Population prevalence and risk factors for iron deficiency in Auckland, New Zealand

Aim:  Previous prevalence estimates of iron deficiency (ID) in young New Zealand children are inaccurate because of sampling bias and imprecise definition of ID. The aim of this study was to estimate the prevalence of ID in children aged 6–23 months and the factors associated with ID. Methods:  An e...

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Published inJournal of paediatrics and child health Vol. 43; no. 7-8; pp. 532 - 538
Main Authors Grant, Cameron C, Wall, Clare R, Brunt, Deborah, Crengle, Sue, Scragg, Robert
Format Journal Article
LanguageEnglish
Published Melbourne, Australia Blackwell Publishing Asia 01.07.2007
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Abstract Aim:  Previous prevalence estimates of iron deficiency (ID) in young New Zealand children are inaccurate because of sampling bias and imprecise definition of ID. The aim of this study was to estimate the prevalence of ID in children aged 6–23 months and the factors associated with ID. Methods:  An ethnically stratified sample identified from random residential address start points. Children resident in Auckland, New Zealand were enrolled from 1999 to 2002. Children with elevated C‐reactive protein (>4 mg/L) were excluded. Iron status was determined in 324 (78%) of 416 enrolled children. Analyses adjusted for clustering and weighted for ethnic stratification. ID defined as abnormal values for two or more of serum ferritin (<10 µg/L), iron saturation (<10%) and mean cell volume (<73 fl). Results:  ID was present in 14% (95% confidence interval (CI) 9–17%). ID prevalence varied with ethnicity (Maori 20%, Pacific 17%, other 27%, New Zealand European 7%, P = 0.005), but not with social deprivation. In a multivariate analysis that adjusted for low birthweight, there was an increased risk of ID associated with a body mass index ≥ 18.5 kg/m2 (RR = 4.34, 95% CI 1.08–10.67), and with receiving no infant or follow on formula (RR = 3.60, 95% CI 1.56–6.49). Conclusions:  ID is prevalent in young New Zealand children. Variance in ID prevalence with ethnicity but not social deprivation implies that cultural practices influence iron status. Young children with more rapid growth are at increased risk of ID as are those receiving milk other than that specifically modified for them.
AbstractList Aim:  Previous prevalence estimates of iron deficiency (ID) in young New Zealand children are inaccurate because of sampling bias and imprecise definition of ID. The aim of this study was to estimate the prevalence of ID in children aged 6–23 months and the factors associated with ID. Methods:  An ethnically stratified sample identified from random residential address start points. Children resident in Auckland, New Zealand were enrolled from 1999 to 2002. Children with elevated C‐reactive protein (>4 mg/L) were excluded. Iron status was determined in 324 (78%) of 416 enrolled children. Analyses adjusted for clustering and weighted for ethnic stratification. ID defined as abnormal values for two or more of serum ferritin (<10 µg/L), iron saturation (<10%) and mean cell volume (<73 fl). Results:  ID was present in 14% (95% confidence interval (CI) 9–17%). ID prevalence varied with ethnicity (Maori 20%, Pacific 17%, other 27%, New Zealand European 7%, P = 0.005), but not with social deprivation. In a multivariate analysis that adjusted for low birthweight, there was an increased risk of ID associated with a body mass index ≥ 18.5 kg/m2 (RR = 4.34, 95% CI 1.08–10.67), and with receiving no infant or follow on formula (RR = 3.60, 95% CI 1.56–6.49). Conclusions:  ID is prevalent in young New Zealand children. Variance in ID prevalence with ethnicity but not social deprivation implies that cultural practices influence iron status. Young children with more rapid growth are at increased risk of ID as are those receiving milk other than that specifically modified for them.
Aim:  Previous prevalence estimates of iron deficiency (ID) in young New Zealand children are inaccurate because of sampling bias and imprecise definition of ID. The aim of this study was to estimate the prevalence of ID in children aged 6–23 months and the factors associated with ID. Methods:  An ethnically stratified sample identified from random residential address start points. Children resident in Auckland, New Zealand were enrolled from 1999 to 2002. Children with elevated C‐reactive protein (>4 mg/L) were excluded. Iron status was determined in 324 (78%) of 416 enrolled children. Analyses adjusted for clustering and weighted for ethnic stratification. ID defined as abnormal values for two or more of serum ferritin (<10 µg/L), iron saturation (<10%) and mean cell volume (<73 fl). Results:  ID was present in 14% (95% confidence interval (CI) 9–17%). ID prevalence varied with ethnicity (Maori 20%, Pacific 17%, other 27%, New Zealand European 7%, P  = 0.005), but not with social deprivation. In a multivariate analysis that adjusted for low birthweight, there was an increased risk of ID associated with a body mass index ≥ 18.5 kg/m 2 (RR = 4.34, 95% CI 1.08–10.67), and with receiving no infant or follow on formula (RR = 3.60, 95% CI 1.56–6.49). Conclusions:  ID is prevalent in young New Zealand children. Variance in ID prevalence with ethnicity but not social deprivation implies that cultural practices influence iron status. Young children with more rapid growth are at increased risk of ID as are those receiving milk other than that specifically modified for them.
Aim: Previous prevalence estimates of iron deficiency (ID) in young New Zealand children are inaccurate because of sampling bias and imprecise definition of ID. The aim of this study was to estimate the prevalence of ID in children aged 6-23 months and the factors associated with ID. Methods: An ethnically stratified sample identified from random residential address start points. Children resident in Auckland, New Zealand were enrolled from 1999 to 2002. Children with elevated C-reactive protein (>4 mg-L) were excluded. Iron status was determined in 324 (78%) of 416 enrolled children. Analyses adjusted for clustering and weighted for ethnic stratification. ID defined as abnormal values for two or more of serum ferritin (<10 mu g-L), iron saturation (<10%) and mean cell volume (<73 fl). Results: ID was present in 14% (95% confidence interval (CI) 9-17%). ID prevalence varied with ethnicity (Maori 20%, Pacific 17%, other 27%, New Zealand European 7%, P = 0.005), but not with social deprivation. In a multivariate analysis that adjusted for low birthweight, there was an increased risk of ID associated with a body mass index greater than or equal to 18.5 kg-m super(2) (RR = 4.34, 95% CI 1.08-10.67), and with receiving no infant or follow on formula (RR = 3.60, 95% CI 1.56-6.49). Conclusions: ID is prevalent in young New Zealand children. Variance in ID prevalence with ethnicity but not social deprivation implies that cultural practices influence iron status. Young children with more rapid growth are at increased risk of ID as are those receiving milk other than that specifically modified for them.
Previous prevalence estimates of iron deficiency (ID) in young New Zealand children are inaccurate because of sampling bias and imprecise definition of ID. The aim of this study was to estimate the prevalence of ID in children aged 6-23 months and the factors associated with ID. An ethnically stratified sample identified from random residential address start points. Children resident in Auckland, New Zealand were enrolled from 1999 to 2002. Children with elevated C-reactive protein (>4 mg/L) were excluded. Iron status was determined in 324 (78%) of 416 enrolled children. Analyses adjusted for clustering and weighted for ethnic stratification. ID defined as abnormal values for two or more of serum ferritin (<10 microg/L), iron saturation (<10%) and mean cell volume (<73 fl). ID was present in 14% (95% confidence interval (CI) 9-17%). ID prevalence varied with ethnicity (Maori 20%, Pacific 17%, other 27%, New Zealand European 7%, P = 0.005), but not with social deprivation. In a multivariate analysis that adjusted for low birthweight, there was an increased risk of ID associated with a body mass index >or= 18.5 kg/m(2) (RR = 4.34, 95% CI 1.08-10.67), and with receiving no infant or follow on formula (RR = 3.60, 95% CI 1.56-6.49). ID is prevalent in young New Zealand children. Variance in ID prevalence with ethnicity but not social deprivation implies that cultural practices influence iron status. Young children with more rapid growth are at increased risk of ID as are those receiving milk other than that specifically modified for them.
AIMPrevious prevalence estimates of iron deficiency (ID) in young New Zealand children are inaccurate because of sampling bias and imprecise definition of ID. The aim of this study was to estimate the prevalence of ID in children aged 6-23 months and the factors associated with ID.METHODSAn ethnically stratified sample identified from random residential address start points. Children resident in Auckland, New Zealand were enrolled from 1999 to 2002. Children with elevated C-reactive protein (>4 mg/L) were excluded. Iron status was determined in 324 (78%) of 416 enrolled children. Analyses adjusted for clustering and weighted for ethnic stratification. ID defined as abnormal values for two or more of serum ferritin (<10 microg/L), iron saturation (<10%) and mean cell volume (<73 fl).RESULTSID was present in 14% (95% confidence interval (CI) 9-17%). ID prevalence varied with ethnicity (Maori 20%, Pacific 17%, other 27%, New Zealand European 7%, P = 0.005), but not with social deprivation. In a multivariate analysis that adjusted for low birthweight, there was an increased risk of ID associated with a body mass index >or= 18.5 kg/m(2) (RR = 4.34, 95% CI 1.08-10.67), and with receiving no infant or follow on formula (RR = 3.60, 95% CI 1.56-6.49).CONCLUSIONSID is prevalent in young New Zealand children. Variance in ID prevalence with ethnicity but not social deprivation implies that cultural practices influence iron status. Young children with more rapid growth are at increased risk of ID as are those receiving milk other than that specifically modified for them.
Author Wall, Clare R
Crengle, Sue
Brunt, Deborah
Scragg, Robert
Grant, Cameron C
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  surname: Scragg
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  organization: Epidemiology and Biostatistics, University of Auckland
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2002; 51
2002; 5
1997; 110
1997; 277
1984; 104
2000; 20
2002; 99
1992; 105
1997
1996
1995
2003; 39
2005
2003
2002
1985; 42
2003; 73
2003; 111
1998; 47
1971; 74
1992; 90
2004; 58
1999; 281
1974; 80
1995; 127
1999; 112
1996; 5
1994; 107
1996; 20
1999; 318
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Rive S (e_1_2_7_12_2) 1996; 109
Statistics New Zealand. (e_1_2_7_19_2) 2003
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e_1_2_7_16_2
e_1_2_7_41_2
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e_1_2_7_43_2
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e_1_2_7_44_2
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Snippet Aim:  Previous prevalence estimates of iron deficiency (ID) in young New Zealand children are inaccurate because of sampling bias and imprecise definition of...
Previous prevalence estimates of iron deficiency (ID) in young New Zealand children are inaccurate because of sampling bias and imprecise definition of ID. The...
Aim:  Previous prevalence estimates of iron deficiency (ID) in young New Zealand children are inaccurate because of sampling bias and imprecise definition of...
Aim: Previous prevalence estimates of iron deficiency (ID) in young New Zealand children are inaccurate because of sampling bias and imprecise definition of...
AIMPrevious prevalence estimates of iron deficiency (ID) in young New Zealand children are inaccurate because of sampling bias and imprecise definition of ID....
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crossref
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wiley
istex
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Publisher
StartPage 532
SubjectTerms anaemia iron deficiency
Anemia, Iron-Deficiency - epidemiology
Body Mass Index
child
diet
ethnic group
Ethnic Groups
Humans
Infant
Infant Nutrition Disorders - epidemiology
Infant Nutritional Physiological Phenomena
iron
Iron - blood
Multivariate Analysis
New Zealand
Prevalence
Risk Factors
Title Population prevalence and risk factors for iron deficiency in Auckland, New Zealand
URI https://api.istex.fr/ark:/67375/WNG-WFXQ5XV1-S/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1440-1754.2007.01129.x
https://www.ncbi.nlm.nih.gov/pubmed/17635681
https://search.proquest.com/docview/20738089
https://search.proquest.com/docview/70749979
Volume 43
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