Post‐natal anaemia and iron deficiency in HIV‐infected women and the health and survival of their children
Identifieur interne : 003F50 ( Istex/Corpus ); précédent : 003F49; suivant : 003F51Post‐natal anaemia and iron deficiency in HIV‐infected women and the health and survival of their children
Auteurs : Sheila Isanaka ; Donna Spiegelman ; Said Aboud ; Karim P. Manji ; Gernard I. Msamanga ; Walter C. Willet ; Christopher Duggan ; Wafaie W. FawziSource :
- Maternal & Child Nutrition [ 1740-8695 ] ; 2012-07.
English descriptors
- KwdEn :
- American journal, Anaemia, Baseline, Blackwell publishing, Body mass index, Breast milk, Breastfeeding, Categorised, Cells world health organization, Child death, Child health, Child mortality, Child nutrition, Clinical nutrition, Clinical stage, Endpoint, Erythrocyte morphology, Fawzi, Folic acid supplementation, Haemoglobin, Harvard school, Hypochromasia, Hypochromic, Hypochromic microcytosis, Hypochromic microcytosis anaemia, Immune, Immune status, Immune syndromes, Infection, Infection status, Infectious diseases, Iron status, Iron supplementation, Isanaka, Malaria infection, Maternal, Maternal anaemia, Maternal hypochromic microcytosis, Maternal iron, Maternal iron status, Microcytic, Microcytic cells, Microcytosis, Muhimbili university, Nations programme, Parent study, Predictor, Pregnancy, Pregnancy outcomes, Pregnant women, Prenatal, Prenatal compliance, Prenatal iron supplementation, Prenatal period, Prenatal visits, Programme, Prospective study, Public health, Severe anaemia, Severe hypochromic microcytosis, Standard deviation, Supplementation, Tanzania, Viral, Viral load, World health organization.
- Teeft :
- American journal, Anaemia, Baseline, Blackwell publishing, Body mass index, Breast milk, Breastfeeding, Categorised, Cells world health organization, Child death, Child health, Child mortality, Child nutrition, Clinical nutrition, Clinical stage, Endpoint, Erythrocyte morphology, Fawzi, Folic acid supplementation, Haemoglobin, Harvard school, Hypochromasia, Hypochromic, Hypochromic microcytosis, Hypochromic microcytosis anaemia, Immune, Immune status, Immune syndromes, Infection, Infection status, Infectious diseases, Iron status, Iron supplementation, Isanaka, Malaria infection, Maternal, Maternal anaemia, Maternal hypochromic microcytosis, Maternal iron, Maternal iron status, Microcytic, Microcytic cells, Microcytosis, Muhimbili university, Nations programme, Parent study, Predictor, Pregnancy, Pregnancy outcomes, Pregnant women, Prenatal, Prenatal compliance, Prenatal iron supplementation, Prenatal period, Prenatal visits, Programme, Prospective study, Public health, Severe anaemia, Severe hypochromic microcytosis, Standard deviation, Supplementation, Tanzania, Viral, Viral load, World health organization.
Abstract
Prenatal iron supplementation may improve pregnancy outcomes and decrease the risk of child mortality. However, little is known about the importance of post‐natal maternal iron status for child health and survival, particularly in the context of HIV infection. We examined the association of maternal anaemia and hypochromic microcytosis, an erythrocyte morphology consistent with iron deficiency, with child health and survival in the first two to five years of life. Repeated measures of maternal anaemia and hypochromic microcytosis from 840 HIV‐positive women enrolled in a clinical trial of vitamin supplementation were prospectively related to child mortality, HIV infection and CD4 T‐cell count. Median duration of follow‐up for the endpoints of child mortality, HIV infection and CD4 cell count was 58, 17 and 23 months, respectively. Maternal anaemia and hypochromic microcytosis were associated with greater risk of child mortality [hazard ratio (HR) for severe anaemia = 2.58, 95% confidence interval (CI): 1.66–4.01, P trend < 0.0001; HR for severe hypochromic microcytosis = 2.36, 95% CI: 1.27–4.38, P trend = 0.001]. Maternal anaemia was not significantly associated with greater risk of child HIV infection (HR for severe anaemia = 1.46, 95% CI: 0.91, 2.33, P trend = 0.08) but predicted lower CD4 T‐cell counts among HIV‐uninfected children (difference in CD4 T‐cell count/µL for severe anaemia: −93, 95% CI: −204–17, P trend = 0.02). The potential child health risks associated with maternal anaemia and iron deficiency may not be limited to the prenatal period. Efforts to reduce maternal anaemia and iron deficiency during pregnancy may need to be expanded to include the post‐partum period.
Url:
DOI: 10.1111/j.1740-8709.2011.00389.x
Links to Exploration step
ISTEX:C251351EF66A46770FB7C50CCD82D3143B31B201Le document en format XML
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UK</pubPlace><date type="published" when="2012-07">2012-07</date></imprint><idno type="ISSN">1740-8695</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1740-8695</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>American journal</term><term>Anaemia</term><term>Baseline</term><term>Blackwell publishing</term><term>Body mass index</term><term>Breast milk</term><term>Breastfeeding</term><term>Categorised</term><term>Cells world health organization</term><term>Child death</term><term>Child health</term><term>Child mortality</term><term>Child nutrition</term><term>Clinical nutrition</term><term>Clinical stage</term><term>Endpoint</term><term>Erythrocyte morphology</term><term>Fawzi</term><term>Folic acid supplementation</term><term>Haemoglobin</term><term>Harvard school</term><term>Hypochromasia</term><term>Hypochromic</term><term>Hypochromic microcytosis</term><term>Hypochromic microcytosis 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microcytosis</term><term>Standard deviation</term><term>Supplementation</term><term>Tanzania</term><term>Viral</term><term>Viral load</term><term>World health organization</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>American journal</term><term>Anaemia</term><term>Baseline</term><term>Blackwell publishing</term><term>Body mass index</term><term>Breast milk</term><term>Breastfeeding</term><term>Categorised</term><term>Cells world health organization</term><term>Child death</term><term>Child health</term><term>Child mortality</term><term>Child nutrition</term><term>Clinical nutrition</term><term>Clinical stage</term><term>Endpoint</term><term>Erythrocyte morphology</term><term>Fawzi</term><term>Folic acid supplementation</term><term>Haemoglobin</term><term>Harvard school</term><term>Hypochromasia</term><term>Hypochromic</term><term>Hypochromic microcytosis</term><term>Hypochromic microcytosis anaemia</term><term>Immune</term><term>Immune status</term><term>Immune syndromes</term><term>Infection</term><term>Infection status</term><term>Infectious diseases</term><term>Iron status</term><term>Iron supplementation</term><term>Isanaka</term><term>Malaria infection</term><term>Maternal</term><term>Maternal anaemia</term><term>Maternal hypochromic microcytosis</term><term>Maternal iron</term><term>Maternal iron status</term><term>Microcytic</term><term>Microcytic cells</term><term>Microcytosis</term><term>Muhimbili university</term><term>Nations programme</term><term>Parent study</term><term>Predictor</term><term>Pregnancy</term><term>Pregnancy outcomes</term><term>Pregnant women</term><term>Prenatal</term><term>Prenatal compliance</term><term>Prenatal iron supplementation</term><term>Prenatal period</term><term>Prenatal visits</term><term>Programme</term><term>Prospective study</term><term>Public health</term><term>Severe anaemia</term><term>Severe hypochromic microcytosis</term><term>Standard deviation</term><term>Supplementation</term><term>Tanzania</term><term>Viral</term><term>Viral load</term><term>World health organization</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Prenatal iron supplementation may improve pregnancy outcomes and decrease the risk of child mortality. However, little is known about the importance of post‐natal maternal iron status for child health and survival, particularly in the context of HIV infection. We examined the association of maternal anaemia and hypochromic microcytosis, an erythrocyte morphology consistent with iron deficiency, with child health and survival in the first two to five years of life. Repeated measures of maternal anaemia and hypochromic microcytosis from 840 HIV‐positive women enrolled in a clinical trial of vitamin supplementation were prospectively related to child mortality, HIV infection and CD4 T‐cell count. Median duration of follow‐up for the endpoints of child mortality, HIV infection and CD4 cell count was 58, 17 and 23 months, respectively. Maternal anaemia and hypochromic microcytosis were associated with greater risk of child mortality [hazard ratio (HR) for severe anaemia = 2.58, 95% confidence interval (CI): 1.66–4.01, P trend < 0.0001; HR for severe hypochromic microcytosis = 2.36, 95% CI: 1.27–4.38, P trend = 0.001]. Maternal anaemia was not significantly associated with greater risk of child HIV infection (HR for severe anaemia = 1.46, 95% CI: 0.91, 2.33, P trend = 0.08) but predicted lower CD4 T‐cell counts among HIV‐uninfected children (difference in CD4 T‐cell count/µL for severe anaemia: −93, 95% CI: −204–17, P trend = 0.02). The potential child health risks associated with maternal anaemia and iron deficiency may not be limited to the prenatal period. Efforts to reduce maternal anaemia and iron deficiency during pregnancy may need to be expanded to include the post‐partum period.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>anaemia</json:string><json:string>microcytosis</json:string><json:string>hypochromic</json:string><json:string>maternal anaemia</json:string><json:string>hypochromic microcytosis</json:string><json:string>hypochromasia</json:string><json:string>supplementation</json:string><json:string>prenatal</json:string><json:string>child mortality</json:string><json:string>tanzania</json:string><json:string>child nutrition</json:string><json:string>blackwell publishing</json:string><json:string>baseline</json:string><json:string>child health</json:string><json:string>immune</json:string><json:string>haemoglobin</json:string><json:string>breastfeeding</json:string><json:string>microcytic</json:string><json:string>microcytic cells</json:string><json:string>viral</json:string><json:string>maternal</json:string><json:string>severe anaemia</json:string><json:string>american journal</json:string><json:string>isanaka</json:string><json:string>categorised</json:string><json:string>world health organization</json:string><json:string>fawzi</json:string><json:string>endpoint</json:string><json:string>iron supplementation</json:string><json:string>iron status</json:string><json:string>predictor</json:string><json:string>viral load</json:string><json:string>programme</json:string><json:string>harvard school</json:string><json:string>malaria infection</json:string><json:string>clinical nutrition</json:string><json:string>public health</json:string><json:string>immune syndromes</json:string><json:string>maternal iron status</json:string><json:string>body mass index</json:string><json:string>prenatal period</json:string><json:string>pregnant women</json:string><json:string>hypochromic microcytosis anaemia</json:string><json:string>clinical stage</json:string><json:string>nations programme</json:string><json:string>muhimbili university</json:string><json:string>infection status</json:string><json:string>severe hypochromic microcytosis</json:string><json:string>erythrocyte morphology</json:string><json:string>cells world health organization</json:string><json:string>child death</json:string><json:string>parent study</json:string><json:string>immune status</json:string><json:string>standard deviation</json:string><json:string>maternal hypochromic microcytosis</json:string><json:string>prospective study</json:string><json:string>prenatal iron supplementation</json:string><json:string>maternal iron</json:string><json:string>prenatal compliance</json:string><json:string>folic acid supplementation</json:string><json:string>prenatal visits</json:string><json:string>breast milk</json:string><json:string>pregnancy outcomes</json:string><json:string>infectious diseases</json:string><json:string>infection</json:string><json:string>pregnancy</json:string></teeft></keywords><author><json:item><name>Sheila Isanaka</name><affiliations><json:string>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</json:string><json:string>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</json:string><json:string>E-mail: sisanaka@hsph.harvard.edu</json:string></affiliations></json:item><json:item><name>Donna Spiegelman</name><affiliations><json:string>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</json:string><json:string>Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA</json:string></affiliations></json:item><json:item><name>Said Aboud</name><affiliations><json:string>Department of Microbiology and Immunology, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania</json:string></affiliations></json:item><json:item><name>Karim P. Manji</name><affiliations><json:string>Department of Pediatrics and Child Health, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania</json:string></affiliations></json:item><json:item><name>Gernard I. Msamanga</name><affiliations><json:string>Department of Community Health, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania</json:string></affiliations></json:item><json:item><name>Walter C. Willet</name><affiliations><json:string>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</json:string><json:string>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</json:string><json:string>Channing Laboratory, Harvard Medical School, Department of Medicine, Boston, Massachusetts, USA</json:string></affiliations></json:item><json:item><name>Christopher Duggan</name><affiliations><json:string>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</json:string><json:string>Division of Gastroenterology and Nutrition, Children's Hospital Boston, Boston, Massachusetts, USA</json:string></affiliations></json:item><json:item><name>Wafaie W. Fawzi</name><affiliations><json:string>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</json:string><json:string>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</json:string><json:string>Department of Global Health and Population, Harvard School of Public Health, Boston, Massachusetts, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>anaemia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>iron deficiency</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>post‐natal</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>HIV</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>child</value></json:item></subject><articleId><json:string>MCN389</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Prenatal iron supplementation may improve pregnancy outcomes and decrease the risk of child mortality. However, little is known about the importance of post‐natal maternal iron status for child health and survival, particularly in the context of HIV infection. We examined the association of maternal anaemia and hypochromic microcytosis, an erythrocyte morphology consistent with iron deficiency, with child health and survival in the first two to five years of life. Repeated measures of maternal anaemia and hypochromic microcytosis from 840 HIV‐positive women enrolled in a clinical trial of vitamin supplementation were prospectively related to child mortality, HIV infection and CD4 T‐cell count. Median duration of follow‐up for the endpoints of child mortality, HIV infection and CD4 cell count was 58, 17 and 23 months, respectively. Maternal anaemia and hypochromic microcytosis were associated with greater risk of child mortality [hazard ratio (HR) for severe anaemia = 2.58, 95% confidence interval (CI): 1.66–4.01, P trend > 0.0001; HR for severe hypochromic microcytosis = 2.36, 95% CI: 1.27–4.38, P trend = 0.001]. Maternal anaemia was not significantly associated with greater risk of child HIV infection (HR for severe anaemia = 1.46, 95% CI: 0.91, 2.33, P trend = 0.08) but predicted lower CD4 T‐cell counts among HIV‐uninfected children (difference in CD4 T‐cell count/µL for severe anaemia: −93, 95% CI: −204–17, P trend = 0.02). The potential child health risks associated with maternal anaemia and iron deficiency may not be limited to the prenatal period. 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E‐mail: sisanaka@hsph.harvard.edu</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Donna</forename><surname>Spiegelman</surname></persName><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA<address><country key="US"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Said</forename><surname>Aboud</surname></persName><affiliation>Department of Microbiology and Immunology, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Karim P.</forename><surname>Manji</surname></persName><affiliation>Department of Pediatrics and Child Health, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Gernard I.</forename><surname>Msamanga</surname></persName><affiliation>Department of Community Health, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Walter C.</forename><surname>Willet</surname></persName><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA<address><country key="US"></country></address></affiliation><affiliation>Channing Laboratory, Harvard Medical School, Department of Medicine, Boston, Massachusetts, USA<address><country key="US"></country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Christopher</forename><surname>Duggan</surname></persName><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA<address><country key="US"></country></address></affiliation><affiliation>Division of Gastroenterology and Nutrition, Children's Hospital Boston, Boston, Massachusetts, USA<address><country key="US"></country></address></affiliation></author><author xml:id="author-0007"><persName><forename type="first">Wafaie W.</forename><surname>Fawzi</surname></persName><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA<address><country key="US"></country></address></affiliation><affiliation>Department of Global Health and Population, Harvard School of Public Health, Boston, Massachusetts, USA<address><country key="US"></country></address></affiliation></author><idno type="istex">C251351EF66A46770FB7C50CCD82D3143B31B201</idno><idno type="ark">ark:/67375/WNG-70XRL16N-1</idno><idno type="DOI">10.1111/j.1740-8709.2011.00389.x</idno><idno type="unit">MCN389</idno><idno type="toTypesetVersion">file:MCN.MCN389.pdf</idno></analytic><monogr><title level="j" type="main">Maternal & Child Nutrition</title><title level="j" type="alt">MATERNAL CHILD NUTRITION</title><idno type="pISSN">1740-8695</idno><idno type="eISSN">1740-8709</idno><idno type="book-DOI">10.1111/(ISSN)1740-8709</idno><idno type="book-part-DOI">10.1111/mcn.2012.8.issue-3</idno><idno type="product">MCN</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">8</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="287">287</biblScope><biblScope unit="page" to="298">298</biblScope><biblScope unit="page-count">12</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2012-07"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><p>Prenatal iron supplementation may improve pregnancy outcomes and decrease the risk of child mortality. However, little is known about the importance of post‐natal maternal iron status for child health and survival, particularly in the context of HIV infection. We examined the association of maternal anaemia and hypochromic microcytosis, an erythrocyte morphology consistent with iron deficiency, with child health and survival in the first two to five years of life. Repeated measures of maternal anaemia and hypochromic microcytosis from 840 HIV‐positive women enrolled in a clinical trial of vitamin supplementation were prospectively related to child mortality, HIV infection and CD4 T‐cell count. Median duration of follow‐up for the endpoints of child mortality, HIV infection and CD4 cell count was 58, 17 and 23 months, respectively. Maternal anaemia and hypochromic microcytosis were associated with greater risk of child mortality [hazard ratio (HR) for severe anaemia = 2.58, 95% confidence interval (CI): 1.66–4.01, <hi rend="italic">P</hi> trend < 0.0001; HR for severe hypochromic microcytosis = 2.36, 95% CI: 1.27–4.38, <hi rend="italic">P</hi> trend = 0.001]. Maternal anaemia was not significantly associated with greater risk of child HIV infection (HR for severe anaemia = 1.46, 95% CI: 0.91, 2.33, <hi rend="italic">P</hi> trend = 0.08) but predicted lower CD4 T‐cell counts among HIV‐uninfected children (difference in CD4 T‐cell count/<hi rend="italic">µ</hi>L for severe anaemia: −93, 95% CI: −204–17, <hi rend="italic">P</hi> trend = 0.02). The potential child health risks associated with maternal anaemia and iron deficiency may not be limited to the prenatal period. Efforts to reduce maternal anaemia and iron deficiency during pregnancy may need to be expanded to include the post‐partum period.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">anaemia</term><term xml:id="k2">iron deficiency</term><term xml:id="k3">post‐natal</term><term xml:id="k4">HIV</term><term xml:id="k5">child</term></keywords><keywords rend="tocHeading1"><term>Original Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/C251351EF66A46770FB7C50CCD82D3143B31B201/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1740-8709</doi><issn type="print">1740-8695</issn><issn type="electronic">1740-8709</issn><idGroup><id type="product" value="MCN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="MATERNAL CHILD NUTRITION">Maternal & Child Nutrition</title></titleGroup></publicationMeta><publicationMeta level="part" position="07103"><doi origin="wiley">10.1111/mcn.2012.8.issue-3</doi><numberingGroup><numbering type="journalVolume" number="8">8</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="2012-07">July 2012</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="3" status="forIssue"><doi origin="wiley">10.1111/j.1740-8709.2011.00389.x</doi><idGroup><id type="unit" value="MCN389"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><copyright>© 2012 Blackwell Publishing Ltd</copyright><eventGroup><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:3.1.5 mode:FullText" date="2012-06-05"></event><event type="publishedOnlineEarlyUnpaginated" date="2012-01-11"></event><event type="firstOnline" date="2012-01-11"></event><event type="publishedOnlineFinalForm" date="2012-06-05"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.3.4 mode:FullText" date="2015-02-25"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="287">287</numbering><numbering type="pageLast" number="298">298</numbering></numberingGroup><correspondenceTo>Sheila Isanaka, Harvard School of Public Health, Department of Nutrition, 665 Huntington Avenue, Boston, MA 02115, USA. E‐mail: <email>sisanaka@hsph.harvard.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MCN.MCN389.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="4"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="40"></count><count type="wordTotal" number="7133"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Post‐natal anaemia and iron deficiency in HIV‐infected women and the health and survival of their children</title><title type="shortAuthors">S. Isanaka <i>et al</i>.</title><title type="short">Post‐natal maternal anaemia and child health</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2" corresponding="yes"><personName><givenNames>Sheila</givenNames><familyName>Isanaka</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1 #a3"><personName><givenNames>Donna</givenNames><familyName>Spiegelman</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a5"><personName><givenNames>Said</givenNames><familyName>Aboud</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a6"><personName><givenNames>Karim P.</givenNames><familyName>Manji</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a7"><personName><givenNames>Gernard I.</givenNames><familyName>Msamanga</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1 #a2 #a8"><personName><givenNames>Walter C.</givenNames><familyName>Willet</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1 #a9"><personName><givenNames>Christopher</givenNames><familyName>Duggan</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a1 #a2 #a4"><personName><givenNames>Wafaie W.</givenNames><familyName>Fawzi</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="US"><unparsedAffiliation>Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="US"><unparsedAffiliation>Department of Global Health and Population, Harvard School of Public Health, Boston, Massachusetts, USA</unparsedAffiliation></affiliation><affiliation xml:id="a5"><unparsedAffiliation>Department of Microbiology and Immunology, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania</unparsedAffiliation></affiliation><affiliation xml:id="a6"><unparsedAffiliation>Department of Pediatrics and Child Health, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania</unparsedAffiliation></affiliation><affiliation xml:id="a7"><unparsedAffiliation>Department of Community Health, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania</unparsedAffiliation></affiliation><affiliation xml:id="a8" countryCode="US"><unparsedAffiliation>Channing Laboratory, Harvard Medical School, Department of Medicine, Boston, Massachusetts, USA</unparsedAffiliation></affiliation><affiliation xml:id="a9" countryCode="US"><unparsedAffiliation>Division of Gastroenterology and Nutrition, Children's Hospital Boston, Boston, Massachusetts, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">anaemia</keyword><keyword xml:id="k2">iron deficiency</keyword><keyword xml:id="k3">post‐natal</keyword><keyword xml:id="k4">HIV</keyword><keyword xml:id="k5">child</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Prenatal iron supplementation may improve pregnancy outcomes and decrease the risk of child mortality. However, little is known about the importance of post‐natal maternal iron status for child health and survival, particularly in the context of HIV infection. We examined the association of maternal anaemia and hypochromic microcytosis, an erythrocyte morphology consistent with iron deficiency, with child health and survival in the first two to five years of life. Repeated measures of maternal anaemia and hypochromic microcytosis from 840 HIV‐positive women enrolled in a clinical trial of vitamin supplementation were prospectively related to child mortality, HIV infection and CD4 T‐cell count. Median duration of follow‐up for the endpoints of child mortality, HIV infection and CD4 cell count was 58, 17 and 23 months, respectively. Maternal anaemia and hypochromic microcytosis were associated with greater risk of child mortality [hazard ratio (HR) for severe anaemia = 2.58, 95% confidence interval (CI): 1.66–4.01, <i>P</i> trend < 0.0001; HR for severe hypochromic microcytosis = 2.36, 95% CI: 1.27–4.38, <i>P</i> trend = 0.001]. Maternal anaemia was not significantly associated with greater risk of child HIV infection (HR for severe anaemia = 1.46, 95% CI: 0.91, 2.33, <i>P</i> trend = 0.08) but predicted lower CD4 T‐cell counts among HIV‐uninfected children (difference in CD4 T‐cell count/<i>µ</i>L for severe anaemia: −93, 95% CI: −204–17, <i>P</i> trend = 0.02). The potential child health risks associated with maternal anaemia and iron deficiency may not be limited to the prenatal period. Efforts to reduce maternal anaemia and iron deficiency during pregnancy may need to be expanded to include the post‐partum period.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Post‐natal anaemia and iron deficiency in HIV‐infected women and the health and survival of their children</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Post‐natal maternal anaemia and child health</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Post‐natal anaemia and iron deficiency in HIV‐infected women and the health and survival of their children</title></titleInfo><name type="personal"><namePart type="given">Sheila</namePart><namePart type="family">Isanaka</namePart><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><affiliation>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><affiliation>E-mail: sisanaka@hsph.harvard.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Donna</namePart><namePart type="family">Spiegelman</namePart><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><affiliation>Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Said</namePart><namePart type="family">Aboud</namePart><affiliation>Department of Microbiology and Immunology, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karim P.</namePart><namePart type="family">Manji</namePart><affiliation>Department of Pediatrics and Child Health, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gernard I.</namePart><namePart type="family">Msamanga</namePart><affiliation>Department of Community Health, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Walter C.</namePart><namePart type="family">Willet</namePart><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><affiliation>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><affiliation>Channing Laboratory, Harvard Medical School, Department of Medicine, Boston, Massachusetts, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christopher</namePart><namePart type="family">Duggan</namePart><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><affiliation>Division of Gastroenterology and Nutrition, Children's Hospital Boston, Boston, Massachusetts, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wafaie W.</namePart><namePart type="family">Fawzi</namePart><affiliation>Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><affiliation>Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><affiliation>Department of Global Health and Population, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2012-07</dateIssued><copyrightDate encoding="w3cdtf">2012</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">0</extent><extent unit="tables">4</extent><extent unit="formulas">0</extent><extent unit="references">40</extent><extent unit="linksCrossRef">0</extent><extent unit="words">7133</extent></physicalDescription><abstract lang="en">Prenatal iron supplementation may improve pregnancy outcomes and decrease the risk of child mortality. However, little is known about the importance of post‐natal maternal iron status for child health and survival, particularly in the context of HIV infection. We examined the association of maternal anaemia and hypochromic microcytosis, an erythrocyte morphology consistent with iron deficiency, with child health and survival in the first two to five years of life. Repeated measures of maternal anaemia and hypochromic microcytosis from 840 HIV‐positive women enrolled in a clinical trial of vitamin supplementation were prospectively related to child mortality, HIV infection and CD4 T‐cell count. Median duration of follow‐up for the endpoints of child mortality, HIV infection and CD4 cell count was 58, 17 and 23 months, respectively. Maternal anaemia and hypochromic microcytosis were associated with greater risk of child mortality [hazard ratio (HR) for severe anaemia = 2.58, 95% confidence interval (CI): 1.66–4.01, P trend < 0.0001; HR for severe hypochromic microcytosis = 2.36, 95% CI: 1.27–4.38, P trend = 0.001]. Maternal anaemia was not significantly associated with greater risk of child HIV infection (HR for severe anaemia = 1.46, 95% CI: 0.91, 2.33, P trend = 0.08) but predicted lower CD4 T‐cell counts among HIV‐uninfected children (difference in CD4 T‐cell count/µL for severe anaemia: −93, 95% CI: −204–17, P trend = 0.02). The potential child health risks associated with maternal anaemia and iron deficiency may not be limited to the prenatal period. Efforts to reduce maternal anaemia and iron deficiency during pregnancy may need to be expanded to include the post‐partum period.</abstract><subject lang="en"><genre>keywords</genre><topic>anaemia</topic><topic>iron deficiency</topic><topic>post‐natal</topic><topic>HIV</topic><topic>child</topic></subject><relatedItem type="host"><titleInfo><title>Maternal & Child Nutrition</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">1740-8695</identifier><identifier type="eISSN">1740-8709</identifier><identifier type="DOI">10.1111/(ISSN)1740-8709</identifier><identifier type="PublisherID">MCN</identifier><part><date>2012</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>287</start><end>298</end><total>12</total></extent></part></relatedItem><identifier type="istex">C251351EF66A46770FB7C50CCD82D3143B31B201</identifier><identifier type="ark">ark:/67375/WNG-70XRL16N-1</identifier><identifier type="DOI">10.1111/j.1740-8709.2011.00389.x</identifier><identifier type="ArticleID">MCN389</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2012 Blackwell Publishing Ltd</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/C251351EF66A46770FB7C50CCD82D3143B31B201/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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