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Postnatal anemia and iron deficiency in HIV-infected women and the health and survival of their children

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Postnatal anemia 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. Fawzi

Source :

RBID : PMC:3330171

Abstract

Prenatal iron supplementation may improve pregnancy outcomes and decrease the risk of child mortality. However, little is known about the importance of postnatal maternal iron status for child health and survival, particularly in the context of HIV infection. We examined the association of maternal anemia 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 anemia 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 anemia and hypochromic microcytosis were associated with greater risk of child mortality (HR for severe anemia=2.58, 95% 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 anemia was not significantly associated with greater risk of child HIV infection (HR for severe anemia=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 anemia:-93, 95% CI: -204-17, P trend=0.02). The potential child health risks associated with maternal anemia and iron deficiency may not be limited to the prenatal period. Efforts to reduce maternal anemia and iron deficiency during pregnancy may need to be expanded to include the postpartum period.


Url:
DOI: 10.1111/j.1740-8709.2011.00389.x
PubMed: 22236211
PubMed Central: 3330171

Links to Exploration step

PMC:3330171

Le document en format XML

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<p id="P1">Prenatal iron supplementation may improve pregnancy outcomes and decrease the risk of child mortality. However, little is known about the importance of postnatal maternal iron status for child health and survival, particularly in the context of HIV infection. We examined the association of maternal anemia 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 anemia 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 anemia and hypochromic microcytosis were associated with greater risk of child mortality (HR for severe anemia=2.58, 95% CI: 1.66-4.01,
<italic>P</italic>
trend<0.0001; HR for severe hypochromic microcytosis=2.36, 95% CI: 1.27-4.38,
<italic>P</italic>
trend=0.001). Maternal anemia was not significantly associated with greater risk of child HIV infection (HR for severe anemia=1.46, 95% CI: 0.91, 2.33,
<italic>P</italic>
trend=0.08) but predicted lower CD4 T-cell counts among HIV-uninfected children (difference in CD4 T-cell count/μL for severe anemia:-93, 95% CI: -204-17,
<italic>P</italic>
trend=0.02). The potential child health risks associated with maternal anemia and iron deficiency may not be limited to the prenatal period. Efforts to reduce maternal anemia and iron deficiency during pregnancy may need to be expanded to include the postpartum period.</p>
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<contrib contrib-type="author">
<name>
<surname>Isanaka</surname>
<given-names>Sheila</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
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<name>
<surname>Spiegelman</surname>
<given-names>Donna</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A3">3</xref>
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<name>
<surname>Aboud</surname>
<given-names>Said</given-names>
</name>
<xref ref-type="aff" rid="A4">4</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Manji</surname>
<given-names>Karim P.</given-names>
</name>
<xref ref-type="aff" rid="A5">5</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Msamanga</surname>
<given-names>Gernard I.</given-names>
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<surname>Willet</surname>
<given-names>Walter C.</given-names>
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<name>
<surname>Duggan</surname>
<given-names>Christopher</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A8">8</xref>
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<name>
<surname>Fawzi</surname>
<given-names>Wafaie W.</given-names>
</name>
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Department of Epidemiology, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02215</aff>
<aff id="A2">
<label>2</label>
Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02215</aff>
<aff id="A3">
<label>3</label>
Department of Biostatistics, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02215</aff>
<aff id="A4">
<label>4</label>
Department of Microbiology and Immunology, Muhimbili University of Health and Allied Sciences, P.O. Box 65001, Dar es Salaam, Tanzania</aff>
<aff id="A5">
<label>5</label>
Department of Pediatrics and Child Health, Muhimbili University of Health and Allied Sciences, P.O. Box 65001, Dar es Salaam, Tanzania</aff>
<aff id="A6">
<label>6</label>
Department of Community Health, Muhimbili University of Health and Allied Sciences, P.O. Box 65001, Dar es Salaam, Tanzania</aff>
<aff id="A7">
<label>7</label>
Channing Laboratory, Harvard Medical School, Department of Medicine, 181 Longwood Avenue, Boston, MA 02115</aff>
<aff id="A8">
<label>8</label>
Division of Gastroenterology and Nutrition, Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115</aff>
<aff id="A9">
<label>9</label>
Department of Global Health and Population, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02215</aff>
<author-notes>
<corresp id="FN1">Corresponding author: S. Isanaka, Harvard School of Public Health, Department of Nutrition, 665 Huntington Avenue, Boston, MA, 02115, Phone: 202 487 0441, Fax: 617 432 2435,
<email>sisanaka@hsph.harvard.edu</email>
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<pub-date pub-type="nihms-submitted">
<day>14</day>
<month>12</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="epub">
<day>11</day>
<month>1</month>
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</pub-date>
<pub-date pub-type="ppub">
<month>7</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>01</day>
<month>7</month>
<year>2013</year>
</pub-date>
<volume>8</volume>
<issue>3</issue>
<fpage>287</fpage>
<lpage>298</lpage>
<abstract>
<p id="P1">Prenatal iron supplementation may improve pregnancy outcomes and decrease the risk of child mortality. However, little is known about the importance of postnatal maternal iron status for child health and survival, particularly in the context of HIV infection. We examined the association of maternal anemia 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 anemia 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 anemia and hypochromic microcytosis were associated with greater risk of child mortality (HR for severe anemia=2.58, 95% CI: 1.66-4.01,
<italic>P</italic>
trend<0.0001; HR for severe hypochromic microcytosis=2.36, 95% CI: 1.27-4.38,
<italic>P</italic>
trend=0.001). Maternal anemia was not significantly associated with greater risk of child HIV infection (HR for severe anemia=1.46, 95% CI: 0.91, 2.33,
<italic>P</italic>
trend=0.08) but predicted lower CD4 T-cell counts among HIV-uninfected children (difference in CD4 T-cell count/μL for severe anemia:-93, 95% CI: -204-17,
<italic>P</italic>
trend=0.02). The potential child health risks associated with maternal anemia and iron deficiency may not be limited to the prenatal period. Efforts to reduce maternal anemia and iron deficiency during pregnancy may need to be expanded to include the postpartum period.</p>
</abstract>
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<funding-group>
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<funding-source country="United States">National Institute of Child Health & Human Development : NICHD</funding-source>
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