Evidence map›Paper›PMID 25519750›Full record

ArticleBlood2015

Hepcidin is suppressed by erythropoiesis in hemoglobin E β-thalassemia and β-thalassemia trait.

Emma Jones, Sant-Rayn Pasricha, Angela Allen, Patricia Evans, Chris A Fisher, Katherine Wray, Anuja Premawardhena, Dyananda Bandara, Ashok Perera, Craig Webster and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 66 citations in OpenAlex.

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  14. Biology of Anemia: A Public Health Perspective.The Journal of nutrition · 2023
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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

17 authors at 9 institutions in 4 countries.

Emma JonesMedical Research Council, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom;
Sant-Rayn PasrichaMedical Research Council, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom;
Angela AllenCollege of Medicine, Swansea University, Swansea, United Kingdom;
Patricia EvansUniversity College of London Cancer Institute, Department of Haematology, University College London, United Kingdom;
Chris A FisherMedical Research Council, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom;
Katherine WrayMedical Research Council, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom;
Anuja PremawardhenaUniversity of Kelaniya, Colombo, Sri Lanka;
Dyananda BandaraNational Thalassaemia Centre, District Hospital, Kurunegala, Sri Lanka;
Ashok PereraNational Thalassaemia Centre, District Hospital, Kurunegala, Sri Lanka;
Craig WebsterDepartment of Biochemistry and Immunology, Birmingham Heartlands Hospital, Birmingham, United Kingdom;
Pamela SturgesDepartment of Biochemistry and Immunology, Birmingham Heartlands Hospital, Birmingham, United Kingdom;
Nancy F OlivieriUniversity Health Network, University of Toronto, ON, Canada; and.
Timothy St PierreSchool of Physics, University of Western Australia, Crawley, Australia.
Andrew E ArmitageMedical Research Council, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom;
John B PorterUniversity College of London Cancer Institute, Department of Haematology, University College London, United Kingdom;
David J WeatherallMedical Research Council, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom;
Hal DrakesmithMedical Research Council, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom;
MRC Weatherall Institute of Molecular Medicine · GBUniversity of Oxford · GBHeartlands Hospital · GBLondon Cancer · GBNational Hospital of Sri Lanka · LKSwansea University · GBThe University of Western Australia · AUUniversity Health Network · CAUniversity of Kelaniya · LK

Funding

Medical Research Council MC_UU_12009/13Medical Research Council MC_UU_12010/10Wellcome Trust
6 · The paper itself

Abstract

Hemoglobin E (HbE) β-thalassemia is the most common severe thalassemia syndrome across Asia, and millions of people are carriers. Clinical heterogeneity in HbE β-thalassemia is incompletely explained by genotype, and the interaction of phenotypic variation with hepcidin is unknown. The effect of thalassemia carriage on hepcidin is also unknown, but it could be relevant for iron supplementation programs aimed at combating anemia. In 62 of 69 Sri Lankan patients with HbE β-thalassemia with moderate or severe phenotype, hepcidin was suppressed, and overall hepcidin inversely correlated with iron accumulation. On segregating by phenotype, there were no differences in hepcidin, erythropoiesis, or hemoglobin between severe or moderate disease, but multiple linear regression showed that erythropoiesis inversely correlated with hepcidin only in severe phenotypes. In moderate disease, no independent predictors of hepcidin were identifiable; nevertheless, the low hepcidin levels indicate a significant risk for iron overload. In a population survey of Sri Lankan schoolchildren, β-thalassemia (but not HbE) trait was associated with increased erythropoiesis and mildly suppressed hepcidin, suggesting an enhanced propensity to accumulate iron. In summary, the influence of erythropoiesis on hepcidin suppression associates with phenotypic disease variation and pathogenesis in HbE β-thalassemia and indicates that the epidemiology of β-thalassemia trait requires consideration when planning public health iron interventions.

Indexed as

AdolescentAdultbeta-Globinsbeta-ThalassemiaCarrier StateCase-Control StudiesChildChild, PreschoolErythropoiesisFemaleGene Expression RegulationGenotypeHemoglobin EHepcidinsHumansIronbeta-GlobinsHAMP protein, humanHemoglobin EHepcidinsIron

Identifiers

PMID25519750
PMCPMC4321326
OpenAlexW2001570896

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.