Evidence map›Paper›PMID 25964669›Full record

ReviewBlood2015

How I treat hypereosinophilic syndromes.

Amy D Klion

Registry-linked trialOpen access · bronzeAbstract readCase ReportsReview
In one paragraph

Review in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00044304 (Efficacy of Tyrosine Kinase Inhibition in Reducing Eosinophilia in Patients With Myeloid and/or Steroid-Refractory Hypereosinophilic Syndrome), which is not on this map. Cited by 133 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 3 pooled it
18.0field-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.

NCT00044304 phase2active not recruitingnot on this map

Efficacy of Tyrosine Kinase Inhibition in Reducing Eosinophilia in Patients With Myeloid and/or Steroid-Refractory Hypereosinophilic Syndrome

TypeinterventionalSponsorNational Institute of Allergy and Infectious Diseases (NIAID)Ran2002 to 2027Enrolled70ConditionsEosinophilic Myeloid Neoplasm, Hypereosinophilic SyndromeArmsImatinib, Ruxolitinib
3 · Its place in the literature

Who cites it

133 citing papers in PubMed, 3 syntheses or guidelines pooled it, 280 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Eosinophils and eosinophil-associated diseases: An update.The Journal of allergy and clinical immunology · 2018
    Pooled it
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Mechanisms of glucocorticoid resistance in hypereosinophilic syndromes.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2019
    Trial
  9. Benralizumab forThe New England journal of medicine · 2019
    Trial
  10. Trial
  11. Hypereosinophilic Syndrome Subtype Predicts Responsiveness to Glucocorticoids.The journal of allergy and clinical immunology. In practice
    Trial
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

73 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

1 author at 1 institution in 1 country.

Amy D KlionHuman Eosinophil Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.ORCID http://orcid.org/0000-0002-4986-5326
National Institutes of Health · US

Funding

Eosinophils and Eosinophil Activation in the Pathogenesis of Human DiseaseZIAAI001130 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KLION, AMY · 2010 to 2025
$22.5M
Intramural NIH HHS
6 · The paper itself

Abstract

Hypereosinophilic syndromes (HESs) are a group of rare disorders characterized by peripheral blood eosinophilia of 1.5 × 10(9)/L or higher and evidence of end organ manifestations attributable to the eosinophilia and not otherwise explained in the clinical setting. HESs are pleomorphic in clinical presentation and can be idiopathic or associated with a variety of underlying conditions, including allergic, rheumatologic, infectious, and neoplastic disorders. Moreover, the etiology of the eosinophilia in HESs can be primary (myeloid), secondary (lymphocyte-driven), or unknown. Although corticosteroids remain the first-line therapy for most forms of HESs, the availability of an increasing number of novel therapeutic agents, including tyrosine kinase inhibitors and monoclonal antibodies, has necessarily altered the approach to treatment of HESs. This review presents an updated treatment-based approach to the classification of patients with presumed HES and discusses the roles of conventional and novel agents in the management of these patients.

Indexed as

Adrenal Cortex HormonesAdultAntibodies, MonoclonalDrug DiscoveryFemaleHumansHypereosinophilic SyndromeImatinib MesylateProtein Kinase InhibitorsAdrenal Cortex HormonesAntibodies, MonoclonalImatinib MesylateProtein Kinase Inhibitors

Identifiers

PMID25964669
PMCPMC4551360
OpenAlexW2096034121

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.