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 in | Journal of neuroimmunology Vol. 139; no. 1; pp. 93 - 101 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier B.V
01.06.2003
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Subjects | |
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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. |
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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. |
Author_xml | – sequence: 1 givenname: Hedley C.A. surname: Emsley fullname: Emsley, Hedley C.A. email: hemsley@fs1.ho.man.ac.uk organization: University of Manchester, Manchester, UK – sequence: 2 givenname: Craig J. surname: Smith fullname: Smith, Craig J. organization: University of Manchester, Manchester, UK – sequence: 3 givenname: Carole M. surname: Gavin fullname: Gavin, Carole M. organization: Department of Emergency Medicine, Hope Hospital, Stott Lane, Salford, UK – sequence: 4 givenname: Rachel F. surname: Georgiou fullname: Georgiou, Rachel F. organization: University of Manchester, Manchester, UK – sequence: 5 givenname: Andy surname: Vail fullname: Vail, Andy organization: Biostatistics Group, University of Manchester, Clinical Sciences Building, Hope Hospital, Eccles Old Road, Salford M6 8HD, UK – sequence: 6 givenname: Elisa M. surname: Barberan fullname: Barberan, Elisa M. organization: Stroke Services, Clinical Sciences Building, Hope Hospital, Eccles Old Road, Salford M6 8HD, UK – sequence: 7 givenname: John M. surname: Hallenbeck fullname: Hallenbeck, John M. organization: Stroke Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD, USA – sequence: 8 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 givenname: Pippa J. surname: Tyrrell fullname: Tyrrell, Pippa J. organization: University of Manchester, Manchester, UK – sequence: 11 givenname: Stephen J. surname: Hopkins fullname: Hopkins, Stephen J. 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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Keywords | Infection Stroke Inflammation C-reactive protein Erythrocyte sedimentation rate IL-6 |
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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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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 |
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