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

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...

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Published inJournal of neuroimmunology Vol. 139; no. 1; pp. 93 - 101
Main Authors Emsley, Hedley C.A., Smith, Craig J., Gavin, Carole M., Georgiou, Rachel F., Vail, Andy, Barberan, Elisa M., Hallenbeck, John M., del Zoppo, Gregory J., Rothwell, Nancy J., Tyrrell, Pippa J., Hopkins, Stephen J.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.06.2003
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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.
AbstractList 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.
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.
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 less than or equal to 0.001) until 3 months (2.90 mg/l) (p less than or equal to 0.01), the greatest elevation occurring at 5-7 days (17.67 mg/l) (p less than or equal to 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 less than or equal to 0.01), and remained elevated at 5-7 days (23 pg/ml) (p less than or equal to 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.
Author Hallenbeck, John M.
Tyrrell, Pippa J.
Gavin, Carole M.
Barberan, Elisa M.
Georgiou, Rachel F.
Hopkins, Stephen J.
Vail, Andy
Smith, Craig J.
Emsley, Hedley C.A.
del Zoppo, Gregory J.
Rothwell, Nancy J.
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  fullname: Smith, Craig J.
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  givenname: Gregory J.
  surname: del Zoppo
  fullname: del Zoppo, Gregory J.
  organization: Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA, USA
– sequence: 9
  givenname: Nancy J.
  surname: Rothwell
  fullname: Rothwell, Nancy J.
  organization: School of Biological Sciences, University of Manchester, 1.124 Stopford Building, Oxford Road, Manchester M13 9PT, UK
– sequence: 10
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  organization: North Western Injury Research Collaboration (NWIRC), Clinical Sciences Building, Hope Hospital, Eccles Old Road, Salford M6 8HD, UK
BackLink https://www.ncbi.nlm.nih.gov/pubmed/12799026$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords Infection
Stroke
Inflammation
C-reactive protein
Erythrocyte sedimentation rate
IL-6
Language English
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PublicationTitle Journal of neuroimmunology
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Snippet Central nervous system and peripheral inflammation is important in the responses to ischaemic stroke, and may also predispose to its development. We aimed to...
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StartPage 93
SubjectTerms acute
Acute Disease
Adult
Arteriosclerosis - blood
Arteriosclerosis - complications
Arteriosclerosis - immunology
Blood Sedimentation
Brain Ischemia - blood
Brain Ischemia - immunology
Brain Ischemia - physiopathology
C-reactive protein
C-Reactive Protein - metabolism
Erythrocyte sedimentation rate
Female
Humans
IL-6
Infection
Inflammation
Inflammation - blood
Inflammation - complications
Inflammation - immunology
Interleukin-6 - blood
Leukocyte Count
Male
Stroke
Stroke - blood
Stroke - immunology
Stroke - physiopathology
Time Factors
Title An early and sustained peripheral inflammatory response in acute ischaemic stroke: relationships with infection and atherosclerosis
URI https://dx.doi.org/10.1016/S0165-5728(03)00134-6
https://www.ncbi.nlm.nih.gov/pubmed/12799026
https://search.proquest.com/docview/18927907
https://search.proquest.com/docview/73373941
Volume 139
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