Evidence map›Paper›PMID 37541168›Full record

ArticleThrombosis research2023

Laboratory and demographic predictors of functional assay positive status in suspected heparin-induced thrombocytopenia: A multicenter retrospective cohort study.

Jason B Giles, Jerome Rollin, Kiana L Martinez, Kathleen Selleng, Thomas Thiele, Claire Pouplard, Jo-Ann I Sheppard, Nancy M Heddle, Elizabeth J Phillips, Dan M Roden and 4 more

Open access · greenAbstract readMulticenter Study
In one paragraph

Article in Thrombosis research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
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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

14 authors at 7 institutions in 4 countries.

Jason B GilesDepartment of Pharmacy Practice and Science, University of Arizona R. Ken Coit College of Pharmacy, Tucson, AZ, USA.
Jerome RollinRegional University Hospital Centre Tours, Department of Hemostasis, Tours, France; University of Tours, EA4245, T2i, Tours, France.
Kiana L MartinezDepartment of Pharmacy Practice and Science, University of Arizona R. Ken Coit College of Pharmacy, Tucson, AZ, USA.
Kathleen SellengInstitute of Immunology and Transfusion Medicine, University of Greifswald, Greifswald, Germany.
Thomas ThieleInstitute of Immunology and Transfusion Medicine, University of Greifswald, Greifswald, Germany.
Claire PouplardRegional University Hospital Centre Tours, Department of Hemostasis, Tours, France; University of Tours, EA4245, T2i, Tours, France.
Jo-Ann I SheppardDepartment of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada.
Nancy M HeddleDepartment of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada.
Elizabeth J PhillipsDepartment of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN, USA.
Dan M RodenDepartment of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Biomedical Informatics, Vanderbilt University Medical Center, Nashville, TN, USA.
Yves GruelRegional University Hospital Centre Tours, Department of Hemostasis, Tours, France; University of Tours, EA4245, T2i, Tours, France.
Theodore E WarkentinDepartment of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada.
Andreas GreinacherInstitute of Immunology and Transfusion Medicine, University of Greifswald, Greifswald, Germany.
Jason H KarnesDepartment of Pharmacy Practice and Science, University of Arizona R. Ken Coit College of Pharmacy, Tucson, AZ, USA; Department of Biomedical Informatics, Vanderbilt University Medical Center, Nashville, TN, USA. Electronic address: karnes@arizona.edu.
McMaster University · CAVanderbilt University Medical Center · USUniversität Greifswald · DEUniversité de Tours · FRUniversity of Arizona · USCentre Hospitalier Universitaire de Tours · FRUniversitätsmedizin Greifswald · DE

Funding

Pharmacogenomics of Arrhythmia TherapyU19HL065962 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RODEN, DAN M · 2010 to 2014
$17.4M
Understanding and preventing HLA-associated drug reactionsP50GM115305 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI DENNY, JOSHUA C. · 2015 to 2019
$13.0M
Training in Environmental Toxicology of Human DiseaseT32ES007091 · NIEHS · UNIVERSITY OF ARIZONA · PI Nathan J Cherrington · 1985 to 2026
$10.7M
Leveraging the Microbiome, Local Admixture, and Machine Learning to Optimize Anticoagulant Pharmacogenomics in Medically Underserved PatientsR01HL158686 · NHLBI · UNIVERSITY OF ARIZONA · PI KARNES, JASON HANSEN · 2021 to 2025
$2.2M
ABO and Immunogenetic Variation in the Pathogenesis of Heparin-Induced ThrombocytopeniaR01HL156993 · NHLBI · UNIVERSITY OF ARIZONA · PI KARNES, JASON HANSEN · 2022 to 2025
$2.0M
Genomic and Transcriptomic Influences on Heparin-Induced ThrombocytopeniaK01HL143137 · NHLBI · UNIVERSITY OF ARIZONA · PI KARNES, JASON HANSEN · 2019 to 2022
$615k
NHLBI NIH HHS K01 HL143137NHLBI NIH HHS L30 HL138782NHLBI NIH HHS R01 HL156993NHLBI NIH HHS R01 HL158686NHLBI NIH HHS U19 HL065962NIEHS NIH HHS T32 ES007091NIGMS NIH HHS P50 GM115305
6 · The paper itself

Abstract

Heparin-induced thrombocytopenia (HIT) is an antibody-mediated immune response against platelet factor 4 (PF4) bound to heparin anticoagulants. A priori identification of patients at-risk for HIT remains elusive and a number of risk factors have been identified, but these associations and their effect sizes have limited validation in large cohorts of suspected HIT patients. The aim of this study was to investigate existing anti-PF4/heparin antibody thresholds and model the relationship of demographic variables and anti-PF4/heparin antibody levels with functional assay positivity across multiple institutions in the absence of detailed clinical data. In a large collection of suspected HIT patients (n = 8904), we tested for associations between laboratory and demographic variables and functional assay positive status as well as anti-PF4/heparin antibody levels. We also tested for correlation between IgG-specific and polyspecific (IgG/IgA/IgM) anti-PF4/heparin antibody values and their ability to predict functional assay positive status using area under the receiver operating characteristic (AUROC). Logistic regression identified increasing anti-PF4/heparin antibody OD levels (OR = 51.84 [37.27-74.34], p < 2.0 × 10

Indexed as

ThrombocytopeniaAnticoagulantsDemographyFemaleHeparinHumansImmunoglobulin AImmunoglobulin GPlatelet Factor 4Retrospective StudiesAnticoagulantsHeparinImmunoglobulin AImmunoglobulin GPlatelet Factor 4Adverse drug reactionAnti-PF4/heparin antibodiesFunctional assay testingHeparinHeparin-induced thrombocytopeniaRisk factors

Identifiers

PMID37541168
PMCPMC10528503
OpenAlexW4384938616

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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.