The Impact of Sex and Age on Serum Prohepcidin Concentration in Healthy Adults

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Abstract

Introduction

Within the last 8 years, it has become evident that hepcidin has a diagnostic and therapeutic potential. Therefore, it is a great need to establish the reference interval for hepcidin and its precursor. The aim of this study was to assess the impact of age and sex on serum prohepcidin concentration in healthy adults. Material and methods: 100 healthy volunteers were enrolled during the 18 months of the study - 56 males and 44 females, mean age 34.8±10.1 yrs. Serum prohepcidin, ferritin, soluble transferring receptor (sTfR) and plasma erythropoietin were examined by enzyme-linked immunosorbent assay (ELISA) kits. Serum iron and unsaturated iron binding capacity were determined on ARCHITECT ci8200 (Abbott Diagnostics) according to the manufacturer’s instructions.

Results

Serum prohepcidin concentrations ranged from 74.9 ng/ml to 300.4 ng/ml in healthy adults of both sexes. However, prohepcidin levels were significantly higher in males (median value 145.7 ng/ml) than in females (median 127.3 ng/ml) (p=0.0016). Serum prohepcidin was not associated with age in the group of healthy adults.

Conclusions

Serum prohepcidin concentrations were found to be related to sex. Significantly lower prohepcidin levels were observed in females compared with males.

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Most cited references 22

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Interleukin-6 induces hepcidin expression through STAT3.

Diedra M Wrighting, Nancy C Andrews (2006)

Iron homeostasis is maintained through meticulous regulation of circulating hepcidin levels. Hepcidin levels that are inappropriately low or high result in iron overload or iron deficiency, respectively. Although hypoxia, erythroid demand, iron, and inflammation are all known to influence hepcidin expression, the mechanisms responsible are not well defined. In this report we show that the inflammatory cytokine interleukin-6 (IL-6) directly regulates hepcidin through induction and subsequent promoter binding of signal transducer and activator of transcription 3 (STAT3). STAT3 is necessary and sufficient for the IL-6 responsiveness of the hepcidin promoter. Our findings provide a mechanism by which hepcidin can be regulated by inflammation or, in the absence of inflammatory stimuli, by alternative mechanisms leading to STAT3 activation.

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TLR4-dependent hepcidin expression by myeloid cells in response to bacterial pathogens.

Victor Nizet, Syd Johnson, Annelies S Zinkernagel … (2006)

Hepcidin is an antimicrobial peptide secreted by the liver during inflammation that plays a central role in mammalian iron homeostasis. Here we demonstrate the endogenous expression of hepcidin by macrophages and neutrophils in vitro and in vivo. These myeloid cell types produced hepcidin in response to bacterial pathogens in a toll-like receptor 4 (TLR4)-dependent fashion. Conversely, bacterial stimulation of macrophages triggered a TLR4-dependent reduction in the iron exporter ferroportin. In vivo, intraperitoneal challenge with Pseudomonas aeruginosa induced TLR4-dependent hepcidin expression and iron deposition in splenic macrophages, findings mirrored in subcutaneous infection with group A Streptococcus where hepcidin induction was further observed in neutrophils migrating to the tissue site of infection. Hepcidin expression in cultured hepatocytes or in the livers of mice infected with bacteria was independent of TLR4, suggesting the TLR4-hepcidin pathway is restricted to myeloid cell types. Our findings identify endogenous myeloid cell hepcidin production as a previously unrecognized component of the host response to bacterial pathogens.

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Inappropriate expression of hepcidin is associated with iron refractory anemia: implications for the anemia of chronic disease.

F Loda, Cindy N Roy, N Roy … (2002)

The anemia of chronic disease is a prevalent, poorly understood condition that afflicts patients with a wide variety of diseases, including infections, malignancies, and rheumatologic disorders. It is characterized by a blunted erythropoietin response by erythroid precursors, decreased red blood cell survival, and a defect in iron absorption and macrophage iron retention, which interrupts iron delivery to erythroid precursor cells. We noted that patients with large hepatic adenomas had severe iron refractory anemia similar to that observed in anemia of chronic disease. This anemia resolved spontaneously after adenoma resection or liver transplantation. We investigated the role of the adenomas in the pathogenesis of the anemia and found that they produce inappropriately high levels of hepcidin mRNA. Hepcidin is a peptide hormone that has been implicated in controlling the release of iron from cells. We conclude that hepcidin plays a major, causative role in the anemia observed in our subgroup of patients with hepatic adenomas, and we speculate that it is important in the pathogenesis of the anemia of chronic disease in general.

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Author and article information

Journal

Journal ID (nlm-ta): EJIFCC

Journal ID (iso-abbrev): EJIFCC

Journal ID (publisher-id): eJIFCC

Title: EJIFCC

Publisher: The Communications and Publications Division (CPD) of the IFCC

ISSN (Electronic): 1650-3414

Publication date (Electronic): 25 August 2009

Publication date Collection: August 2009

Volume: 20

Issue: 2

Pages: 129-135

Affiliations

[1 ]Department of Pathophysiology, University of Nicolaus Copernicus , Bydgoszcz, Poland

[2 ] Department of Laboratory Medicine, Collegium Medicum, University of Nicolaus Copernicus , Bydgoszcz, Poland

Author notes

Corresponding author: Department of Pathophysiology, Nicolaus Copernicus University, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Poland; M. Sklodowskiej-Curie 9, 85-094 Bydgoszcz, Poland; +48 52 585 35 95; zhemostazy@ 123456cm.umk.pl

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Publisher ID: ejifcc-20-129

PMC ID: 4975280

SO-VID: 2ad8d2ca-f8b5-4e51-9364-cec534ba9570

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

The Impact of Sex and Age on Serum Prohepcidin Concentration in Healthy Adults

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Abstract

Introduction

Results

Conclusions

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Pneumonia, sex, and the environment

Most cited references 22

Interleukin-6 induces hepcidin expression through STAT3.

TLR4-dependent hepcidin expression by myeloid cells in response to bacterial pathogens.

Inappropriate expression of hepcidin is associated with iron refractory anemia: implications for the anemia of chronic disease.

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