Evidence map›Paper›PMID 19787824›Full record

ReviewWorld journal of gastroenterology2009

An update on iron physiology.

Manuel Muñoz, Isabel Villar, José Antonio García-Erce

2 registry-linked trialsOpen access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 112 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 3 pooled it
13.0field-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.

NCT04778072 naunknown statusnot on this mapstarted 2018, after this paper: background citation

A Randomised, Double-blinded, Parallel Group Study to Demonstrate the Adherence and Efficacy of Different Doses of Iron Supplement in Subjects With or At-risk of Iron Deficiency With a History of Intolerance to Oral Iron

TypeinterventionalSponsorSolvotrin Innovations LtdRan2018 to 2021Enrolled60ConditionsPremenopause, Iron-deficiency, Iron Adverse Reaction, Iron Deficiency AnemiaArmsFerrous sulfate 14mg once daily, Ferrous sulfate 25mg once daily, Ferrous sulfate 25mg twice daily
NCT06321887 phase3unknown statusnot on this mapstarted 2023, after this paper: background citation

A Pilot Study to Assess the Efficacy and Tolerability of Reduced Dose Oral Iron in the Treatment of Iron Deficiency Anaemia in Inflammatory Bowel Disease Patients.

TypeinterventionalSponsorLiverpool University Hospitals NHS Foundation TrustRan2023 to 2025Enrolled30ConditionsInflammatory Bowel Disease, Iron Deficiency AnemiaArmsFerrous fumarate syrup 2.5ml/70mg (22.5mg elemental iron), Ferrous fumarate syrup 2.5ml/70mg(45mg elemental iron), Ferrous fumarate syrup 2.5ml/70mg (90mg elemental iron)
3 · Its place in the literature

Who cites it

112 citing papers in PubMed, 3 syntheses or guidelines pooled it, 365 citations in OpenAlex.

  1. Pooled it
  2. Iron therapy for preoperative anaemia.The Cochrane database of systematic reviews · 2019
    Pooled it
  3. Erythropoiesis-stimulating agents for anemia in rheumatoid arthritis.The Cochrane database of systematic reviews · 2013
    Pooled it
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52 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

3 authors at 1 institution in 2 countries.

Manuel MuñozTransfusion Medicine, School of Medicine, University of Málaga, Málaga 29071, Spain. mmunoz@uma.es.
Isabel Villar
José Antonio García-Erce
Universidad de Málaga · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron is an essential micronutrient, as it is required for adequate erythropoietic function, oxidative metabolism and cellular immune responses. Although the absorption of dietary iron (1-2 mg/d) is regulated tightly, it is just balanced with losses. Therefore, internal turnover of iron is essential to meet the requirements for erythropoiesis (20-30 mg/d). Increased iron requirements, limited external supply, and increased blood loss may lead to iron deficiency (ID) and iron-deficiency anemia. Hepcidin, which is made primarily in hepatocytes in response to liver iron levels, inflammation, hypoxia and anemia, is the main iron regulatory hormone. Once secreted into the circulation, hepcidin binds ferroportin on enterocytes and macrophages, which triggers its internalization and lysosomal degradation. Thus, in chronic inflammation, the excess of hepcidin decreases iron absorption and prevents iron recycling, which results in hypoferremia and iron-restricted erythropoiesis, despite normal iron stores (functional ID), and anemia of chronic disease (ACD), which can evolve to ACD plus true ID (ACD + ID). In contrast, low hepcidin expression may lead to iron overload, and vice versa. Laboratory tests provide evidence of iron depletion in the body, or reflect iron-deficient red cell production. The appropriate combination of these laboratory tests help to establish a correct diagnosis of ID status and anemia.

Indexed as

Anemia, Iron-DeficiencyAntimicrobial Cationic PeptidesCation Transport ProteinsEnterocytesErythrocytesErythropoiesisFerroportinHepcidinsHomeostasisHumansInflammationIronIron DeficienciesMacrophagesTransferrinAntimicrobial Cationic PeptidesCation Transport ProteinsFerroportinHAMP protein, humanHepcidinsIronTransferrin

Identifiers

PMID19787824
PMCPMC2754509
OpenAlexW2113462770

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.