Evidence map›Paper›PMID 33188723›Full record

ArticleJournal of thrombosis and haemostasis : JTH2021

Plasma levels of S100A8/A9, histone/DNA complexes, and cell-free DNA predict adverse outcomes of immune thrombotic thrombocytopenic purpura.

Jingrui Sui, Ruinan Lu, Konstantine Halkidis, Nicole K Kocher, Wenjing Cao, Marisa B Marques, X Long Zheng

Open access · bronzeAbstract read
In one paragraph

Article in Journal of thrombosis and haemostasis : JTH, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

26 citing papers in PubMed, 27 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Jingrui SuiDivision of Laboratory Medicine, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Ruinan LuDivision of Laboratory Medicine, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Konstantine HalkidisDivision of Laboratory Medicine, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Nicole K KocherDivision of Laboratory Medicine, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Wenjing CaoDivision of Laboratory Medicine, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Marisa B MarquesDivision of Laboratory Medicine, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
X Long ZhengDivision of Laboratory Medicine, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.ORCID 0000-0003-1680-5295
University of Alabama at Birmingham · US

Funding

Pathogenesis of thrombotic microangiopathiesR01HL164016 · NHLBI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI X. Long Zheng · 2023 to 2026
$2.1M
Pathogenesis of Thrombotic MicroangiopathyR01HL126724 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZHENG, X. LONG · 2015 to 2018
$1.8M
Novel Therapeutics for Acquired Thrombotic Thrombocytopenic PurpuraR01HL144552 · NHLBI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI ZHENG, X. LONG · 2019 to 2022
$1.8M
Novel Therapeutics for Acquired Thrombotic Thrombocytopenic PurpuraR01HL115187 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZHENG, X. LONG · 2013 to 2016
$1.6M
NHLBI NIH HHS HL126724NHLBI NIH HHS R01 HL115187NHLBI NIH HHS R01 HL126724NHLBI NIH HHS R01 HL144552NHLBI NIH HHS R01 HL164016
6 · The paper itself

Abstract

backgroundImmune thrombotic thrombocytopenic purpura (iTTP) is a life-threatening blood disorder, primarily resulting from autoantibodies against ADAMTS13. Infection or inflammation often precedes acute iTTP. However, the association of inflammation and inflammatory mediators with disease severity and outcome of acute iTTP is not fully assessed.

objectivesHere, we determined plasma levels of S100A8/A9, histone/DNA complexes, citrullinated histone H3 (CitH3), and cell-free DNA (cfDNA) in a cohort of 108 acute episodes from 94 unique iTTP patients and healthy controls, and assessed the association of each of these biomarkers with the disease severity and mortality.

resultsAll acute iTTP patients had significantly increased plasma levels of S100A8/A9 (median 84.8, interquartile range [IQR] 31.2-157.4 µg/mL), histone/DNA complexes (median 55.7, IQR 35.8-130.8 U/mL), CitH3 (median 3.8, IQR 2.2-6.4 ng/mL), and cfDNA (median 937.7, IQR 781.3-1420.0 ng/mL) on the admission blood samples when compared with healthy controls. An increased plasma level of S100A8/A9, histone/DNA complex and cfDNA was associated with organ damage, coagulopathy, and mortality in iTTP. After being adjusted for age and history of hypertension, Cox proportional hazard regression analysis demonstrated that a hazard ratio (95% confidence interval) for an elevated plasma level of S100A8/A9, histone/DNA complexes, and cfDNA was 11.5 (1.4-90.9) (P = .021), 10.3 (2.7-38.5) (P = .001), and 12.8 (3.9-42.0) (P = .014), respectively.

conclusionThese results indicate that inflammation or plasma inflammatory mediators such as S100A8/A9 or NETosis markers such as histone/DNA complexes and cfDNA may play a role in pathogenesis of iTTP, which may help stratify patients with a high risk of death during acute iTTP episodes.

Indexed as

Cell-Free Nucleic AcidsHistonesPurpura, Thrombocytopenic, IdiopathicPurpura, Thrombotic ThrombocytopenicCalgranulin ACalgranulin BDNAHumansCalgranulin ACalgranulin BCell-Free Nucleic AcidsDNAHistonesS100A8 protein, humanS100A9 protein, humanand mortalityinflammationNETosisneutrophil activationthrombosis

Identifiers

PMID33188723
PMCPMC8058879
OpenAlexW3105093159

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.