Evidence map›Paper›PMID 36549913›Full record

ArticleNeurology2023

Association of Soluble ST2 With Functional Outcome, Perihematomal Edema, and Immune Response After Intraparenchymal Hemorrhage.

Matthew B Bevers, Caroline Booraem, Karen Li, Anirudh Sreekrishnan, Cristina Sastre, Guido J Falcone, Kevin Navin Sheth, Lauren H Sansing, W Taylor Kimberly

Open access · greenAbstract read
In one paragraph

Article in Neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 30% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Matthew B BeversFrom the Division of Neurocritical Care (M.B.B., C.B., K.L., A.S.), Brigham and Women's Hospital; Division of Neurocritical Care (C.S., G.J.F., W.T.K.), Center for Genomic Medicine, Massachusetts General Hospital, Boston; and Department of Neurology (K.N.S., L.H.S.), Yale-New Haven Hospital, CT. mbevers@bwh.harvard.edu.
Caroline BooraemFrom the Division of Neurocritical Care (M.B.B., C.B., K.L., A.S.), Brigham and Women's Hospital; Division of Neurocritical Care (C.S., G.J.F., W.T.K.), Center for Genomic Medicine, Massachusetts General Hospital, Boston; and Department of Neurology (K.N.S., L.H.S.), Yale-New Haven Hospital, CT.
Karen LiFrom the Division of Neurocritical Care (M.B.B., C.B., K.L., A.S.), Brigham and Women's Hospital; Division of Neurocritical Care (C.S., G.J.F., W.T.K.), Center for Genomic Medicine, Massachusetts General Hospital, Boston; and Department of Neurology (K.N.S., L.H.S.), Yale-New Haven Hospital, CT.
Anirudh SreekrishnanFrom the Division of Neurocritical Care (M.B.B., C.B., K.L., A.S.), Brigham and Women's Hospital; Division of Neurocritical Care (C.S., G.J.F., W.T.K.), Center for Genomic Medicine, Massachusetts General Hospital, Boston; and Department of Neurology (K.N.S., L.H.S.), Yale-New Haven Hospital, CT.
Cristina SastreFrom the Division of Neurocritical Care (M.B.B., C.B., K.L., A.S.), Brigham and Women's Hospital; Division of Neurocritical Care (C.S., G.J.F., W.T.K.), Center for Genomic Medicine, Massachusetts General Hospital, Boston; and Department of Neurology (K.N.S., L.H.S.), Yale-New Haven Hospital, CT.
Guido J FalconeFrom the Division of Neurocritical Care (M.B.B., C.B., K.L., A.S.), Brigham and Women's Hospital; Division of Neurocritical Care (C.S., G.J.F., W.T.K.), Center for Genomic Medicine, Massachusetts General Hospital, Boston; and Department of Neurology (K.N.S., L.H.S.), Yale-New Haven Hospital, CT.ORCID 0000-0002-6407-0302
Kevin Navin ShethFrom the Division of Neurocritical Care (M.B.B., C.B., K.L., A.S.), Brigham and Women's Hospital; Division of Neurocritical Care (C.S., G.J.F., W.T.K.), Center for Genomic Medicine, Massachusetts General Hospital, Boston; and Department of Neurology (K.N.S., L.H.S.), Yale-New Haven Hospital, CT.
Lauren H SansingFrom the Division of Neurocritical Care (M.B.B., C.B., K.L., A.S.), Brigham and Women's Hospital; Division of Neurocritical Care (C.S., G.J.F., W.T.K.), Center for Genomic Medicine, Massachusetts General Hospital, Boston; and Department of Neurology (K.N.S., L.H.S.), Yale-New Haven Hospital, CT.
W Taylor KimberlyFrom the Division of Neurocritical Care (M.B.B., C.B., K.L., A.S.), Brigham and Women's Hospital; Division of Neurocritical Care (C.S., G.J.F., W.T.K.), Center for Genomic Medicine, Massachusetts General Hospital, Boston; and Department of Neurology (K.N.S., L.H.S.), Yale-New Haven Hospital, CT.ORCID 0000-0002-2519-8530
Brigham and Women's Hospital · US

Funding

Dynamic Neuroimmune Profiling in Patients with Acute Intracerebral HemorrhageR01NS097728 · NINDS · YALE UNIVERSITY · PI SANSING, LAUREN H · 2016 to 2020
$2.8M
Metabolomic predictors of stroke in REGARDSR01NS099209 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI KIMBERLY, WILLIAM TAYLOR · 2017 to 2021
$2.4M
Role of Soluble ST2 in Immune Cell Regulation and Secondary Neurologic Injury After Intracerebral HemorrhageK23NS112474 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI BEVERS, MATTHEW BRADFORD · 2020 to 2024
$1.1M
Modulating Monocyte Responses to Reduce Injury after Intracerebral HemorrhageR21NS088972 · NINDS · YALE UNIVERSITY · PI SANSING, LAUREN H · 2014 to 2015
$458k
Brain endothelium and innate immune responses after strokeR21NS120002 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI KIMBERLY, WILLIAM TAYLOR · 2021 to 2021
$451k
NINDS NIH HHS K23 NS112474NINDS NIH HHS R01 NS097728NINDS NIH HHS R01 NS099209NINDS NIH HHS R21 NS088972NINDS NIH HHS R21 NS120002
6 · The paper itself

Abstract

BACKGROUND AND

objectivesPerihematomal edema (PHE) contributes to poor outcome after deep intraparenchymal hemorrhage (IPH), which is characterized by neuroinflammation and an influx of peripherally derived innate immune cells. We previously identified soluble ST2 (sST2) as a candidate for immune-mediated secondary brain injury. Leveraging prospectively collected cohorts from 2 centers, we sought to determine whether sST2 was associated with functional outcome, PHE, and the immune response following IPH.

methodsPatients with deep IPH were enrolled within 36 hours of ictus, and blood was collected for sST2 and immune cell measurement. Hematoma volume and PHE were measured on serial CT scans. Good outcome was defined as a modified Rankin Scale score of 0-3 at 90 days. Linear mixed-effects models were used to analyze the relationship between sST2 and PHE over time. Flow cytometry was used to identify shifts in immune cell populations associated with sST2. Immunohistochemistry of human brain tissue was used to identify ST2-expressing cells in the perihematomal region.

resultsThe 55 included patients had a median admission Glasgow Coma Scale score of 14 (interquartile range [IQR] 9-15), an intracerebral hemorrhage (ICH) score of 1 (IQR 1-2), and a hematoma volume of 8.6 mL (IQR 3.4-13.8 mL). Receiver operating curve analysis found the sST2 level to be predictive of poor outcome with an area under the curve of 0.763 (95% CI 0.632-0.894) and Youden optimum cut point of 61.8 ng/mL ( DISCUSSION: Our findings demonstrate that elevated sST2 links the peripheral innate immune response to PHE volume and outcome after IPH. This knowledge is relevant to future studies that seek to identify patients with IPH at highest risk for immune-mediated injury or limit injury through targeted interventions.

Indexed as

Brain EdemaInterleukin-1 Receptor-Like 1 ProteinCerebral HemorrhageEdemaHematomaHumansImmunityRetrospective StudiesInterleukin-1 Receptor-Like 1 Protein

Identifiers

PMID36549913
PMCPMC10065211
OpenAlexW4312114302

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.