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 in | Journal of paediatrics and child health Vol. 43; no. 7-8; pp. 532 - 538 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Melbourne, Australia
Blackwell Publishing Asia
01.07.2007
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Subjects | |
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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. |
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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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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/17635681$$D View this record in MEDLINE/PubMed |
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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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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 |
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