Evidence map›Paper›PMID 21173098›Full record

ArticleHaematologica2011

A time course of hepcidin response to iron challenge in patients with HFE and TFR2 hemochromatosis.

Domenico Girelli, Paola Trombini, Fabiana Busti, Natascia Campostrini, Marco Sandri, Sara Pelucchi, Mark Westerman, Tomas Ganz, Elizabeta Nemeth, Alberto Piperno and 1 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Primary Non-HFE Hemochromatosis: A Review.Journal of clinical and translational hepatology · 2023
    Review
  5. Managing the Dual Nature of Iron to Preserve Health.International journal of molecular sciences · 2023
    Review
  6. Hepcidin and Iron in Health and Disease.Annual review of medicine · 2023
    Review
  7. The mutual crosstalk between iron and erythropoiesis.International journal of hematology · 2022
    Review
  8. Article
  9. Article
  10. Reduced iron export associated with hepcidin resistance can explain the iron overload spectrum in ferroportin disease.Liver international : official journal of the International Association for the Study of the Liver · 2020
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Biomarkers of Functional Outcome in Intracerebral Hemorrhage: Interplay between Clinical Metrics, CD163, and Ferritin.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2017
    Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 2 countries.

Domenico GirelliDepartment of Medicine, University of Verona, Policlinico GB Rossi, 37134 Verona, Italy. domenico.girelli@univr.it
Paola Trombini
Fabiana Busti
Natascia Campostrini
Marco Sandri
Sara Pelucchi
Mark Westerman
Tomas Ganz
Elizabeta Nemeth
Alberto Piperno
Clara Camaschella
University of Verona · ITUniversity of Milano-Bicocca · ITUniversity of California, Los Angeles · USIntrinsic LifeSciences (United States) · USVita-Salute San Raffaele University · IT

Funding

Telethon GGP06213Telethon GGP08089
6 · The paper itself

Abstract

backgroundInadequate hepcidin production leads to iron overload in nearly all types of hemochromatosis. We explored the acute response of hepcidin to iron challenge in 25 patients with HFE-hemochromatosis, in two with TFR2-hemochromatosis and in 13 controls. Sixteen patients (10 C282Y/C282Y homozygotes, 6 C282Y/H63D compound heterozygotes) had increased iron stores, while nine (6 C282Y/C282Y homozygotes, 3 C282Y/H63D compound heterozygotes) were studied after phlebotomy-induced normalization of iron stores. DESIGN AND

methodsWe analyzed serum iron, transferrin saturation, and serum hepcidin by both enzyme-linked immunosorbent assay and mass-spectrometry at baseline, and 4, 8, 12 and 24 hours after a single 65-mg dose of oral iron.

resultsSerum iron and transferrin saturation significantly increased at 4 hours and returned to baseline values at 8-12 hours in all groups, except in the iron-normalized patients who showed the highest and longest increase of both parameters. The level of hepcidin increased significantly at 4 hours and returned to baseline at 24 hours in controls and in the C282Y/H63D compound heterozygotes at diagnosis. The hepcidin response was smaller in C282Y-homozygotes than in controls, barely detectable in the patients with iron-depleted HFE-hemochromatosis and absent in those with TFR2-hemochromatosis. Conclusions Our results are consistent with a scenario in which TFR2 plays a prominent and HFE a contributory role in the hepcidin response to a dose of oral iron. In iron-normalized patients with HFE hemochromatosis, both the low baseline hepcidin level and the weak response to iron contribute to hyperabsorption of iron.

Indexed as

AdultAntimicrobial Cationic PeptidesFerritinsGenotypeHemochromatosisHemochromatosis ProteinHepcidinsHistocompatibility Antigens Class IHumansIronMaleMembrane ProteinsMiddle AgedReceptors, TransferrinTime FactorsAntimicrobial Cationic PeptidesFerritinsHAMP protein, humanHemochromatosis ProteinHepcidinsHFE protein, humanHistocompatibility Antigens Class IIronMembrane ProteinsReceptors, TransferrinTFR2 protein, human

Identifiers

PMID21173098
PMCPMC3069225
OpenAlexW1989331670

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.