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An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis

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An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis. / Emsley, Hedley C. A.; Smith, Craig J.; Gavin, Carole M. et al.
In: Journal of Neuroimmunology, Vol. 139, No. 1-2, 06.2003, p. 93-101.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Emsley, HCA, Smith, CJ, Gavin, CM, Georgiou, RF, Vail, A, Barberan, EM, Hallenbeck, JM, Del Zoppo, GJ, Rothwell, NJ, Tyrrell, PJ & Hopkins, SJ 2003, 'An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis', Journal of Neuroimmunology, vol. 139, no. 1-2, pp. 93-101. https://doi.org/10.1016/S0165-5728(03)00134-6

APA

Emsley, H. C. A., Smith, C. J., Gavin, C. M., Georgiou, R. F., Vail, A., Barberan, E. M., Hallenbeck, J. M., Del Zoppo, G. J., Rothwell, N. J., Tyrrell, P. J., & Hopkins, S. J. (2003). An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis. Journal of Neuroimmunology, 139(1-2), 93-101. https://doi.org/10.1016/S0165-5728(03)00134-6

Vancouver

Emsley HCA, Smith CJ, Gavin CM, Georgiou RF, Vail A, Barberan EM et al. An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis. Journal of Neuroimmunology. 2003 Jun;139(1-2):93-101. Epub 2003 May 21. doi: 10.1016/S0165-5728(03)00134-6

Author

Emsley, Hedley C. A. ; Smith, Craig J. ; Gavin, Carole M. et al. / An early and sustained peripheral inflammatory response in acute ischaemic stroke : relationships with infection and atherosclerosis. In: Journal of Neuroimmunology. 2003 ; Vol. 139, No. 1-2. pp. 93-101.

Bibtex

@article{9c476712069c4eb288c408d6beae4c42,
title = "An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis",
abstract = "Central nervous system and peripheral inflammation is important in the responses to ischaemic stroke, and may also predispose to its development. We aimed to identify (1) the extent to which a peripheral inflammatory response is activated in patients following acute stroke, and (2) whether there was evidence for preexisting peripheral inflammation. Thirty-six patients with ischaemic stroke within 12 h of onset of symptoms had serial blood samples taken up to 12 months for analysis of markers of inflammation. Thirty-six control subjects, individually matched for age, sex and degree of atherosclerosis, were also studied. Median C-reactive protein (CRP) was elevated, relative to controls (2.08 mg/l), from admission (4.31 mg/l) (p≤0.001) until 3 months (2.90 mg/l) (p≤0.01), the greatest elevation occurring at 5-7 days (17.67 mg/l) (p≤0.001). Elevations were also seen in erythrocyte sedimentation rate (ESR) and white blood cell (WBC) count until 3 months. Median plasma IL-6 was also elevated, relative to controls (9 pg/ml), by 24 h after onset of symptoms (22 pg/ml) (p≤0.01), and remained elevated at 5-7 days (23 pg/ml) (p≤0.01), but not at 3 months. Less marked elevations in these markers were seen in patients without evidence of infection except for IL-6, which was not increased in the absence of infection. These data provide evidence of an early and sustained peripheral inflammatory response to acute ischaemic stroke in patients with or without evidence of infection. The very early increase in concentrations of inflammatory markers after stroke may either be induced by stroke itself, or may indicate a preexisting inflammatory condition in stroke patients which may contribute to the development of stroke.",
keywords = "Acute, C-reactive protein, Erythrocyte sedimentation rate, IL-6, Infection, Inflammation, Stroke",
author = "Emsley, {Hedley C. A.} and Smith, {Craig J.} and Gavin, {Carole M.} and Georgiou, {Rachel F.} and Andy Vail and Barberan, {Elisa M.} and Hallenbeck, {John M.} and {Del Zoppo}, {Gregory J.} and Rothwell, {Nancy J.} and Tyrrell, {Pippa J.} and Hopkins, {Stephen J.}",
year = "2003",
month = jun,
doi = "10.1016/S0165-5728(03)00134-6",
language = "English",
volume = "139",
pages = "93--101",
journal = "Journal of Neuroimmunology",
issn = "0165-5728",
publisher = "Elsevier",
number = "1-2",

}

RIS

TY - JOUR

T1 - An early and sustained peripheral inflammatory response in acute ischaemic stroke

T2 - relationships with infection and atherosclerosis

AU - Emsley, Hedley C. A.

AU - Smith, Craig J.

AU - Gavin, Carole M.

AU - Georgiou, Rachel F.

AU - Vail, Andy

AU - Barberan, Elisa M.

AU - Hallenbeck, John M.

AU - Del Zoppo, Gregory J.

AU - Rothwell, Nancy J.

AU - Tyrrell, Pippa J.

AU - Hopkins, Stephen J.

PY - 2003/6

Y1 - 2003/6

N2 - Central nervous system and peripheral inflammation is important in the responses to ischaemic stroke, and may also predispose to its development. We aimed to identify (1) the extent to which a peripheral inflammatory response is activated in patients following acute stroke, and (2) whether there was evidence for preexisting peripheral inflammation. Thirty-six patients with ischaemic stroke within 12 h of onset of symptoms had serial blood samples taken up to 12 months for analysis of markers of inflammation. Thirty-six control subjects, individually matched for age, sex and degree of atherosclerosis, were also studied. Median C-reactive protein (CRP) was elevated, relative to controls (2.08 mg/l), from admission (4.31 mg/l) (p≤0.001) until 3 months (2.90 mg/l) (p≤0.01), the greatest elevation occurring at 5-7 days (17.67 mg/l) (p≤0.001). Elevations were also seen in erythrocyte sedimentation rate (ESR) and white blood cell (WBC) count until 3 months. Median plasma IL-6 was also elevated, relative to controls (9 pg/ml), by 24 h after onset of symptoms (22 pg/ml) (p≤0.01), and remained elevated at 5-7 days (23 pg/ml) (p≤0.01), but not at 3 months. Less marked elevations in these markers were seen in patients without evidence of infection except for IL-6, which was not increased in the absence of infection. These data provide evidence of an early and sustained peripheral inflammatory response to acute ischaemic stroke in patients with or without evidence of infection. The very early increase in concentrations of inflammatory markers after stroke may either be induced by stroke itself, or may indicate a preexisting inflammatory condition in stroke patients which may contribute to the development of stroke.

AB - Central nervous system and peripheral inflammation is important in the responses to ischaemic stroke, and may also predispose to its development. We aimed to identify (1) the extent to which a peripheral inflammatory response is activated in patients following acute stroke, and (2) whether there was evidence for preexisting peripheral inflammation. Thirty-six patients with ischaemic stroke within 12 h of onset of symptoms had serial blood samples taken up to 12 months for analysis of markers of inflammation. Thirty-six control subjects, individually matched for age, sex and degree of atherosclerosis, were also studied. Median C-reactive protein (CRP) was elevated, relative to controls (2.08 mg/l), from admission (4.31 mg/l) (p≤0.001) until 3 months (2.90 mg/l) (p≤0.01), the greatest elevation occurring at 5-7 days (17.67 mg/l) (p≤0.001). Elevations were also seen in erythrocyte sedimentation rate (ESR) and white blood cell (WBC) count until 3 months. Median plasma IL-6 was also elevated, relative to controls (9 pg/ml), by 24 h after onset of symptoms (22 pg/ml) (p≤0.01), and remained elevated at 5-7 days (23 pg/ml) (p≤0.01), but not at 3 months. Less marked elevations in these markers were seen in patients without evidence of infection except for IL-6, which was not increased in the absence of infection. These data provide evidence of an early and sustained peripheral inflammatory response to acute ischaemic stroke in patients with or without evidence of infection. The very early increase in concentrations of inflammatory markers after stroke may either be induced by stroke itself, or may indicate a preexisting inflammatory condition in stroke patients which may contribute to the development of stroke.

KW - Acute

KW - C-reactive protein

KW - Erythrocyte sedimentation rate

KW - IL-6

KW - Infection

KW - Inflammation

KW - Stroke

U2 - 10.1016/S0165-5728(03)00134-6

DO - 10.1016/S0165-5728(03)00134-6

M3 - Journal article

C2 - 12799026

AN - SCOPUS:0037532616

VL - 139

SP - 93

EP - 101

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

SN - 0165-5728

IS - 1-2

ER -