Evidence map›Paper›PMID 36759502›Full record

ArticleAnnals of clinical biochemistry2023

Hepcidin analysis in pneumonia: Comparison of immunoassay and LC-MS/MS.

Kjersti Oppen, Cato Brede, Øyvind Skadberg, Trude Steinsvik, Jan Cato Holter, Annika E Michelsen, Lars Heggelund

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Article in Annals of clinical biochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Kjersti OppenDepartment of Laboratory Medicine, Drammen Hospital, Vestre Viken Hospital Trust, Norway.ORCID 0000-0002-0853-5769
Cato BredeDepartment of Medical Biochemistry, Stavanger University Hospital, Norway.ORCID 0000-0003-2691-6052
Øyvind SkadbergDepartment of Medical Biochemistry, Stavanger University Hospital, Norway.
Trude SteinsvikDepartment of Laboratory Medicine, Drammen Hospital, Vestre Viken Hospital Trust, Norway.
Jan Cato HolterInstitute of Clinical Medicine, University of Oslo, Norway.ORCID 0000-0003-1618-5022
Annika E MichelsenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Norway.
Lars HeggelundDepartment of Internal Medicine, Drammen Hospital, Vestre Viken Hospital Trust, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe iron-regulatory hormone hepcidin is a promising biomarker to differentiate anaemia of inflammation from iron deficiency. Plasma hepcidin concentrations increase substantially during inflammation, and the amount of smaller, non-biologically active isoforms of hepcidin increase in inflammatory conditions. These smaller isoforms are measured in some, but not all analytical methods. Thus, we evaluated the comparability of two analytical methods with different isoform selectivity during and after acute-phase pneumonia as a highly inflammatory model disease.

methodsBlood samples from a cohort of 267 hospitalized community-acquired pneumonia patients collected at admission and a 6-week follow-up were analysed. Hepcidin was measured in plasma by an immunoassay, which recognizes all hepcidin isoforms, and a liquid chromatography tandem mass spectrometry (LC-MS/MS), which selectively measures the bioactive hepcidin-25. Additionally, a subset of serum samples was analysed by LC-MS/MS.

resultsHepcidin measurements by immunoassay were higher compared with LC-MS/MS. The relative mean difference of hepcidin plasma concentrations between the two analytical methods was larger in admission samples than in follow-up samples (admission samples <200 ng/mL: 37%, admission samples >200 ng/mL: 78%, follow-up samples >10 ng/mL: 22%). During acute-phase pneumonia, serum concentrations were on average 22% lower than plasma concentrations when measured by LC-MS/MS.

conclusionsImmunoassay measured higher hepcidin concentrations compared with LC-MS/MS, with more pronounced differences in high-concentration samples during acute-phase pneumonia. These findings should be considered in local method validations and in future harmonization and standardization optimization of hepcidin measurements.

Indexed as

HepcidinsPneumoniaChromatography, LiquidHumansImmunoassayInflammationProtein IsoformsTandem Mass SpectrometryHepcidinsProtein IsoformsbiomarkersHepcidinimmunoassayLC-MS/MSpneumonia

Identifiers

PMID36759502
PMCPMC10552342

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