Evidence map›Paper›PMID 24895335›Full record

ArticleHaematologica2014

Hepcidin as a predictive factor and therapeutic target in erythropoiesis-stimulating agent treatment for anemia of chronic disease in rats.

Milan Theurl, Manfred Nairz, Andrea Schroll, Thomas Sonnweber, Malte Asshoff, David Haschka, Markus Seifert, Wolfgang Willenbacher, Doris Wilflingseder, Wilfried Posch and 4 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Anemia of Inflammation.Advances in experimental medicine and biology · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Atopic Disease and Anemia in Korean Patients: Cross-Sectional Study with Propensity Score Analysis.International journal of environmental research and public health · 2020
    Article
  8. Review
  9. Review
  10. Hepcidin Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2018
    Review
  11. Article
  12. Review
  13. Article
  14. Role of hepcidin-ferroportin axis in the pathophysiology, diagnosis, and treatment of anemia of chronic inflammation.Hemodialysis international. International Symposium on Home Hemodialysis · 2017
    Review
  15. Anaemia of Chronic Disease: An In-Depth Review.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2017
    Review
  16. Review
  17. Hepcidin regulation in the anemia of inflammation.Current opinion in hematology · 2016
    Review
  18. Mice with hepcidin-resistant ferroportin accumulate iron in the retina.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  19. [Hepcidin for iron homeostasis and target therapy in ironrelated disorders].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2015
    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

14 authors at 2 institutions in 2 countries.

Milan TheurlDepartment of Internal Medicine VI, Innsbruck Medical University, Innsbruck, Austria Department of Ophthalmology and Optometry, Innsbruck Medical University, Innsbruck, Austria.
Manfred NairzDepartment of Internal Medicine VI, Innsbruck Medical University, Innsbruck, Austria.
Andrea SchrollDepartment of Internal Medicine VI, Innsbruck Medical University, Innsbruck, Austria.
Thomas SonnweberDepartment of Internal Medicine VI, Innsbruck Medical University, Innsbruck, Austria.
Malte AsshoffDepartment of Internal Medicine VI, Innsbruck Medical University, Innsbruck, Austria.
David HaschkaDepartment of Internal Medicine VI, Innsbruck Medical University, Innsbruck, Austria.
Markus SeifertDepartment of Internal Medicine VI, Innsbruck Medical University, Innsbruck, Austria.
Wolfgang WillenbacherDepartment of Internal Medicine V, Innsbruck Medical University, Innsbruck, Austria.
Doris WilflingsederDivision of Hygiene and Medical Microbiology, Innsbruck Medical University, Innsbruck, Austria.
Wilfried PoschDivision of Hygiene and Medical Microbiology, Innsbruck Medical University, Innsbruck, Austria.
Anthony T MurphyBiotechnology Discovery Research, Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN, USA.
Derrick R WitcherBiotechnology Discovery Research, Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN, USA.
Igor TheurlDepartment of Internal Medicine VI, Innsbruck Medical University, Innsbruck, Austria guenter.weiss@i-med.ac.at igor.theurl@i-med.ac.at.
Günter WeissDepartment of Internal Medicine VI, Innsbruck Medical University, Innsbruck, Austria guenter.weiss@i-med.ac.at igor.theurl@i-med.ac.at.
Innsbruck Medical University · ATEli Lilly (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anemia of chronic disease is a multifactorial disorder, resulting mainly from inflammation-driven reticuloendothelial iron retention, impaired erythropoiesis, and reduced biological activity of erythropoietin. Erythropoiesis-stimulating agents have been used for the treatment of anemia of chronic disease, although with varying response rates and potential adverse effects. Serum concentrations of hepcidin, a key regulator of iron homeostasis, are increased in patients with anemia of chronic disease and linked to the pathogenesis of this disease, because hepcidin blocks cellular iron egress, thus limiting availability of iron for erythropoiesis. We tested whether serum hepcidin levels can predict and affect the therapeutic efficacy of erythropoiesis-stimulating agent treatment using a well-established rat model of anemia of chronic disease. We found that high pre-treatment hepcidin levels correlated with an impaired hematologic response to an erythropoiesis-stimulating agent in rats with anemia of chronic disease. Combined treatment with an erythropoiesis-stimulating agent and an inhibitor of hepcidin expression, LDN-193189, significantly reduced serum hepcidin levels, mobilized iron from tissue stores, increased serum iron levels and improved hemoglobin levels more effectively than did the erythropoiesis-stimulating agent or LDN-193189 monotherapy. In parallel, both the erythropoiesis-stimulating agent and erythropoiesis-stimulating agent/LDN-193189 combined reduced the expression of cytokines known to inhibit erythropoiesis. We conclude that serum hepcidin levels can predict the hematologic responsiveness to erythropoiesis-stimulating agent therapy in anemia of chronic disease. Pharmacological inhibition of hepcidin formation improves the erythropoiesis-stimulating agent's therapeutic efficacy, which may favor a reduction of erythropoiesis-stimulating agent dosages, costs and side effects.

Indexed as

AnemiaAnimalsBiomarkersChronic DiseaseDrug CombinationsDrug SynergismErythropoiesisErythropoietinFemaleGene ExpressionHematinicsHepcidinsHumansInterferon-gammaIronPolysaccharides, BacterialBiomarkersDrug CombinationsErythropoietinHamp protein, ratHematinicsHepcidinsInterferon-gammaIronLDN 193189Polysaccharides, BacterialPyrazolesPyrimidinesRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID24895335
PMCPMC4562542
OpenAlexW1992361061

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.