Serum hepcidin levels, iron status, and HFE gene alterations during the first year of life in healthy Spanish infants
The aims of this study were to describe hepcidin levels and to assess their associations with iron status and the main variants in the HFE gene in healthy and full-term newborns during the first year of life, as a longitudinal study conducted on 140 infants. Anthropometric and biochemical parameters...
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Veröffentlicht in: | Annals of hematology 2018-06, Vol.97 (6), p.1071-1080 |
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creator | Aranda, Nuria Bedmar, Cristina Arija, Victoria Jardí, Cristina Jimenez-Feijoo, Rosa Ferré, Natalia Tous, Monica |
description | The aims of this study were to describe hepcidin levels and to assess their associations with iron status and the main variants in the
HFE
gene in healthy and full-term newborns during the first year of life, as a longitudinal study conducted on 140 infants. Anthropometric and biochemical parameters, hepcidin, hemoglobin (Hb), serum ferritin (SF), transferrin saturation (TS), mean corpuscular volume (MCV), and C-reactive protein (CRP), were assessed in 6- and 12-month-olds. Infants were genotyped for the three main
HFE
variants: C282Y, H63D, and S65C. Hepcidin levels increased from 6 to 12 months of age (43.7 ± 1.5 to 52.0 ± 1.5 ng/mL;
p
|
doi_str_mv | 10.1007/s00277-018-3256-2 |
format | Article |
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HFE
gene in healthy and full-term newborns during the first year of life, as a longitudinal study conducted on 140 infants. Anthropometric and biochemical parameters, hepcidin, hemoglobin (Hb), serum ferritin (SF), transferrin saturation (TS), mean corpuscular volume (MCV), and C-reactive protein (CRP), were assessed in 6- and 12-month-olds. Infants were genotyped for the three main
HFE
variants: C282Y, H63D, and S65C. Hepcidin levels increased from 6 to 12 months of age (43.7 ± 1.5 to 52.0 ± 1.5 ng/mL;
p
< 0.001), showing higher levels in infants with better iron status compared to those with iron deficiency (ID) (44.8 ± 1.5 vs 37.9 ± 1.3 ng/mL,
p
< 0.018, and 54.3 ± 1.5 vs 44.0 ± 1.4 ng/mL,
p
< 0.038, in 6- and 12-month-olds, respectively). In multivariate linear regression models, iron status was found to be associated with hepcidin levels in infants with wild-type HFE gene (
p
= 0.046 and
p
= 0.048 in 6- and 12-month-olds, respectively). However, this association was not found in HFE-alteration-carrying infants. Hepcidin levels increased in healthy infants during the first year of life and were positively associated with iron levels only in infants with wild-type HFE gene, a situation that requires further investigation.</description><identifier>ISSN: 0939-5555</identifier><identifier>EISSN: 1432-0584</identifier><identifier>DOI: 10.1007/s00277-018-3256-2</identifier><identifier>PMID: 29404719</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Hematology ; Hemoglobin ; Iron ; Medicine ; Medicine & Public Health ; Oncology ; Original Article</subject><ispartof>Annals of hematology, 2018-06, Vol.97 (6), p.1071-1080</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2018</rights><rights>Annals of Hematology is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-92373d11052582dcacb8906df7db0e40b05ba133d10afb088f2afc7d74f370823</citedby><cites>FETCH-LOGICAL-c372t-92373d11052582dcacb8906df7db0e40b05ba133d10afb088f2afc7d74f370823</cites><orcidid>0000-0003-0104-9511</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00277-018-3256-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00277-018-3256-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29404719$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aranda, Nuria</creatorcontrib><creatorcontrib>Bedmar, Cristina</creatorcontrib><creatorcontrib>Arija, Victoria</creatorcontrib><creatorcontrib>Jardí, Cristina</creatorcontrib><creatorcontrib>Jimenez-Feijoo, Rosa</creatorcontrib><creatorcontrib>Ferré, Natalia</creatorcontrib><creatorcontrib>Tous, Monica</creatorcontrib><creatorcontrib>Defensas Study investigators</creatorcontrib><title>Serum hepcidin levels, iron status, and HFE gene alterations during the first year of life in healthy Spanish infants</title><title>Annals of hematology</title><addtitle>Ann Hematol</addtitle><addtitle>Ann Hematol</addtitle><description>The aims of this study were to describe hepcidin levels and to assess their associations with iron status and the main variants in the
HFE
gene in healthy and full-term newborns during the first year of life, as a longitudinal study conducted on 140 infants. Anthropometric and biochemical parameters, hepcidin, hemoglobin (Hb), serum ferritin (SF), transferrin saturation (TS), mean corpuscular volume (MCV), and C-reactive protein (CRP), were assessed in 6- and 12-month-olds. Infants were genotyped for the three main
HFE
variants: C282Y, H63D, and S65C. Hepcidin levels increased from 6 to 12 months of age (43.7 ± 1.5 to 52.0 ± 1.5 ng/mL;
p
< 0.001), showing higher levels in infants with better iron status compared to those with iron deficiency (ID) (44.8 ± 1.5 vs 37.9 ± 1.3 ng/mL,
p
< 0.018, and 54.3 ± 1.5 vs 44.0 ± 1.4 ng/mL,
p
< 0.038, in 6- and 12-month-olds, respectively). In multivariate linear regression models, iron status was found to be associated with hepcidin levels in infants with wild-type HFE gene (
p
= 0.046 and
p
= 0.048 in 6- and 12-month-olds, respectively). However, this association was not found in HFE-alteration-carrying infants. Hepcidin levels increased in healthy infants during the first year of life and were positively associated with iron levels only in infants with wild-type HFE gene, a situation that requires further investigation.</description><subject>Hematology</subject><subject>Hemoglobin</subject><subject>Iron</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><subject>Original Article</subject><issn>0939-5555</issn><issn>1432-0584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp1kcFq3DAQhkVoaTZpHyCXIuilh7gdSfbKOoaQNIVAD2nPQrZGsYJXdiQ5sG9fuZuGEqgug8Q3_4j5CDlj8IUByK8JgEtZAWsrwZttxY_IhtWCV9C09RuyASVU1ZRzTE5SegBgvK35O3LMVQ21ZGpDljuMy44OOPfe-kBHfMIxnVMfp0BTNnkpFxMsvbm-ovcYkJoxYzTZTyFRu0Qf7mkekDofU6Z7NJFOjo7eIS1xAxZ82NO72QSfhvLkTMjpPXnrzJjww3M9Jb-ur35e3lS3P759v7y4rXohea4UF1JYxqDhTcttb_quVbC1TtoOsIYOms4wURAwroO2ddy4XlpZOyGh5eKUfD7kznF6XDBlvfOpx3E0AaclaaZUw7YgGlXQT6_Qh2mJofxupWoOavsnkB2oPk4pRXR6jn5n4l4z0KsTfXCiixO9OtFrz8fn5KXboX3p-CuhAPwApHldJ8Z_Rv839TfpzpZ1</recordid><startdate>20180601</startdate><enddate>20180601</enddate><creator>Aranda, Nuria</creator><creator>Bedmar, Cristina</creator><creator>Arija, Victoria</creator><creator>Jardí, Cristina</creator><creator>Jimenez-Feijoo, Rosa</creator><creator>Ferré, Natalia</creator><creator>Tous, Monica</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0104-9511</orcidid></search><sort><creationdate>20180601</creationdate><title>Serum hepcidin levels, iron status, and HFE gene alterations during the first year of life in healthy Spanish infants</title><author>Aranda, Nuria ; Bedmar, Cristina ; Arija, Victoria ; Jardí, Cristina ; Jimenez-Feijoo, Rosa ; Ferré, Natalia ; Tous, Monica</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-92373d11052582dcacb8906df7db0e40b05ba133d10afb088f2afc7d74f370823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Hematology</topic><topic>Hemoglobin</topic><topic>Iron</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><topic>Original Article</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aranda, Nuria</creatorcontrib><creatorcontrib>Bedmar, Cristina</creatorcontrib><creatorcontrib>Arija, Victoria</creatorcontrib><creatorcontrib>Jardí, Cristina</creatorcontrib><creatorcontrib>Jimenez-Feijoo, Rosa</creatorcontrib><creatorcontrib>Ferré, Natalia</creatorcontrib><creatorcontrib>Tous, Monica</creatorcontrib><creatorcontrib>Defensas Study investigators</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of hematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aranda, Nuria</au><au>Bedmar, Cristina</au><au>Arija, Victoria</au><au>Jardí, Cristina</au><au>Jimenez-Feijoo, Rosa</au><au>Ferré, Natalia</au><au>Tous, Monica</au><aucorp>Defensas Study investigators</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serum hepcidin levels, iron status, and HFE gene alterations during the first year of life in healthy Spanish infants</atitle><jtitle>Annals of hematology</jtitle><stitle>Ann Hematol</stitle><addtitle>Ann Hematol</addtitle><date>2018-06-01</date><risdate>2018</risdate><volume>97</volume><issue>6</issue><spage>1071</spage><epage>1080</epage><pages>1071-1080</pages><issn>0939-5555</issn><eissn>1432-0584</eissn><abstract>The aims of this study were to describe hepcidin levels and to assess their associations with iron status and the main variants in the
HFE
gene in healthy and full-term newborns during the first year of life, as a longitudinal study conducted on 140 infants. Anthropometric and biochemical parameters, hepcidin, hemoglobin (Hb), serum ferritin (SF), transferrin saturation (TS), mean corpuscular volume (MCV), and C-reactive protein (CRP), were assessed in 6- and 12-month-olds. Infants were genotyped for the three main
HFE
variants: C282Y, H63D, and S65C. Hepcidin levels increased from 6 to 12 months of age (43.7 ± 1.5 to 52.0 ± 1.5 ng/mL;
p
< 0.001), showing higher levels in infants with better iron status compared to those with iron deficiency (ID) (44.8 ± 1.5 vs 37.9 ± 1.3 ng/mL,
p
< 0.018, and 54.3 ± 1.5 vs 44.0 ± 1.4 ng/mL,
p
< 0.038, in 6- and 12-month-olds, respectively). In multivariate linear regression models, iron status was found to be associated with hepcidin levels in infants with wild-type HFE gene (
p
= 0.046 and
p
= 0.048 in 6- and 12-month-olds, respectively). However, this association was not found in HFE-alteration-carrying infants. Hepcidin levels increased in healthy infants during the first year of life and were positively associated with iron levels only in infants with wild-type HFE gene, a situation that requires further investigation.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>29404719</pmid><doi>10.1007/s00277-018-3256-2</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-0104-9511</orcidid></addata></record> |
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language | eng |
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source | SpringerLink Journals |
subjects | Hematology Hemoglobin Iron Medicine Medicine & Public Health Oncology Original Article |
title | Serum hepcidin levels, iron status, and HFE gene alterations during the first year of life in healthy Spanish infants |
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