The association between early neurological deterioration and whole blood purine concentration during acute stroke.
Cerebrovascular disease
Deterioration
Penumbra
Purines
Stroke
Journal
Biomarker research
ISSN: 2050-7771
Titre abrégé: Biomark Res
Pays: England
ID NLM: 101607860
Informations de publication
Date de publication:
2019
2019
Historique:
received:
08
01
2019
accepted:
27
03
2019
entrez:
17
4
2019
pubmed:
17
4
2019
medline:
17
4
2019
Statut:
epublish
Résumé
Early neurological deterioration (END) is common after stroke. Prediction could identify patients requiring additional monitoring and intervention. Purines, breakdown products of adenosine triphosphate which accumulate during acute hypoxia, may reflect the subclinical presence of vulnerable tissue. We considered whether whole blood purine concentration (WBPC) measurements during acute stroke were associated with subsequent END. Patients within 4.5 h of stroke onset underwent point-of-care finger-prick measurement of WBPC and blinded assessment of symptom severity using the National Institutes of Health Stroke Scale (NIHSS). END was defined as an NIHSS increase ≥2 points at 24-36 h compared to baseline. 15/152 (9.8%) patients experienced END with a median [IQR] NIHSS increase of 4 [2-7] points. There were no strong associations between END and baseline NIHSS, clinical stroke subtype, thrombolytic therapy, physiological characteristics or time to assay. The median [IQR] WBPC concentration (uM) was higher before the occurrence of END but without statistical significance (7.21 [4.77-10.65] versus 4.83 [3.00-9.02]; Although the study lacked statistical power, early WBPC measurement could be a convenient biomarker for identifying acute stroke patients at risk of END, but further evaluation is required.
Sections du résumé
BACKGROUND
BACKGROUND
Early neurological deterioration (END) is common after stroke. Prediction could identify patients requiring additional monitoring and intervention. Purines, breakdown products of adenosine triphosphate which accumulate during acute hypoxia, may reflect the subclinical presence of vulnerable tissue. We considered whether whole blood purine concentration (WBPC) measurements during acute stroke were associated with subsequent END.
METHODS
METHODS
Patients within 4.5 h of stroke onset underwent point-of-care finger-prick measurement of WBPC and blinded assessment of symptom severity using the National Institutes of Health Stroke Scale (NIHSS). END was defined as an NIHSS increase ≥2 points at 24-36 h compared to baseline.
RESULTS
RESULTS
15/152 (9.8%) patients experienced END with a median [IQR] NIHSS increase of 4 [2-7] points. There were no strong associations between END and baseline NIHSS, clinical stroke subtype, thrombolytic therapy, physiological characteristics or time to assay. The median [IQR] WBPC concentration (uM) was higher before the occurrence of END but without statistical significance (7.21 [4.77-10.65] versus 4.83 [3.00-9.02];
CONCLUSION
CONCLUSIONS
Although the study lacked statistical power, early WBPC measurement could be a convenient biomarker for identifying acute stroke patients at risk of END, but further evaluation is required.
Identifiants
pubmed: 30988953
doi: 10.1186/s40364-019-0158-y
pii: 158
pmc: PMC6448300
doi:
Types de publication
Journal Article
Langues
eng
Pagination
7Déclaration de conflit d'intérêts
Ethics approval was granted by the National Research Ethics Service in England (reference 16/WM/0164). All participants or their personal consultee gave informed consent consistent with the principles of the Declaration of Helsinki.Not applicable.Faming Tian is an employee of Sarissa Biomedical Ltd., manufacturer of the biosensor used, and is named on patents that are owned or licensed by Sarissa Biomedical. Nicholas Dale is a Director and Founder of Sarissa Biomedical Ltd., holds equity in that company and is named on patents that are owned or licensed by Sarissa Biomedical. All other authors declare that they have no competing interest.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Références
Lancet. 1991 Jun 22;337(8756):1521-6
pubmed: 1675378
Anal Chem. 2007 Sep 1;79(17):6760-6
pubmed: 17672522
Stroke. 2009 Jun;40(6):e443-50
pubmed: 19390076
Int J Stroke. 2012 Jun;7(4):321-9
pubmed: 22463492
J Stroke Cerebrovasc Dis. 2013 Jul;22(5):675-82
pubmed: 22727922
Neurology. 2012 Sep 25;79(13 Suppl 1):S79-85
pubmed: 23008418
N Engl J Med. 2013 Jun 20;368(25):2355-65
pubmed: 23713578
ISRN Neurosci. 2013 May 08;2013:327968
pubmed: 24967309
J Neurol Neurosurg Psychiatry. 2015 Jan;86(1):87-94
pubmed: 24970907
BMJ Open. 2015 Jul 28;5(7):e008563
pubmed: 26220872
Purinergic Signal. 2017 Dec;13(4):521-528
pubmed: 28803399
N Engl J Med. 2018 Jan 4;378(1):11-21
pubmed: 29129157