Evidence map›Paper›PMID 24252885›Full record

ReviewPediatric research2014

Emerging science of hydroxyurea therapy for pediatric sickle cell disease.

Nancy S Green, Sandra Barral

Open access · bronzeAbstract readReview
In one paragraph

Review in Pediatric research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.

  1. Hydroxyurea (hydroxycarbamide) for sickle cell disease.The Cochrane database of systematic reviews · 2022
    Pooled it
  2. Hydroxyurea (hydroxycarbamide) for sickle cell disease.The Cochrane database of systematic reviews · 2017
    Pooled it
  3. Trial
  4. Review
  5. Role ofLife (Basel, Switzerland) · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Sickle cell cerebrovascular reactivity to a COFrontiers in physiology · 2022
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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 at 1 institution in 1 country.

Nancy S GreenDivision of Pediatric Hematology/Oncology/Stem Cell Transplantation, Department of Pediatrics, Columbia University, New York, New York.
Sandra BarralG.H.Sergievsky Center, Department of Neurology, Columbia University, New York, New York.
Columbia University · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024156 · NCRR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2006 to 2011
$53.0M
NCRR NIH HHS 5UL1RR024156NCRR NIH HHS UL1 RR024156
6 · The paper itself

Abstract

Hydroxyurea (HU) is the sole approved pharmacological therapy for sickle cell disease (SCD). Higher levels of fetal hemoglobin (HbF) diminish deoxygenated sickle globin polymerization in vitro and clinically reduce the incidence of disease morbidities. Clinical and laboratory effects of HU largely result from induction of HbF expression, though to a highly variable extent. Baseline and HU-induced HbF expression are both inherited complex traits. In children with SCD, baseline HbF remains the best predictor of drug-induced levels, but this accounts for only a portion of the induction. A limited number of validated genetic loci are strongly associated with higher baseline HbF levels in SCD. For induced HbF levels, genetic approaches using candidate single-nucleotide polymorphisms (SNPs) have identified some of these same loci as being also associated with induction. However, SNP associations with induced HbF are only partially independent of baseline levels. Additional approaches to understanding the impact of HU on HbF and its other therapeutic effects on SCD include pharmacokinetic, gene expression-based, and epigenetic analyses in patients and through studies in existing murine models for SCD. Understanding the genetic and other factors underlying the variability in therapeutic effects of HU for pediatric SCD is critical for prospectively predicting good responders and for designing other effective therapies.

Indexed as

Age FactorsAnemia, Sickle CellAnimalsAntisickling AgentsChildChild, PreschoolFetal HemoglobinGenetic MarkersGenetic Predisposition to DiseaseHumansHydroxyureaInfantInfant, NewbornPhenotypePolymorphism, Single NucleotideRisk FactorsAntisickling AgentsFetal HemoglobinGenetic MarkersHydroxyurea

Identifiers

PMID24252885
PMCPMC3917141
OpenAlexW2073853004

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.