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High natural killer cell number might identify stroke patients at risk of developing infections
OBJECTIVE: To investigate early changes in leukocyte subsets and autonomic function as predictors of the development of poststroke infections. METHODS: We assessed the time course of leukocyte subsets in the blood of 59 patients with acute ischemic stroke. We divided the patients into 2 groups: thos...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Lippincott Williams & Wilkins
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4335818/ https://www.ncbi.nlm.nih.gov/pubmed/25738168 http://dx.doi.org/10.1212/NXI.0000000000000071 |
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author | De Raedt, Sylvie De Vos, Aurelie Van Binst, Anne-Marie De Waele, Marc Coomans, Danny Buyl, Ronald De Keyser, Jacques |
author_facet | De Raedt, Sylvie De Vos, Aurelie Van Binst, Anne-Marie De Waele, Marc Coomans, Danny Buyl, Ronald De Keyser, Jacques |
author_sort | De Raedt, Sylvie |
collection | PubMed |
description | OBJECTIVE: To investigate early changes in leukocyte subsets and autonomic function as predictors of the development of poststroke infections. METHODS: We assessed the time course of leukocyte subsets in the blood of 59 patients with acute ischemic stroke. We divided the patients into 2 groups: those who developed infections during the first 7 days after stroke onset and those who did not. We measured urinary norepinephrine and epinephrine concentrations and pulse rate variability indices within 24 hours of admission. RESULTS: We found that the number of circulating natural killer (NK) cells within the first hours after stroke was higher in stroke patients who developed infections (mean 435 cells/mL; 95% confidence interval [CI] 321–588) than in stroke patients who did not develop infections (mean 236 cells/mL; 95% CI 186–300; p = 0.001). This was followed by a decrease in all lymphocyte subsets from admission to day 1, varying between 22% and 40%, which was not seen in patients without poststroke infection (mean increase varied between 2% and 23%; all p < 0.005). In the group that developed infections, pulse rate variability revealed a decreased high frequency component. These findings all remained significant after adjustment for age and stroke volume. CONCLUSIONS: High circulating NK cell count within the first hours after ischemic stroke onset followed by a drop in all lymphocyte subsets identified patients who developed infections and may be caused by a sympathovagal imbalance with sympathetic overweight. These findings need to be validated in larger studies. |
format | Online Article Text |
id | pubmed-4335818 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Lippincott Williams & Wilkins |
record_format | MEDLINE/PubMed |
spelling | pubmed-43358182015-03-03 High natural killer cell number might identify stroke patients at risk of developing infections De Raedt, Sylvie De Vos, Aurelie Van Binst, Anne-Marie De Waele, Marc Coomans, Danny Buyl, Ronald De Keyser, Jacques Neurol Neuroimmunol Neuroinflamm Article OBJECTIVE: To investigate early changes in leukocyte subsets and autonomic function as predictors of the development of poststroke infections. METHODS: We assessed the time course of leukocyte subsets in the blood of 59 patients with acute ischemic stroke. We divided the patients into 2 groups: those who developed infections during the first 7 days after stroke onset and those who did not. We measured urinary norepinephrine and epinephrine concentrations and pulse rate variability indices within 24 hours of admission. RESULTS: We found that the number of circulating natural killer (NK) cells within the first hours after stroke was higher in stroke patients who developed infections (mean 435 cells/mL; 95% confidence interval [CI] 321–588) than in stroke patients who did not develop infections (mean 236 cells/mL; 95% CI 186–300; p = 0.001). This was followed by a decrease in all lymphocyte subsets from admission to day 1, varying between 22% and 40%, which was not seen in patients without poststroke infection (mean increase varied between 2% and 23%; all p < 0.005). In the group that developed infections, pulse rate variability revealed a decreased high frequency component. These findings all remained significant after adjustment for age and stroke volume. CONCLUSIONS: High circulating NK cell count within the first hours after ischemic stroke onset followed by a drop in all lymphocyte subsets identified patients who developed infections and may be caused by a sympathovagal imbalance with sympathetic overweight. These findings need to be validated in larger studies. Lippincott Williams & Wilkins 2015-02-12 /pmc/articles/PMC4335818/ /pubmed/25738168 http://dx.doi.org/10.1212/NXI.0000000000000071 Text en © 2015 American Academy of Neurology This is an open access article distributed under the terms of the Creative Commons Attribution-Noncommercial No Derivative 3.0 License, which permits downloading and sharing the work provided it is properly cited. The work cannot be changed in any way or used commercially. |
spellingShingle | Article De Raedt, Sylvie De Vos, Aurelie Van Binst, Anne-Marie De Waele, Marc Coomans, Danny Buyl, Ronald De Keyser, Jacques High natural killer cell number might identify stroke patients at risk of developing infections |
title | High natural killer cell number might identify stroke patients at risk of developing infections |
title_full | High natural killer cell number might identify stroke patients at risk of developing infections |
title_fullStr | High natural killer cell number might identify stroke patients at risk of developing infections |
title_full_unstemmed | High natural killer cell number might identify stroke patients at risk of developing infections |
title_short | High natural killer cell number might identify stroke patients at risk of developing infections |
title_sort | high natural killer cell number might identify stroke patients at risk of developing infections |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4335818/ https://www.ncbi.nlm.nih.gov/pubmed/25738168 http://dx.doi.org/10.1212/NXI.0000000000000071 |
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