne-Cain, M. (2007) Infection and IL-6 are independent risk factors for a poor functional outcome from ischemic stroke. In European Stroke Conference (Supplement Issue: Cerebrovascular Diseases 2007, Vol. 23, Suppl. 2 ). Karger. p.64 . (doi:10.1159/000103854).

Record type: Conference or Workshop Item (Paper)

Abstract

Background: Infections cause an inflammatory response that may activate the endothelial cells lining blood vessels. Infections affect stroke outcome but the mechanisms have not been elucidated. Our hypothesis is that inflammation due to infections may increase endothelial cell activation, causing prothrombotic changes in coagulation, thereby causing more severe strokes. Methods: People suffering an ischemic stroke in the last 72 hours (n=85) were recruited. Information on infections was collected from patient notes. ELISAs were used to measure plasma markers of endothelial cell activation, inflammation and coagulation. Results: 32% of people with an acute stroke had an infection in the 7 days post stroke. There were no differences in characteristics of the groups, except that 77% of people without an infection took aspirin compared with 46% of people with an infection (p=0.005). Infection, in particular pneumonia, was related to the subclass of stroke (OCSP) (p=0.036, with more TACS and fewer LACS in the infection group). There was a trend for those with an infection to have a larger infarct volume. Stroke functional outcome was worse in those people with an infection (p<0.001 for Rankin’s, Barthel and NIHSS scores). Infection was also related to destination on discharge. People with infections had increased inflammation (IL-6: p<0.001), increased coagulation (F1+2, p=0.048) and a trend for increased endothelial activation (vWF, p=0.125). IL-6 was correlated with vWF (R=0.371, p<0.001) and F1+2 (0.210, p=0.079). 41% of the variation in functional outcome was explained by linear regression models containing infection + IL-6 + stroke subtype, or 28% by infection + IL-6 + infarct volume. Discussion: These data are consistent with our hypothesis that infection increases inflammation, resulting in a poorer functional outcome. We suggest that IL-6 is associated with endothelial cell activation and coagulation, and that infection and IL-6 are independent risk factors for a poor functional outcome.

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More information

Published date: 30 May 2007
Venue - Dates: 16th European Stroke Conference, Glasgow, UK, 2007-05-30
Keywords: stroke, risk factors, risk

Identifiers

Local EPrints ID: 61094
URI: http://eprints.soton.ac.uk/id/eprint/61094
ISBN: 9783805583084
PURE UUID: 0726c371-bcbc-4474-aa08-ff5a8c3e81a4
ORCID for N.A. Englyst: ORCID iD orcid.org/0000-0003-0508-8323
ORCID for T. Bryant: ORCID iD orcid.org/0000-0001-6322-7753

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Date deposited: 24 Nov 2008
Last modified: 16 Mar 2024 03:14

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Contributors

Author: N.A. Englyst ORCID iD
Author: J. Kwan
Author: G. Horsfield
Author: T. Bryant ORCID iD
Author: M. Gawne-Cain

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