Evidence map›Paper›PMID 35126147›Full record

ReviewFrontiers in pharmacology2021

Elucidation of Cellular Contributions to Heparin-Induced Thrombocytopenia Using Omic Approaches.

Jason B Giles, Elise C Miller, Heidi E Steiner, Jason H Karnes

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. The immunogenicity and safety of adenoviral-based vaccines.Current opinion in allergy and clinical immunology · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
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

4 authors at 2 institutions in 1 country.

Jason B GilesDepartment of Pharmacy Practice and Science, University of Arizona College of Pharmacy, Tucson, AZ, United States.
Elise C MillerDepartment of Pharmacy Practice and Science, University of Arizona College of Pharmacy, Tucson, AZ, United States.
Heidi E SteinerDepartment of Pharmacy Practice and Science, University of Arizona College of Pharmacy, Tucson, AZ, United States.
Jason H KarnesDepartment of Pharmacy Practice and Science, University of Arizona College of Pharmacy, Tucson, AZ, United States.
University of Arizona · USVanderbilt University Medical Center · US

Funding

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
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 R01 HL158686NIEHS NIH HHS T32 ES007091
6 · The paper itself

Abstract

Heparin-induced thrombocytopenia (HIT) is an unpredictable, complex, immune-mediated adverse drug reaction associated with a high mortality. Despite decades of research into HIT, fundamental knowledge gaps persist regarding HIT likely due to the complex and unusual nature of the HIT immune response. Such knowledge gaps include the identity of a HIT immunogen, the intrinsic roles of various cell types and their interactions, and the molecular basis that distinguishes pathogenic and non-pathogenic PF4/heparin antibodies. While a key feature of HIT, thrombocytopenia, implicates platelets as a seminal cell fragment in HIT pathogenesis, strong evidence exists for critical roles of multiple cell types. The rise in omic technologies over the last decade has resulted in a number of agnostic, whole system approaches for biological research that may be especially informative for complex phenotypes. Applying multi-omics techniques to HIT has the potential to bring new insights into HIT pathophysiology and identify biomarkers with clinical utility. In this review, we review the clinical, immunological, and molecular features of HIT with emphasis on key cell types and their roles. We then address the applicability of several omic techniques underutilized in HIT, which have the potential to fill knowledge gaps related to HIT biology.

Indexed as

adverse drug reactiongenomicsheparin-induced thrombocytopeniametagenomicneutrophilproteomict-celltranscriptomics

Identifiers

PMID35126147
PMCPMC8814424
OpenAlexW4206768604

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.