Correlating maternal iodine status with neonatal thyroid function in two hospital populations in Ghana: a multicenter cross-sectional pilot study
Congenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs play an important role in the early detection and treatment of congenital hypothyroidism. However, an estimated 71% of children are born in countries such as Ghana...
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Published in | BMC pediatrics Vol. 20; no. 1; p. 26 |
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Language | English |
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21.01.2020
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Abstract | Congenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs play an important role in the early detection and treatment of congenital hypothyroidism. However, an estimated 71% of children are born in countries such as Ghana, which does not have a screening program. Iodine deficiency, a common cause of congenital hypothyroidism, is present in the Ghanaian population. Mild to moderate maternal iodine deficiency may negatively impact cognitive function in children. A structured approach to examine the association between maternal iodine levels and infant thyroid function may have important ramifications on our understanding of congenital hypothyroidism in Ghana. We investigated the hypothesis that maternal iodine deficiency impacts infant thyroid function, using Thyroid Stimulating Hormone (TSH) as a marker of thyroid function. We also explored potential opportunities and barriers to newborn screening for congenital hypothyroidism in Ghana.
This was a cross-sectional, multicenter pilot study of 250 women and their neonates recruited from post-natal clinics in Accra and Tamale, Ghana. We compared maternal urine iodine concentration and infant TSH, as well as maternal sociodemographic and nutrition information. Regression models were used to model the relationship between variables.
Median infant TSH was 4.7 μIU/ml (95% CI: 3.9-5.5) in Accra. In Tamale, the median infant TSH was 3.5 μIU/ml (95%CI: 3.3 to 3.6) (Δ: 1.3 μIU/ml, 95% CI: 0.5-2.1, p = 0.002). Median maternal urine iodine concentrations were 141.0 μg/L (95% CI: 115.7 to 166.3) and 142.5 μg/L (95% CI: 125.1 to 160.0) in Accra and Tamale, respectively (Δ: - 1.5 μIU/ml, 95% CI: - 32.2 - 29.2, p = 0.925). There was a weakly positive correlation between maternal urine iodine and infant TSH (rho 0.1, p = 0.02). Almost one-third (30%) of women in both locations had biochemical evidence of iodine deficiency. Mothers with any formal education were more likely to have higher iodine levels than their counterparts who had no formal education (coefficient 0.31, p = 0.006).
Maternal iodine deficiency is prevalent in Ghana and is correlated to infant thyroid function. We recommend studies with larger sample sizes to assess the true scope of this relationship. |
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AbstractList | Background Congenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs play an important role in the early detection and treatment of congenital hypothyroidism. However, an estimated 71% of children are born in countries such as Ghana, which does not have a screening program. Iodine deficiency, a common cause of congenital hypothyroidism, is present in the Ghanaian population. Mild to moderate maternal iodine deficiency may negatively impact cognitive function in children. A structured approach to examine the association between maternal iodine levels and infant thyroid function may have important ramifications on our understanding of congenital hypothyroidism in Ghana. We investigated the hypothesis that maternal iodine deficiency impacts infant thyroid function, using Thyroid Stimulating Hormone (TSH) as a marker of thyroid function. We also explored potential opportunities and barriers to newborn screening for congenital hypothyroidism in Ghana. Methods This was a cross-sectional, multicenter pilot study of 250 women and their neonates recruited from post-natal clinics in Accra and Tamale, Ghana. We compared maternal urine iodine concentration and infant TSH, as well as maternal sociodemographic and nutrition information. Regression models were used to model the relationship between variables. Results Median infant TSH was 4.7 [mu]IU/ml (95% CI: 3.9-5.5) in Accra. In Tamale, the median infant TSH was 3.5 [mu]IU/ml (95%CI: 3.3 to 3.6) ([DELA]: 1.3 [mu]IU/ml, 95% CI: 0.5-2.1, p = 0.002). Median maternal urine iodine concentrations were 141.0 [mu]g/L (95% CI: 115.7 to 166.3) and 142.5 [mu]g/L (95% CI: 125.1 to 160.0) in Accra and Tamale, respectively ([DELA]: - 1.5 [mu]IU/ml, 95% CI: - 32.2 - 29.2, p = 0.925). There was a weakly positive correlation between maternal urine iodine and infant TSH (rho 0.1, p = 0.02). Almost one-third (30%) of women in both locations had biochemical evidence of iodine deficiency. Mothers with any formal education were more likely to have higher iodine levels than their counterparts who had no formal education (coefficient 0.31, p = 0.006). Conclusions Maternal iodine deficiency is prevalent in Ghana and is correlated to infant thyroid function. We recommend studies with larger sample sizes to assess the true scope of this relationship. Keywords: Iodine deficiency, Congenital hypothyroidism, Ghana Congenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs play an important role in the early detection and treatment of congenital hypothyroidism. However, an estimated 71% of children are born in countries such as Ghana, which does not have a screening program. Iodine deficiency, a common cause of congenital hypothyroidism, is present in the Ghanaian population. Mild to moderate maternal iodine deficiency may negatively impact cognitive function in children. A structured approach to examine the association between maternal iodine levels and infant thyroid function may have important ramifications on our understanding of congenital hypothyroidism in Ghana. We investigated the hypothesis that maternal iodine deficiency impacts infant thyroid function, using Thyroid Stimulating Hormone (TSH) as a marker of thyroid function. We also explored potential opportunities and barriers to newborn screening for congenital hypothyroidism in Ghana. This was a cross-sectional, multicenter pilot study of 250 women and their neonates recruited from post-natal clinics in Accra and Tamale, Ghana. We compared maternal urine iodine concentration and infant TSH, as well as maternal sociodemographic and nutrition information. Regression models were used to model the relationship between variables. Median infant TSH was 4.7 μIU/ml (95% CI: 3.9-5.5) in Accra. In Tamale, the median infant TSH was 3.5 μIU/ml (95%CI: 3.3 to 3.6) (Δ: 1.3 μIU/ml, 95% CI: 0.5-2.1, p = 0.002). Median maternal urine iodine concentrations were 141.0 μg/L (95% CI: 115.7 to 166.3) and 142.5 μg/L (95% CI: 125.1 to 160.0) in Accra and Tamale, respectively (Δ: - 1.5 μIU/ml, 95% CI: - 32.2 - 29.2, p = 0.925). There was a weakly positive correlation between maternal urine iodine and infant TSH (rho 0.1, p = 0.02). Almost one-third (30%) of women in both locations had biochemical evidence of iodine deficiency. Mothers with any formal education were more likely to have higher iodine levels than their counterparts who had no formal education (coefficient 0.31, p = 0.006). Maternal iodine deficiency is prevalent in Ghana and is correlated to infant thyroid function. We recommend studies with larger sample sizes to assess the true scope of this relationship. Abstract Background Congenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs play an important role in the early detection and treatment of congenital hypothyroidism. However, an estimated 71% of children are born in countries such as Ghana, which does not have a screening program. Iodine deficiency, a common cause of congenital hypothyroidism, is present in the Ghanaian population. Mild to moderate maternal iodine deficiency may negatively impact cognitive function in children. A structured approach to examine the association between maternal iodine levels and infant thyroid function may have important ramifications on our understanding of congenital hypothyroidism in Ghana. We investigated the hypothesis that maternal iodine deficiency impacts infant thyroid function, using Thyroid Stimulating Hormone (TSH) as a marker of thyroid function. We also explored potential opportunities and barriers to newborn screening for congenital hypothyroidism in Ghana. Methods This was a cross-sectional, multicenter pilot study of 250 women and their neonates recruited from post-natal clinics in Accra and Tamale, Ghana. We compared maternal urine iodine concentration and infant TSH, as well as maternal sociodemographic and nutrition information. Regression models were used to model the relationship between variables. Results Median infant TSH was 4.7 μIU/ml (95% CI: 3.9–5.5) in Accra. In Tamale, the median infant TSH was 3.5 μIU/ml (95%CI: 3.3 to 3.6) (Δ: 1.3 μIU/ml, 95% CI: 0.5–2.1, p = 0.002). Median maternal urine iodine concentrations were 141.0 μg/L (95% CI: 115.7 to 166.3) and 142.5 μg/L (95% CI: 125.1 to 160.0) in Accra and Tamale, respectively (Δ: − 1.5 μIU/ml, 95% CI: − 32.2 – 29.2, p = 0.925). There was a weakly positive correlation between maternal urine iodine and infant TSH (rho 0.1, p = 0.02). Almost one-third (30%) of women in both locations had biochemical evidence of iodine deficiency. Mothers with any formal education were more likely to have higher iodine levels than their counterparts who had no formal education (coefficient 0.31, p = 0.006). Conclusions Maternal iodine deficiency is prevalent in Ghana and is correlated to infant thyroid function. We recommend studies with larger sample sizes to assess the true scope of this relationship. Background Congenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs play an important role in the early detection and treatment of congenital hypothyroidism. However, an estimated 71% of children are born in countries such as Ghana, which does not have a screening program. Iodine deficiency, a common cause of congenital hypothyroidism, is present in the Ghanaian population. Mild to moderate maternal iodine deficiency may negatively impact cognitive function in children. A structured approach to examine the association between maternal iodine levels and infant thyroid function may have important ramifications on our understanding of congenital hypothyroidism in Ghana. We investigated the hypothesis that maternal iodine deficiency impacts infant thyroid function, using Thyroid Stimulating Hormone (TSH) as a marker of thyroid function. We also explored potential opportunities and barriers to newborn screening for congenital hypothyroidism in Ghana. Methods This was a cross-sectional, multicenter pilot study of 250 women and their neonates recruited from post-natal clinics in Accra and Tamale, Ghana. We compared maternal urine iodine concentration and infant TSH, as well as maternal sociodemographic and nutrition information. Regression models were used to model the relationship between variables. Results Median infant TSH was 4.7 μIU/ml (95% CI: 3.9–5.5) in Accra. In Tamale, the median infant TSH was 3.5 μIU/ml (95%CI: 3.3 to 3.6) (Δ: 1.3 μIU/ml, 95% CI: 0.5–2.1, p = 0.002). Median maternal urine iodine concentrations were 141.0 μg/L (95% CI: 115.7 to 166.3) and 142.5 μg/L (95% CI: 125.1 to 160.0) in Accra and Tamale, respectively (Δ: − 1.5 μIU/ml, 95% CI: − 32.2 – 29.2, p = 0.925). There was a weakly positive correlation between maternal urine iodine and infant TSH (rho 0.1, p = 0.02). Almost one-third (30%) of women in both locations had biochemical evidence of iodine deficiency. Mothers with any formal education were more likely to have higher iodine levels than their counterparts who had no formal education (coefficient 0.31, p = 0.006). Conclusions Maternal iodine deficiency is prevalent in Ghana and is correlated to infant thyroid function. We recommend studies with larger sample sizes to assess the true scope of this relationship. BACKGROUNDCongenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs play an important role in the early detection and treatment of congenital hypothyroidism. However, an estimated 71% of children are born in countries such as Ghana, which does not have a screening program. Iodine deficiency, a common cause of congenital hypothyroidism, is present in the Ghanaian population. Mild to moderate maternal iodine deficiency may negatively impact cognitive function in children. A structured approach to examine the association between maternal iodine levels and infant thyroid function may have important ramifications on our understanding of congenital hypothyroidism in Ghana. We investigated the hypothesis that maternal iodine deficiency impacts infant thyroid function, using Thyroid Stimulating Hormone (TSH) as a marker of thyroid function. We also explored potential opportunities and barriers to newborn screening for congenital hypothyroidism in Ghana. METHODSThis was a cross-sectional, multicenter pilot study of 250 women and their neonates recruited from post-natal clinics in Accra and Tamale, Ghana. We compared maternal urine iodine concentration and infant TSH, as well as maternal sociodemographic and nutrition information. Regression models were used to model the relationship between variables. RESULTSMedian infant TSH was 4.7 μIU/ml (95% CI: 3.9-5.5) in Accra. In Tamale, the median infant TSH was 3.5 μIU/ml (95%CI: 3.3 to 3.6) (Δ: 1.3 μIU/ml, 95% CI: 0.5-2.1, p = 0.002). Median maternal urine iodine concentrations were 141.0 μg/L (95% CI: 115.7 to 166.3) and 142.5 μg/L (95% CI: 125.1 to 160.0) in Accra and Tamale, respectively (Δ: - 1.5 μIU/ml, 95% CI: - 32.2 - 29.2, p = 0.925). There was a weakly positive correlation between maternal urine iodine and infant TSH (rho 0.1, p = 0.02). Almost one-third (30%) of women in both locations had biochemical evidence of iodine deficiency. Mothers with any formal education were more likely to have higher iodine levels than their counterparts who had no formal education (coefficient 0.31, p = 0.006). CONCLUSIONSMaternal iodine deficiency is prevalent in Ghana and is correlated to infant thyroid function. We recommend studies with larger sample sizes to assess the true scope of this relationship. Congenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs play an important role in the early detection and treatment of congenital hypothyroidism. However, an estimated 71% of children are born in countries such as Ghana, which does not have a screening program. Iodine deficiency, a common cause of congenital hypothyroidism, is present in the Ghanaian population. Mild to moderate maternal iodine deficiency may negatively impact cognitive function in children. A structured approach to examine the association between maternal iodine levels and infant thyroid function may have important ramifications on our understanding of congenital hypothyroidism in Ghana. We investigated the hypothesis that maternal iodine deficiency impacts infant thyroid function, using Thyroid Stimulating Hormone (TSH) as a marker of thyroid function. We also explored potential opportunities and barriers to newborn screening for congenital hypothyroidism in Ghana. This was a cross-sectional, multicenter pilot study of 250 women and their neonates recruited from post-natal clinics in Accra and Tamale, Ghana. We compared maternal urine iodine concentration and infant TSH, as well as maternal sociodemographic and nutrition information. Regression models were used to model the relationship between variables. Median infant TSH was 4.7 [mu]IU/ml (95% CI: 3.9-5.5) in Accra. In Tamale, the median infant TSH was 3.5 [mu]IU/ml (95%CI: 3.3 to 3.6) ([DELA]: 1.3 [mu]IU/ml, 95% CI: 0.5-2.1, p = 0.002). Median maternal urine iodine concentrations were 141.0 [mu]g/L (95% CI: 115.7 to 166.3) and 142.5 [mu]g/L (95% CI: 125.1 to 160.0) in Accra and Tamale, respectively ([DELA]: - 1.5 [mu]IU/ml, 95% CI: - 32.2 - 29.2, p = 0.925). There was a weakly positive correlation between maternal urine iodine and infant TSH (rho 0.1, p = 0.02). Almost one-third (30%) of women in both locations had biochemical evidence of iodine deficiency. Mothers with any formal education were more likely to have higher iodine levels than their counterparts who had no formal education (coefficient 0.31, p = 0.006). Maternal iodine deficiency is prevalent in Ghana and is correlated to infant thyroid function. We recommend studies with larger sample sizes to assess the true scope of this relationship. Abstract Background Congenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs play an important role in the early detection and treatment of congenital hypothyroidism. However, an estimated 71% of children are born in countries such as Ghana, which does not have a screening program. Iodine deficiency, a common cause of congenital hypothyroidism, is present in the Ghanaian population. Mild to moderate maternal iodine deficiency may negatively impact cognitive function in children. A structured approach to examine the association between maternal iodine levels and infant thyroid function may have important ramifications on our understanding of congenital hypothyroidism in Ghana. We investigated the hypothesis that maternal iodine deficiency impacts infant thyroid function, using Thyroid Stimulating Hormone (TSH) as a marker of thyroid function. We also explored potential opportunities and barriers to newborn screening for congenital hypothyroidism in Ghana. Methods This was a cross-sectional, multicenter pilot study of 250 women and their neonates recruited from post-natal clinics in Accra and Tamale, Ghana. We compared maternal urine iodine concentration and infant TSH, as well as maternal sociodemographic and nutrition information. Regression models were used to model the relationship between variables. Results Median infant TSH was 4.7 μIU/ml (95% CI: 3.9–5.5) in Accra. In Tamale, the median infant TSH was 3.5 μIU/ml (95%CI: 3.3 to 3.6) (Δ: 1.3 μIU/ml, 95% CI: 0.5–2.1, p = 0.002). Median maternal urine iodine concentrations were 141.0 μg/L (95% CI: 115.7 to 166.3) and 142.5 μg/L (95% CI: 125.1 to 160.0) in Accra and Tamale, respectively (Δ: − 1.5 μIU/ml, 95% CI: − 32.2 – 29.2, p = 0.925). There was a weakly positive correlation between maternal urine iodine and infant TSH (rho 0.1, p = 0.02). Almost one-third (30%) of women in both locations had biochemical evidence of iodine deficiency. Mothers with any formal education were more likely to have higher iodine levels than their counterparts who had no formal education (coefficient 0.31, p = 0.006). Conclusions Maternal iodine deficiency is prevalent in Ghana and is correlated to infant thyroid function. We recommend studies with larger sample sizes to assess the true scope of this relationship. |
ArticleNumber | 26 |
Audience | Academic |
Author | Aliyu, Muktar H Dei-Tutu, Selorm A Oppong, Samuel A Moore, Daniel J Malechi, Hawa Russell, William E Heimburger, Douglas C Manful, Adoma |
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References | A-R Abizari (1932_CR29) 2017; 20 D Chirawurah (1932_CR15) 2015; 5 1932_CR16 M Moleti (1932_CR18) 2016; 26 JT Dunn (1932_CR11) 2001; 86 1932_CR17 R Sinha (1932_CR5) 2000 RO Nyumuah (1932_CR13) 2012; 33 JF Rovet (1932_CR8) 2014; 26 SC Bath (1932_CR19) 2013; 382 C Buxton (1932_CR14) 2012; 70 DL Simpong (1932_CR27) 2016; 74 SS Chan (1932_CR30) 2003; 13 J Bernal (1932_CR7) 2000 SB Nøhr (1932_CR31) 2000; 85 H Stephen (1932_CR4) 2014; 10 DS Saleh (1932_CR21) 2016; 16 MV Rastogi (1932_CR2) 2010; 5 PA Harris (1932_CR23) 2009; 42 G Ford (1932_CR1) 2014; 28 S Lain (1932_CR20) 2017; 177 1932_CR28 1932_CR25 1932_CR26 AC Ojule (1932_CR24) 1998; 27 J Ehrenkranz (1932_CR22) 2011; 21 AM Giacobbe (1932_CR9) 2015; 292 MB Zimmermann (1932_CR12) 2012; 26 JC Dillon (1932_CR10) 2000; 107 1932_CR3 1932_CR6 |
References_xml | – volume: 26 start-page: 26 year: 2014 ident: 1932_CR8 publication-title: Paediatr Thyroidol doi: 10.1159/000363153 contributor: fullname: JF Rovet – volume: 33 start-page: S293 issue: 4 Suppl year: 2012 ident: 1932_CR13 publication-title: Food Nutr Bull doi: 10.1177/15648265120334S305 contributor: fullname: RO Nyumuah – volume: 20 start-page: 1107 issue: 6 year: 2017 ident: 1932_CR29 publication-title: Public Health Nutr doi: 10.1017/S1368980016003098 contributor: fullname: A-R Abizari – ident: 1932_CR25 – volume: 86 start-page: 2360 issue: 6 year: 2001 ident: 1932_CR11 publication-title: J Clin Endocrinol Metab doi: 10.1210/jcem.86.6.7611 contributor: fullname: JT Dunn – ident: 1932_CR3 doi: 10.1542/peds.2006-0915 – volume: 5 start-page: 17 year: 2010 ident: 1932_CR2 publication-title: Orphanet J Rare Dis doi: 10.1186/1750-1172-5-17 contributor: fullname: MV Rastogi – volume: 10 start-page: 115 issue: 2 year: 2014 ident: 1932_CR4 publication-title: US Endocrinol doi: 10.17925/USE.2014.10.02.115 contributor: fullname: H Stephen – ident: 1932_CR16 – volume: 27 start-page: 57 issue: 1–2 year: 1998 ident: 1932_CR24 publication-title: Nigeria Afr J Med Med Sci contributor: fullname: AC Ojule – volume: 13 start-page: 873 issue: 9 year: 2003 ident: 1932_CR30 publication-title: Thyroid. doi: 10.1089/105072503322401078 contributor: fullname: SS Chan – volume-title: Cellular action of thyroid hormone. In: Feingold KR, Anawalt B, Boyce a, Chrousos G, Dungan K, Grossman a, et al., editors year: 2000 ident: 1932_CR5 contributor: fullname: R Sinha – volume: 16 start-page: 24 year: 2016 ident: 1932_CR21 publication-title: BMC Pediatr doi: 10.1186/s12887-016-0559-0 contributor: fullname: DS Saleh – volume: 26 start-page: 296 issue: 2 year: 2016 ident: 1932_CR18 publication-title: Thyroid Off J Am Thyroid Assoc doi: 10.1089/thy.2015.0336 contributor: fullname: M Moleti – volume: 74 start-page: 8 issue: 1 year: 2016 ident: 1932_CR27 publication-title: Arch Public Health doi: 10.1186/s13690-016-0119-y contributor: fullname: DL Simpong – ident: 1932_CR28 – volume: 107 start-page: 631 issue: 5 year: 2000 ident: 1932_CR10 publication-title: BJOG Int J Obstet Gynaecol doi: 10.1111/j.1471-0528.2000.tb13305.x contributor: fullname: JC Dillon – ident: 1932_CR26 – volume: 26 start-page: 108 issue: Suppl 1 year: 2012 ident: 1932_CR12 publication-title: Paediatr Perinat Epidemiol doi: 10.1111/j.1365-3016.2012.01275.x contributor: fullname: MB Zimmermann – volume: 42 start-page: 377 issue: 2 year: 2009 ident: 1932_CR23 publication-title: J Biomed Inform doi: 10.1016/j.jbi.2008.08.010 contributor: fullname: PA Harris – volume: 382 start-page: 331 issue: 9889 year: 2013 ident: 1932_CR19 publication-title: Lancet Lond Engl doi: 10.1016/S0140-6736(13)60436-5 contributor: fullname: SC Bath – volume: 21 start-page: 183 issue: 2 year: 2011 ident: 1932_CR22 publication-title: Thyroid doi: 10.1089/thy.2009.0358 contributor: fullname: J Ehrenkranz – ident: 1932_CR17 – volume: 292 start-page: 995 issue: 5 year: 2015 ident: 1932_CR9 publication-title: Arch Gynecol Obstet doi: 10.1007/s00404-015-3741-y contributor: fullname: AM Giacobbe – volume: 177 start-page: D1 issue: 5 year: 2017 ident: 1932_CR20 publication-title: Eur J Endocrinol doi: 10.1530/EJE-17-0107 contributor: fullname: S Lain – volume: 85 start-page: 623 issue: 2 year: 2000 ident: 1932_CR31 publication-title: J Clin Endocrinol Metab contributor: fullname: SB Nøhr – volume: 28 start-page: 175 issue: 2 year: 2014 ident: 1932_CR1 publication-title: Best Pract Res Clin Endocrinol Metab doi: 10.1016/j.beem.2013.05.008 contributor: fullname: G Ford – ident: 1932_CR6 – volume: 5 start-page: 70 issue: 3 year: 2015 ident: 1932_CR15 publication-title: Food Public Health contributor: fullname: D Chirawurah – volume-title: Thyroid hormones in brain development and function. In: Feingold KR, Anawalt B, Boyce a, Chrousos G, Dungan K, Grossman a, et al., editors year: 2000 ident: 1932_CR7 contributor: fullname: J Bernal – volume: 70 start-page: 5 issue: 1 year: 2012 ident: 1932_CR14 publication-title: Arch Public Health. doi: 10.1186/0778-7367-70-5 contributor: fullname: C Buxton |
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Snippet | Congenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs play an important role... Abstract Background Congenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs... Background Congenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs play an... BACKGROUNDCongenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs play an... Abstract Background Congenital hypothyroidism is a common, yet easily treatable cause of poor growth and intellectual disability. Newborn screening programs... |
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SubjectTerms | Child Complications and side effects Congenital diseases Congenital hypothyroidism Cross-Sectional Studies Diseases Female Food and nutrition Ghana Ghana - epidemiology Hormones Hospitals Humans Infant, Newborn Intellectual disabilities Iodine Iodine deficiency Iodine deficiency diseases Laboratories Newborn babies Physiological aspects Pilot Projects Pregnant women Risk factors Thyroid Gland Thyrotropin Womens health |
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Title | Correlating maternal iodine status with neonatal thyroid function in two hospital populations in Ghana: a multicenter cross-sectional pilot study |
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