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      High prevalence of iodine deficiency in pregnant women living in adequate iodine area

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          Abstract

          Objectives

          Iodine deficiency during pregnancy is associated with obstetric and neonatal adverse outcomes. Serum thyroglobulin (sTg) and thyroid volume (TV) are optional tools to urinary iodine concentration (UIC) for defining iodine status. This cross-sectional study aims to evaluate the iodine status of pregnant women living in iodine-adequate area by spot UIC and correlation with sTg, TV and thyroid function.

          Methods

          Two hundred and seventy-three pregnant women were evaluated at three trimesters. All had no previous thyroid disease, no iodine supplementation and negative thyroperoxidase and thyroglobulin antibodies. Thyroid function and sTg were measured using electrochemiluminescence immunoassays. TV was determined by ultrasonography; UIC was determined using a modified Sandell–Kolthoff method.

          Results

          Median UIC was 146 µg/L, being 52% iodine deficient and only 4% excessive. TSH values were 1.50 ± 0.92, 1.50 ± 0.92 and 1.91 ± 0.96 mIU/L, respectively, in each trimester ( P = 0.001). sTg did not change significantly during trimesters with median 11.2 ng/mL and only 3.3% had above 40 ng/mL. Mean TV was 9.3 ± 3.4 mL, which positively correlated with body mass index, but not with sTg. Only 4.5% presented with goitre.

          When pregnant women were categorized as iodine deficient (UIC < 150 µg/L), adequate (≥150 and <250 µg/L) and excessive (≥250 µg/L), sTg, thyroid hormones and TV at each trimester showed no statistical differences.

          Conclusions

          Iodine deficiency was detected frequently in pregnant women living in iodine-adequate area. sTg concentration and TV did not correlate to UIC. Our observation also demonstrated that the Brazilian salt-iodization programme prevents deficiency, but does not maintain iodine status within adequate and recommended ranges for pregnant women.

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          Most cited references15

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          Iodine deficiency.

          Iodine deficiency has multiple adverse effects in humans, termed iodine deficiency disorders, due to inadequate thyroid hormone production. Globally, it is estimated that 2 billion individuals have an insufficient iodine intake, and South Asia and sub-Saharan Africa are particularly affected. However, about 50% of Europe remains mildly iodine deficient, and iodine intakes in other industrialized countries, including the United States and Australia, have fallen in recent years. Iodine deficiency during pregnancy and infancy may impair growth and neurodevelopment of the offspring and increase infant mortality. Deficiency during childhood reduces somatic growth and cognitive and motor function. Assessment methods include urinary iodine concentration, goiter, newborn TSH, and blood thyroglobulin. But assessment of iodine status in pregnancy is difficult, and it remains unclear whether iodine intakes are sufficient in this group, leading to calls for iodine supplementation during pregnancy in several industrialized countries. In most countries, the best strategy to control iodine deficiency in populations is carefully monitored universal salt iodization, one of the most cost-effective ways to contribute to economic and social development. Achieving optimal iodine intakes from iodized salt (in the range of 150-250 microg/d for adults) may minimize the amount of thyroid dysfunction in populations. Ensuring adequate iodine status during parenteral nutrition has become important, particularly in preterm infants, as the use of povidone-iodine disinfectants has declined. Introduction of iodized salt to regions of chronic iodine deficiency may transiently increase the incidence of thyroid disorders, but overall, the relatively small risks of iodine excess are far outweighed by the substantial risks of iodine deficiency.
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            Ten repeat collections for urinary iodine from spot samples or 24-hour samples are needed to reliably estimate individual iodine status in women.

            Although the median urinary iodine concentration (UIC) is a good indicator of iodine status in populations, there is no established biomarker for individual iodine status. If the UIC were to be used to assess individuals, it is unclear how many repeat urine collections would be needed and if the collections should be spot samples or 24-h samples. In a prospective, longitudinal, 15-mo study, healthy Swiss women (n = 22) aged 52-77 y collected repeated 24-h urine samples (total n = 341) and corresponding fasting, second-void, morning spot urine samples (n = 177). From the UIC in spot samples, 24-h urinary iodine excretion (UIE) was extrapolated based on the age- and sex-adjusted iodine:creatinine ratio. Measured UIE in 24-h samples, estimated 24-h UIE, and UIC in spot samples were (geometric mean ± SD) 103 ± 28 μg/24 h, 86 ± 33 μg/24 h, and 68 ± 28 μg/L, respectively, with no seasonal differences. Intra-individual variation (mean CV) was comparable for measured UIE (32%) and estimated UIE (33%). The CV tended to be higher for the spot UIC (38%) than for the estimated 24-h UIE (33%) (P = 0.12). In this population, 10 spot urine samples or 24-h urine samples were needed to assess individual iodine status with 20% precision. Spot samples would likely be preferable because of their ease of collection. However, the large number of repeated urine samples needed to estimate individual iodine status is a major limitation and emphasizes the need for further investigation of more practical biomarkers of individual iodine status.
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              Iodine deficiency and brain development in the first half of pregnancy.

              An inadequate supply of iodine during gestation results in damage to the foetal brain that is irreversible by mid-gestation unless timely interventions can correct the accompanying maternal hypothyroxinemia. Even mild to moderate maternal hypothyroxinemia may result in suboptimal neurodevelopment. This review mainly focuses on iodine and thyroid hormone economy up to mid-gestation, a period during which the mother is the only source for the developing brain of the foetus. The cerebral cortex of the foetus depends on maternal thyroxine (T4) for the production of the 3',3,5-tri-iodothyronine (T3) for nuclear receptor-binding and biological effectiveness. Maternal hypothyroxinemia early in pregnancy is potentially damaging for foetal brain development. Direct evidence has been obtained from experiments on animals: even a relatively mild and transient hypothyroxinemia during corticogenesis, which takes place mostly before mid-gestation in humans, affects the migration of radial neurons, which settle permanently in heterotopic locations within the cortex and hippocampus. Behavioural defects have also been detected. The conceptus imposes important early changes on maternal thyroid hormone economy that practically doubles the amount of T4 secreted something that requires a concordant increase in the availability of iodine, from 150 to 250-300 microg I day- 1. Women who are unable to increase their production of T4 early in pregnancy constitute a population at risk for having children with neurological disabilities. As a mild to moderate iodine deficiency is still the most widespread cause of maternal hypothyroxinemia, the birth of many children with learning disabilities may be prevented by advising women to take iodine supplements as soon as pregnancy starts, or earlier if possible, in order to ensure that their requirements for iodine are met.

                Author and article information

                Journal
                Endocr Connect
                Endocr Connect
                EC
                Endocrine Connections
                Bioscientifica Ltd (Bristol )
                2049-3614
                May 2018
                26 April 2018
                : 7
                : 5
                : 762-767
                Affiliations
                [1 ]Thyroid Unit Division of Endocrinology and Metabolism, Hospital das Clinicas HCFMUSP-Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Sao Paulo, Brazil
                [2 ]Ultrasound Unit Department of Radiology, Hospital das Clinicas HCFMUSP-Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Sao Paulo, Brazil
                [3 ]Clinic of the Paraisópolis Community Einstein Project Jewish School of Health Sciences Albert Einstein, Sao Paulo, Sao Paulo, Brazil
                [4 ]Hematology and Biochemistry Center of Pathology, Adolfo Lutz Institute, Sao Paulo, Sao Paulo, Brazil
                Author notes
                Correspondence should be addressed to S Marui: suemimar@ 123456usp.br
                Article
                EC180131
                10.1530/EC-18-0131
                5958744
                29700098
                41b26d3b-fd0b-4694-8eb5-00fea0b17762
                © 2018 The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 23 April 2018
                : 26 April 2018
                Categories
                Research

                iodine,pregnancy,thyroglobulin,thyroid function tests
                iodine, pregnancy, thyroglobulin, thyroid function tests

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