Soluble ST2 links inflammation to outcome after subarachnoid hemorrhage.


Journal

Annals of neurology
ISSN: 1531-8249
Titre abrégé: Ann Neurol
Pays: United States
ID NLM: 7707449

Informations de publication

Date de publication:
09 2019
Historique:
received: 11 03 2019
revised: 08 07 2019
accepted: 08 07 2019
pubmed: 11 7 2019
medline: 14 4 2020
entrez: 11 7 2019
Statut: ppublish

Résumé

To investigate whether soluble growth stimulation expressed gene 2 (sST2), a prognostic marker in cardiovascular and inflammatory disorders, is associated with neurological injury after aneurysmal subarachnoid hemorrhage (SAH). We studied SAH patients from 2 independent cohorts. Outcome assessments included functional status at 90 days using the modified Rankin Scale (mRS), mortality, and delayed cerebral ischemia (DCI). The relationships between sST2 plasma level and outcome measures were assessed in both cross-sectional and longitudinal analysis. Primary blood mononuclear cells from SAH patients and elective aneurysm controls were analyzed by multiparameter flow cytometry. In the discovery cohort, sST2 predicted 90-day mRS 3-6 (C index = 0.724, p < 0.001) and mortality in Kaplan-Meier analysis (p < 0.001). The association with functional status was independent of age, sex, World Federation of Neurosurgical Societies score, modified Fisher score, treatment modality, and cardiac comorbidities (adjusted odds ratio = 2.28, 95% confidence interval = 1.04-5.00, p = 0.039). Higher sST2 concentration was observed in those patients with DCI (90.8 vs 53.7ng/ml, p = 0.003). These associations were confirmed in a replication cohort. In patients with high sST2, flow cytometry identified decreased expression of CD14 (4.27 × 10 Plasma sST2 predicts DCI, functional outcome, and mortality after SAH, independent of clinical and radiographic markers. Elevated sST2 is also associated with changes in CD14

Identifiants

pubmed: 31291030
doi: 10.1002/ana.25545
pmc: PMC6727654
mid: NIHMS1048440
doi:

Substances chimiques

IL1RL1 protein, human 0
Inflammation Mediators 0
Interleukin-1 Receptor-Like 1 Protein 0
Lipopolysaccharide Receptors 0
Receptors, IgG 0

Types de publication

Journal Article Multicenter Study Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

384-394

Subventions

Organisme : American Heart Association
ID : 17CSA33550004
Pays : International
Organisme : NINDS NIH HHS
ID : R01 NS099209
Pays : United States
Organisme : NINDS NIH HHS
ID : K23 NS076597
Pays : United States
Organisme : NINDS NIH HHS
ID : L30 NS097948
Pays : United States
Organisme : American Academy of Neurology
ID : AI18-0000000062
Pays : International

Informations de copyright

© 2019 American Neurological Association.

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Auteurs

Matthew B Bevers (MB)

Divisions of Stroke, Cerebrovascular, and Critical Care Neurology, Brigham and Women's Hospital, Boston, MA.

Zoe Wolcott (Z)

Division of Neurocritical Care, Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA.

Søren Bache (S)

Department of Neuroanesthesiology, Rigshospitalet, Copenhagen, Denmark.

Christina Hansen (C)

Division of Neurocritical Care, Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA.

Cristina Sastre (C)

Division of Neurocritical Care, Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA.

Ravi Mylvaganam (R)

Department of Pathology, Massachusetts General Hospital, Boston, MA.

Matthew J Koch (MJ)

Department of Neurosurgery, Massachusetts General Hospital, Boston, MA.

Aman B Patel (AB)

Department of Neurosurgery, Massachusetts General Hospital, Boston, MA.

Kirsten Møller (K)

Department of Neuroanesthesiology, Rigshospitalet, Copenhagen, Denmark.

W Taylor Kimberly (WT)

Division of Neurocritical Care, Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA.

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Classifications MeSH