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Preconceptual Health
Published in Michelle Tollefson, Nancy Eriksen, Neha Pathak, Improving Women's Health Across the Lifespan, 2021
Nancy L. Eriksen, Kristi R. VanWinden, John McHugh
Iodine deficiency has largely not been a problem in developing countries until recently. Over the last few decades, the number of reproductive-age women who are iodine deficient has increased nearly seven times.85 Most likely this is due to increased consumption of non-iodized salt in Western countries. Iodine is important for proper metabolic function primarily via the thyroid gland. Lack of iodine during pregnancy can result in a severe form of growth and developmental disabilities known as cretinism. The RDA is 150 μg per day, the amount in one half teaspoon of iodized salt.84 However, the American Thyroid Association recommends women planning to become pregnant consume 220–290 μg /day of iodine to account for pregnancy and fetal requirements.85 Good plant-based sources of iodine include sea vegetables and plants grown in iodine-rich soil.
Thyroid disease
Published in Judy Bothamley, Maureen Boyle, Medical Conditions Affecting Pregnancy and Childbirth, 2020
Pregnancy is characterised by a significant demand for iodine with thyroid iodine uptake increasing. However, more iodine is excreted through renal clearance subsequent to the increased glomerular filtration rate of pregnancy and there is transfer of iodine to the developing fetus (Blackburn, 2007; Girling, 2006; Ramsey, 1998). The thyroid gland compensates for the increased loss of iodine by enlarging. Kenyon and Nelson-Piercy (2005) suggest a physiological goitre (enlarged thyroid) may be seen on ultrasound, but it would not be apparent when looking at the woman. A goitre that is clinically apparent suggests an iodine deficiency or some other kind of pathology. In women with severe iodine deficiency, trapping mechanisms override fetal demand, conserving iodine for maternal use but resulting in fetal cretinism (poor growth and mental retardation).
The endocrine system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Hypothyroisim in infancy is called cretinism. Normal brain development is dependent on the presence of thyroid hormones. Children with a lack of thyroid hormone show learning disabilities, neuromuscular abnormalities, and retarded growth. The causes of cretinism include severe iodine deficiency and rare inherited conditions affecting enzymes involved in thyroid hormone synthesis. Rarely, thyroid agenesis or hypoplasia can occur. Early diagnosis of cretinism is essential, because prompt hormone replacement is potentially curative.
Availability of adequately iodised salt at household level and its associated factors in Robe town, Bale Zone, South East Ethiopia: community-based cross-sectional study
Published in South African Journal of Clinical Nutrition, 2020
Nagasa Dida, Abiyot Legese, Abdurhim Aman, Bilkisa Muhamed, Teshome Damise, Tizita Birhanu, Sintayehu Hailu, Jiregna Darega, Bedasa Woldamichael, Eshetu Gadisa
Iodine deficiency is the world’s major cause of preventable mental retardation.4,6 Around 2 billion people in 130 countries worldwide have insufficient intakes of iodine. Europe (57%), the Eastern Mediterranean (54%), Africa (43%), Southeast Asia (40%), the Western Pacific (24%), and the Americas (10%) are the countries most affected.4,7 Nearly 38 million newborns in developing countries every year remain unprotected from the lifelong effect of brain damage due to iodine deficiency disorders (IDD).8 In Africa about 260 million people have inadequate iodine intake resulting in iodine deficiency states, which may be related to a 10–15% lowering of average intellectual capacity.9 Severity of iodine deficiency can range from mild intellectual blunting to frank cretinism. Impairment of the developing brain results in individuals being poorly equipped to achieve their intellectual potential, work effectively and have healthy birth outcomes. The consequences of iodine deficiency disorders affect all stages of life from foetus to adulthood as well as old age.4,8,10
Trimester-specific reference intervals of thyroid function tests in Turkish pregnants
Published in Gynecological Endocrinology, 2020
Oktay Bulur, Zeliha Atak, Derun Taner Ertugrul, Esin Beyan, Emre Gunakan, Serdar Karakaya, Kubilay Sahin, Kursat Dal
Physiological adaptations and changes in hormone levels occur in thyroid gland during pregnancy. Recognizable changes in thyroid gland are both morphological and physiological. Thyroid gland enlarges in pregnancy. Thyroid-binding globulin, plasma volume, type III 5– deiodinase, iodine clearance, and human chorionic gonadotrophin (β-hCG) levels increase. These adaptations result to a rise in total T4, total T3, free T4, T4, and T3 pool size according to requirement for increased production of these hormones, and decrease in TSH, serum thyroglobulin. Thyroid dysfunction during pregnancy is common, with a prevalence of 2–4% [1,2].Thyroid dysfunctions in pregnancy may cause worst consequences like gestational hypertension, low birth weight, low APGAR score, cretinism, abruptio placenta, fetal and neonatal death, respiratory distress syndrome, and necrotizing enterocolitis [3,4]. Therefore, screening of the thyroid hormone levels are important during follow-up of pregnancy. Due to physiological changes during trimesters in pregnancy, clinicians need trimester-specific reference intervals. For this purpose, several clinical studies have been done in different countries, and several guidelines were proposed for pregnancy. But there is no consensus on reference intervals because there are differences in thyroid function reference intervals between different populations. American Thyroid Association (ATA), European Thyroid Association (ETA), and the Endocrine Society (ES) guidelines recommend the use of trimester-specific reference ranges indigenous to populations [5–7]. The aim of this study is to determine trimester-specific thyroid function reference intervals for pregnancy in Turkish population.
Toward a science-based testing strategy to identify maternal thyroid hormone imbalance and neurodevelopmental effects in the progeny – part I: which parameters from human studies are most relevant for toxicological assessments?
Published in Critical Reviews in Toxicology, 2020
Ursula G. Sauer, Alex Asiimwe, Philip A. Botham, Alex Charlton, Nina Hallmark, Sylvia Jacobi, Sue Marty, Stephanie Melching-Kollmuss, Joana A. Palha, Volker Strauss, Bennard van Ravenzwaay, Gerard Swaen
The present first review addressing the human evidence on how lower maternal thyroid hormone levels affect child neurodevelopment was aligned with the topics of Appendix A of the EFSA and ECHA (2018) Guidance. With respect to maternal serum parameters, hypothyroidism (low fT4 with concordant high TSH) and hypothyroxinaemia (isolated low fT4) were addressed. Importantly, focus is not on severe states of congenital hypothyroidism caused by e.g. pronounced maternal iodine deficiency leading to cretinism (Boyages and Halpern 1993), but rather on more subtle effects on maternal thyroid function.