Evidence map›Paper›PMID 32417430›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2020

Pathogenesis of heparin-induced thrombocytopenia.

Gowthami M Arepally, Douglas B Cines

Open access · greenAbstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 2 pooled it
13.3field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 109 citations in OpenAlex.

  1. Pooled it
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  15. Cloning of Antibodies from Patients with Heparin-Induced Thrombocytopenia.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

8 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

2 authors at 2 institutions in 1 country.

Gowthami M ArepallyDivision of Hematology, Duke University Medical Center, Durham, North Carolina. Electronic address: arepa001@mc.duke.edu.
Douglas B CinesDepartment of Pathology and Laboratory Medicine, Perelman-University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania.
Duke Medical Center · USUniversity of Pennsylvania · US

Funding

Structure-based Design of Rational PF4 Inhibitors in HITR01HL142122 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI CINES, DOUGLAS BROCK, PONCZ, MORTIMER · 2018 to 2021
$2.3M
Complement and CR2/CD21 in the Immune Pathogenesis of HITR01HL136512 · NHLBI · DUKE UNIVERSITY · PI AREPALLY, GOWTHAMI M · 2018 to 2021
$2.1M
Structural analysis of the HIT immune complexR01HL128895 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI ZHANG, HONGTAO · 2015 to 2019
$2.0M
Role of the Endothelium and Neutrophils in the Prothrombotic Nature of HITR01HL139448 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI PONCZ, MORTIMER · 2018 to 2020
$1.4M
NHLBI NIH HHS R01 HL128895NHLBI NIH HHS R01 HL136512NHLBI NIH HHS R01 HL139448NHLBI NIH HHS R01 HL142122
6 · The paper itself

Abstract

There are currently no effective substitutes for high intensity therapy with unfractionated heparin (UFH) for cardiovascular procedures based on its rapid onset of action, ease of monitoring and reversibility. The continued use of UFH in these and other settings requires vigilance for its most serious nonhemorrhagic complication, heparin induced thrombocytopenia (HIT). HIT is an immune prothrombotic disorder caused by antibodies that recognize complexes between platelet factor 4 (PF4) and polyanions such as heparin (H).The pathogenicity of anti-PF4/H antibodies is likely due to the formation of immune complexes that initiate intense procoagulant responses by vascular and hematopoietic cells that lead to the generation of platelet microparticles, monocyte and endothelial cell procoagulant activity, and neutrophil extracellular traps, among other outcomes. The development of anti-PF4/H antibodies after exposure to UFH greatly exceeds the incidence of clinical disease, but the biochemical features that distinguish pathogenic from nonpathogenic antibodies have not been identified. Diagnosis relies on pretest clinical probability, screening for anti-PF4/H antibodies and documentation of their platelet activating capacity. However, both clinical algorithms and test modalities have limited predictive values making diagnosis and management challenging. Given the unacceptable rates of recurrent thromboembolism and bleeding associated with current therapies, there is an unmet need for novel rational nonanticoagulant therapeutics based on the pathogenesis of HIT. We will review recent developments in our understanding of the pathogenesis of HIT and its implications for future approaches to diagnosis and management.

Indexed as

AnticoagulantsHeparinHumansThrombocytopeniaAnticoagulantsHeparin

Identifiers

PMID32417430
PMCPMC7487042
OpenAlexW3024213168

What OpenQuestion holds

Textmetadata
LicenceTDM
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.