Evidence map›Paper›PMID 20425445›Full record

ReviewCurrent hematologic malignancy reports2008

Primary eosinophilic disorders: a concise review.

Animesh Pardanani, Ayalew Tefferi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hematologic malignancy reports, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Animesh PardananiDivision of Hematology, Mayo Clinic, Rochester, MN 55905, USA.
Ayalew Tefferi

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary eosinophilic disorders include hypereosinophilic syndrome (HES); chronic eosinophilic leukemia, not otherwise categorized (CEL-NOC); platelet-derived growth factor receptor (PDGFR)-rearranged myeloid neoplasms; and other myeloid malignancies associated with prominent blood eosinophilia. According to the World Health Organization consensus criteria, the diagnosis of HES requires the absence of clonal cytogenetic or molecular markers of an underlying myeloid or lymphoid neoplasm. CEL-NOC constitutes an HES-like phenotype associated with an abnormal karyotype or excess blasts in blood (> 2%) or bone marrow (> 5%). HES and CEL-NOC are considered distinct from molecularly defined eosinophilic disorders, such as those associated with activating mutations of PDGFR (PDGFRA and PDGFRB) and fibroblast growth factor receptor-1. This is an important distinction because PDGFR-mutated but not other eosinophilic neoplasms are effectively treated with imatinib. Current management in HES includes observation only for asymptomatic patients with no evidence of organ damage, systemic corticosteroid therapy for acute control of symptoms, and interferon-alfa-2a or hydroxyurea as steroid-sparing agents. In patients with HES who are refractory to usual therapy and have life-threatening disease complications, the use of investigational drugs such as alemtuzumab or mepolizumab might be considered, but data on long-term efficacy and safety are limited.

Indexed as

EosinophiliaHumansHypereosinophilic SyndromeMyeloproliferative DisordersReceptors, Platelet-Derived Growth FactorReceptors, Platelet-Derived Growth Factor

Identifiers

What OpenQuestion holds

Textmetadata
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.