Evidence map›Paper›PMID 21490337›Full record

ReviewBlood2011

Fetal hemoglobin in sickle cell anemia.

Idowu Akinsheye, Abdulrahman Alsultan, Nadia Solovieff, Duyen Ngo, Clinton T Baldwin, Paola Sebastiani, David H K Chui, Martin H Steinberg

Open access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 243 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
243citing papers in PubMed, 11 pooled it
11.1field-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

243 citing papers in PubMed, 11 syntheses or guidelines pooled it, 532 citations in OpenAlex.

  1. Pooled it
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  5. Interventions for chronic kidney disease in people with sickle cell disease.The Cochrane database of systematic reviews · 2023
    Pooled it
  6. Preoperative blood transfusions for sickle cell disease.The Cochrane database of systematic reviews · 2020
    Pooled it
  7. Pooled it
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  9. Interventions for chronic kidney disease in people with sickle cell disease.The Cochrane database of systematic reviews · 2017
    Pooled it
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  11. Preoperative blood transfusions for sickle cell disease.The Cochrane database of systematic reviews · 2016
    Pooled it
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183 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

8 authors at 2 institutions in 2 countries.

Idowu AkinsheyeDepartment of Medicine, Boston University School of Medicine, Boston, MA, USA.
Abdulrahman Alsultan
Nadia Solovieff
Duyen Ngo
Clinton T Baldwin
Paola Sebastiani
David H K Chui
Martin H Steinberg
Boston University · USKing Saud University · SA

Funding

Genetic Modulation of Sickle Cell DiseaseR01HL068970 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI STEINBERG, MARTIN H. · 2001 to 2010
$7.0M
Determinants of HbF Response to HydroxyureaR01HL070735 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI STEINBERG, MARTIN H. · 2002 to 2005
$2.9M
Genetic Modulation of HbF in Beta ThalassemiaR01DK069646 · NIDDK · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CHUI, DAVID H K · 2005 to 2009
$2.9M
Genetic Dissection of Sickle Cell Anemia PhenotypesR21HL080463 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SEBASTIANI, PAOLA · 2005 to 2006
$319k
NHLBI NIH HHS R01 HL068970NHLBI NIH HHS R01 HL070735NHLBI NIH HHS R01 HL68970NHLBI NIH HHS R01 HL70735NHLBI NIH HHS R21 HL080463NHLBI NIH HHS RC2 HL101211NIDDK NIH HHS R01 DK069646
6 · The paper itself

Abstract

Fetal hemoglobin (HbF) is the major genetic modulator of the hematologic and clinical features of sickle cell disease, an effect mediated by its exclusion from the sickle hemoglobin polymer. Fetal hemoglobin genes are genetically regulated, and the level of HbF and its distribution among sickle erythrocytes is highly variable. Some patients with sickle cell disease have exceptionally high levels of HbF that are associated with the Senegal and Saudi-Indian haplotype of the HBB-like gene cluster; some patients with different haplotypes can have similarly high HbF. In these patients, high HbF is associated with generally milder but not asymptomatic disease. Studying these persons might provide additional insights into HbF gene regulation. HbF appears to benefit some complications of disease more than others. This might be related to the premature destruction of erythrocytes that do not contain HbF, even though the total HbF concentration is high. Recent insights into HbF regulation have spurred new efforts to induce high HbF levels in sickle cell disease beyond those achievable with the current limited repertory of HbF inducers.

Indexed as

Anemia, Sickle CellErythrocytesFetal HemoglobinHaplotypesHumansSeverity of Illness IndexFetal Hemoglobin

Identifiers

PMID21490337
PMCPMC3139383
OpenAlexW1990599619

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.