Evidence map›Paper›PMID 26560343›Full record

Observational studyJournal of neurotrauma2016

Plasma Anti-Glial Fibrillary Acidic Protein Autoantibody Levels during the Acute and Chronic Phases of Traumatic Brain Injury: A Transforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot Study.

Kevin K W Wang, Zhihui Yang, John K Yue, Zhiqun Zhang, Ethan A Winkler, Ava M Puccio, Ramon Diaz-Arrastia, Hester F Lingsma, Esther L Yuh, Pratik Mukherjee and 13 more

Open access · greenAbstract readMulticenter StudyObservational Study
In one paragraph

Observational study in Journal of neurotrauma, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 2 pooled it
4.7field-weighted citation impact, top 5% 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

61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 82 citations in OpenAlex.

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1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors at 10 institutions in 5 countries.

Kevin K W Wang1 Departments of Psychiatry and Neuroscience, University of Florida , Gainesville, Florida.
Zhihui Yang1 Departments of Psychiatry and Neuroscience, University of Florida , Gainesville, Florida.
John K Yue2 Brain and Spinal Injury Center, San Francisco General Hospital , San Francisco, California.
Zhiqun Zhang1 Departments of Psychiatry and Neuroscience, University of Florida , Gainesville, Florida.
Ethan A Winkler2 Brain and Spinal Injury Center, San Francisco General Hospital , San Francisco, California.
Ava M Puccio4 Department of Neurological Surgery, University of Pittsburgh Medical Center , Pittsburgh, Pennsylvania.
Ramon Diaz-Arrastia5 Department of Neurology, Uniformed Services University of the Health Sciences , and Center for Neuroscience and Regenerative Medicine, Bethesda, Maryland.
Hester F Lingsma6 Department of Public Health, Erasmus Medical Center , Rotterdam, The Netherlands .
Esther L Yuh2 Brain and Spinal Injury Center, San Francisco General Hospital , San Francisco, California.
Pratik Mukherjee2 Brain and Spinal Injury Center, San Francisco General Hospital , San Francisco, California.
Alex B Valadka8 Seton Brain and Spine Institute , Austin, Texas.
Wayne A Gordon9 Department of Rehabilitation Medicine, Mount Sinai School of Medicine , New York, New York.
David O Okonkwo4 Department of Neurological Surgery, University of Pittsburgh Medical Center , Pittsburgh, Pennsylvania.
Geoffrey T Manley2 Brain and Spinal Injury Center, San Francisco General Hospital , San Francisco, California.
Shelly R Cooper2 Brain and Spinal Injury Center, San Francisco General Hospital , San Francisco, California.
Kristen Dams-O'Connor9 Department of Rehabilitation Medicine, Mount Sinai School of Medicine , New York, New York.
Allison J Hricik4 Department of Neurological Surgery, University of Pittsburgh Medical Center , Pittsburgh, Pennsylvania.
Tomoo Inoue2 Brain and Spinal Injury Center, San Francisco General Hospital , San Francisco, California.
Andrew I R Maas10 Department of Neurosurgery, Antwerp University Hospital , Edegem, Belgium .
David K Menon11 Division of Anaesthesia, University of Cambridge and Addenbrooke's Hospital , Cambridge, United Kingdom .
David M Schnyer12 Department of Psychology, University of Texas , Austin, Texas.
Tuhin K Sinha7 Department of Radiology, University of California , San Francisco, San Francisco, California.
Mary J Vassar2 Brain and Spinal Injury Center, San Francisco General Hospital , San Francisco, California.
San Francisco General Hospital · USUniversity of Florida · USUniversity of Pittsburgh Medical Center · USAddenbrooke's Hospital · GBErasmus MC · NLIcahn School of Medicine at Mount Sinai · USNeurogen Brain & Spine Institute · INUniformed Services University of the Health Sciences · USUniversity of California, San Francisco · USUniversity of Cambridge · GB

Funding

Elucidate Consequences of Autoimmune Response to Protease-modified GFAP in TBIR21NS085455 · NINDS · UNIVERSITY OF FLORIDA · PI WANG, KEVIN KA WANG · 2014 to 2015
$397k
NINDS NIH HHS R21 NS085455
6 · The paper itself

Abstract

We described recently a subacute serum autoantibody response toward glial fibrillary acidic protein (GFAP) and its breakdown products 5-10 days after severe traumatic brain injury (TBI). Here, we expanded our anti-GFAP autoantibody (AutoAb[GFAP]) investigation to the multicenter observational study Transforming Research and Clinical Knowledge in TBI Pilot (TRACK-TBI Pilot) to cover the full spectrum of TBI (Glasgow Coma Scale 3-15) by using acute (<24 h) plasma samples from 196 patients with acute TBI admitted to three Level I trauma centers, and a second cohort of 21 participants with chronic TBI admitted to inpatient TBI rehabilitation. We find that acute patients self-reporting previous TBI with loss of consciousness (LOC) (n = 43) had higher day 1 AutoAb[GFAP] (mean ± standard error: 9.11 ± 1.42; n = 43) than healthy controls (2.90 ± 0.92; n = 16; p = 0.032) and acute patients reporting no previous TBI (2.97 ± 0.37; n = 106; p < 0.001), but not acute patients reporting previous TBI without LOC (8.01 ± 1.80; n = 47; p = 0.906). These data suggest that while exposure to TBI may trigger the AutoAb[GFAP] response, circulating antibodies are elevated specifically in acute TBI patients with a history of TBI. AutoAb[GFAP] levels for participants with chronic TBI (average post-TBI time 176 days or 6.21 months) were also significantly higher (15.08 ± 2.82; n = 21) than healthy controls (p < 0.001). These data suggest a persistent upregulation of the autoimmune response to specific brain antigen(s) in the subacute to chronic phase after TBI, as well as after repeated TBI insults. Hence, AutoAb[GFAP] may be a sensitive assay to study the dynamic interactions between post-injury brain and patient-specific autoimmune responses across acute and chronic settings after TBI.

Indexed as

Acute DiseaseAdolescentAdultAgedAged, 80 and overAutoantibodiesBrain Injuries, TraumaticChronic DiseaseFemaleGlial Fibrillary Acidic ProteinHumansMaleMiddle AgedPilot ProjectsYoung AdultAutoantibodiesGlial Fibrillary Acidic Proteinautoantibodyautoimmunitybiomarkersgliatraumatic brain injury

Identifiers

PMID26560343
PMCPMC4931336
OpenAlexW2179071311

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.