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Background: Autism spectrum disorder (ASD) is a neurodevelopmental condition with unknown etiology. Both genetic and environmental factors have been associated with ASD. Environmental exposures during the prenatal period may play an important role in ASD development. This narrative review critically examines the evidence for a relationship between maternal thyroid dysfunction during pregnancy and ASD in the child. Summary: Studies that assessed the associations of hypothyroidism, hyperthyroidism, hypothyroxinemia, thyroid hormone concentrations, or autoimmune thyroid disease with ASD outcomes were included. Most research focused on the relationship between hypothyroidism and ASD. Multiple population-based studies found that maternal hypothyroidism was associated with higher likelihood of an ASD diagnosis in offspring. Associations with other forms of maternal thyroid dysfunction were less consistent. Findings may have been affected by misclassification bias, survival bias, or publication bias. Studies using medical records may have misclassified subclinical thyroid dysfunction as euthyroidism. Two studies that assessed children at early ages may have misclassified those with ASD as typically developing. Most studies adjusted for maternal body mass index (BMI) and/or mental illness, but not interpregnancy interval or pesticide exposure, all factors associated with fetal survival and ASD. Most studies reported a combination of null and statistically significant findings, although publication bias is still possible. Conclusions: Overall, evidence supported a positive association between maternal thyroid dysfunction during pregnancy and ASD outcomes in the child, especially for hypothyroidism. Future studies could reduce misclassification bias by using laboratory measures instead of medical records to ascertain thyroid dysfunction and evaluating children for ASD at an age when it can be reliably detected. Survival bias could be further mitigated by adjusting models for more factors associated with fetal survival and ASD. Additional research is needed to comprehensively understand the roles of maternal levothyroxine treatment, iodine deficiency, or exposure to thyroid-disrupting compounds in the relationship between maternal thyroid dysfunction and child ASD outcomes.

Ensuring optimal iodine nutrition in pregnant women is a global public health concern. However, there is no direct data on safe tolerable upper intake levels (ULs) for pregnant women. A cross-sectional study was performed to determine the ULs of pregnant women. A total of 744 pregnant women were enrolled in this study. The median (IQR) urinary iodine concentration (UIC) in pregnant women was 150.2 (87.6, 268.0) μg/L, and the urinary iodine excretion (UIE) over 24 h was 204.2 (116.0, 387.0) μg/day. Compared with those with a UIE figure of between 150-250 μg/day, the reference group, the prevalence of thyroid dysfunction was 5.7 times higher (95%CI: 1.7, 19.2) in pregnant women with a UIE figure of between 450-550 μg/day, and 3.9 times higher (95%CI: 1.5, 10.3) in pregnant women with a UIE figure of ≥550 μg/day. Compared with an estimated iodine intake (EII) of between 100-200 μg/day, the reference group, the prevalence of thyroid dysfunction was 4.3 times higher (95%CI: 1.3, 14.4) in pregnant women with a UIE figure of between 500-600 μg/day, and 3.6 times higher (95%CI: 1.5, 8.9) in pregnant women with UIE of ≥600 μg/day. In general, our cross-sectional study found that excessive iodine intake during pregnancy appears to directly increase the risk of thyroid dysfunction. Avoiding chronic iodine intakes of 500 μg/day or higher or having a UIE figure of ≥450 μg/day is recommended for pregnant women in China.

Background Graves' disease occurrence during pregnancy is not a frequent event, showing an incidence of 0.2-0.4% in unselected pregnant women. Depending on their functional properties, TSH-receptor antibodies can induce hypothyroidism or hyperthyroidism. Recognizing the signs of altered thyroid function is essential to prevent possible complications on the fetus. Materials and methods The case of a pregnant woman without previous history of thyroid disease presenting with severe overt hypothyroidism during the first trimester is reported. Levothyroxine therapy was started and 6 weeks later overt hyperthyroidism was observed. TRAb were detected at high titers. Levothyroxine was withdrawn and low dose methimazole was started. Serial obstetric ultrasound scans were negative for indirect signs of fetal thyroid dysfunctions and no fetal goiter was visualized throughout pregnancy. Spontaneous delivery occurred without complications at 39 weeks of gestation. In the post-partum, severe overt hypothyroidism recurred, thus methimazole was discontinued and levothyroxine was restarted. TRAb persisted at high levels. The infant experienced a transient thyrotoxicosis, which fully resolved in three months with normalization of thyroid function and negativization of TRAb levels. Results The present case report allows us to overview the challenges related to the management of hypo and hyperthyroidism in patients with high TRAb levels, requiring strict monitoring aimed at early detection of both maternal and fetal consequences. Conclusions This case underlines the importance of close follow-up and the need of collaboration in a multidisciplinary team when Graves's disease is diagnosed in a pregnant woman to prevent adverse neonatal outcomes.

Objectives: Thyroid autoimmunity is common in pregnant women and associated with thyroid dysfunction and adverse obstetric outcomes. Most studies focus on thyroid peroxidase antibodies (TPOAbs) assessed by a negative-positive dichotomy and rarely take into account thyroglobulin antibodies (TgAbs). This study aimed at determining the association of TPOAbs and TgAbs, respectively, and interdependently, with maternal thyroid function. Methods: This was a meta-analysis of individual participant cross-sectional data from 20 cohorts in the Consortium on Thyroid and Pregnancy. Women with multiple pregnancy, pregnancy by assisted reproductive technology, history of thyroid disease, or use of thyroid interfering medication were excluded. Associations of (log2) TPOAbs and TgAbs (with/without mutual adjustment) with cohort-specific z-scores of (log2) thyrotropin (TSH), free triiodothyronine (fT3), total triiodothyronine (TT3), free thyroxine (fT4), total thyroxine (TT4), or triiodothyronine:thyroxine (T3:T4) ratio were evaluated in a linear mixed model. Results: In total, 51,138 women participated (51,094 had TPOAb-data and 27,874 had TgAb-data). Isolated TPOAb positivity was present in 4.1% [95% confidence interval, CI: 3.0 to 5.2], isolated TgAb positivity in 4.8% [CI: 2.9 to 6.6], and positivity for both antibodies in 4.7% [CI: 3.1 to 6.3]. Compared with antibody-negative women, TSH was higher in women with isolated TPOAb positivity (z-score increment 0.40, CI: 0.16 to 0.64) and TgAb positivity (0.21, CI: 0.10 to 0.32), but highest in those positive for both antibodies (0.54, CI: 0.36 to 0.71). There was a dose-response effect of higher TPOAb and TgAb concentrations with higher TSH (TSH z-score increment for TPOAbs 0.12, CI: 0.09 to 0.15, TgAbs 0.08, CI: 0.02 to 0.15). When adjusting analyses for the other antibody, only the association of TPOAbs remained statistically significant. A higher TPOAb concentration was associated with lower fT4 ( p  < 0.001) and higher T3:T4 ratio (0.09, CI: 0.03 to 0.14), however, the association with fT4 was not significant when adjusting for TgAbs ( p  = 0.16). Conclusions: This individual participant data meta-analysis demonstrated an increase in TSH with isolated TPOAb positivity and TgAb positivity, respectively, which was amplified for individuals positive for both antibodies. There was a dose-dependent association of TPOAbs, but not TgAbs, with TSH when adjusting for the other antibody. This supports current practice of using TPOAbs in initial laboratory testing of pregnant women suspected of autoimmune thyroid disease. However, studies on the differences between TPOAb- and TgAb-positive women are needed to fully understand the spectrum of phenotypes.

Background: Adequate maternal thyroid function is important for an uncomplicated pregnancy. Although multiple observational studies have evaluated the association between thyroid dysfunction and hypertensive disorders of pregnancy, the methods and definitions of abnormalities in thyroid function tests were heterogeneous, and the results were conflicting. We aimed to examine the association between abnormalities in thyroid function tests and risk of gestational hypertension and pre-eclampsia., Methods: In this systematic review and meta-analysis of individual-participant data, we searched MEDLINE (Ovid), Embase, Scopus, and the Cochrane Database of Systematic Reviews from date of inception to Dec 27, 2019, for prospective cohort studies with data on maternal concentrations of thyroid-stimulating hormone (TSH), free thyroxine (FT 4 ), thyroid peroxidase (TPO) antibodies, individually or in combination, as well as on gestational hypertension, pre-eclampsia, or both. We issued open invitations to study authors to participate in the Consortium on Thyroid and Pregnancy and to share the individual-participant data. We excluded participants who had pre-existing thyroid disease or multifetal pregnancy, or were taking medications that affect thyroid function. The primary outcomes were documented gestational hypertension and pre-eclampsia. Individual-participant data were analysed using logistic mixed-effects regression models adjusting for maternal age, BMI, smoking, parity, ethnicity, and gestational age at blood sampling. The study protocol was registered with PROSPERO, CRD42019128585., Findings: We identified 1539 published studies, of which 33 cohorts met the inclusion criteria and 19 cohorts were included after the authors agreed to participate. Our study population comprised 46 528 pregnant women, of whom 39 826 (85·6%) women had sufficient data (TSH and FT 4 concentrations and TPO antibody status) to be classified according to their thyroid function status. Of these women, 1275 (3·2%) had subclinical hypothyroidism, 933 (2·3%) had isolated hypothyroxinaemia, 619 (1·6%) had subclinical hyperthyroidism, and 337 (0·8%) had overt hyperthyroidism. Compared with euthyroidism, subclinical hypothyroidism was associated with a higher risk of pre-eclampsia (2·1% vs 3·6%; OR 1·53 [95% CI 1·09-2·15]). Subclinical hyperthyroidism, isolated hypothyroxinaemia, or TPO antibody positivity were not associated with gestational hypertension or pre-eclampsia. In continuous analyses, both a higher and a lower TSH concentration were associated with a higher risk of pre-eclampsia (p=0·0001). FT 4 concentrations were not associated with the outcomes measured., Interpretation: Compared with euthyroidism, subclinical hypothyroidism during pregnancy was associated with a higher risk of pre-eclampsia. There was a U-shaped association of TSH with pre-eclampsia. These results quantify the risks of gestational hypertension or pre-eclampsia in women with thyroid function test abnormalities, adding to the total body of evidence on the risk of adverse maternal and fetal outcomes of thyroid dysfunction during pregnancy. These findings have potential implications for defining the optimal treatment target in women treated with levothyroxine during pregnancy, which needs to be assessed in future interventional studies., Funding: Arkansas Biosciences Institute and Netherlands Organization for Scientific Research., Competing Interests: Declaration of interests SB declares consulting fees from Sonic Healthcare. PT reports a travel grant from Society for Endocrinology (leadership development award). EO reports grants from the National Institutes of Health. ENG received speaker's fees and payment for expert testimony from Merck and consulting fees from Brunel Rus. TGMV reports grants from the Netherlands Organization for Health Research and Development. EKA reports consultancy with Roche Diagnostics. LC received travel support by Pfizer. CD reports grants from the Chief Scientist Office (Scotland) and the British Heart Foundation. JERvL declares grant or contract support from the Dutch Heart Foundation and Amryt. SMN has received consultancy, speakers' fees, or travel support from Access Fertility, Beckman Coulter, Ferring Pharmaceuticals, Merck, Modern Fertility, Roche Diagnostics, and The Fertility Partnership. SMN also reports payments for medical–legal work and investment in The Fertility Partnership. TIMK reports lectureship fees from Berlin-Chemie, Goodlife Healthcare, Institut Biochimique SA, Merck, and Quidel. All other authors declare no competing interests., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Thyroid disorders are prevalent in pregnant women. Furthermore, thyroid hormone has a critical role in fetal development and thyroid dysfunction can adversely affect obstetric outcomes. Thus, the appropriate management of hyperthyroidism, most commonly caused by Graves disease, and hypothyroidism, which in iodine sufficient regions is most commonly caused by Hashimoto thyroiditis, in pregnancy is important for the health of both pregnant women and their offspring. Gestational transient thyrotoxicosis can also occur during pregnancy and should be differentiated from Graves disease. Effects of thyroid autoimmunity and subclinical hypothyroidism in pregnancy remain controversial. Iodine deficiency is the leading cause of hypothyroidism worldwide. Despite global efforts to eradicate iodine deficiency disorders, pregnant women remain at risk of iodine deficiency due to increased iodine requirements during gestation. The incidence of thyroid cancer is increasing worldwide, including in young adults. As such, the diagnosis of thyroid nodules or thyroid cancer during pregnancy is becoming more frequent. The evaluation and management of thyroid nodules and thyroid cancer in pregnancy pose a particular challenge. Postpartum thyroiditis can occur up to 1 year after delivery and must be differentiated from other forms of thyroid dysfunction, as treatment differs. This Review provides current evidence and recommendations for the evaluation and management of thyroid disorders in pregnancy and in the postpartum period., (© 2022. Springer Nature Limited.)

Both hyperthyroidism and hypothyroidism can have adverse effects in pregnancy. The most common causes of thyrotoxicosis in pregnancy are gestational transient thyrotoxicosis and Graves' disease. It is important to distinguish between these entities as treatment options differ. Women of reproductive age who are diagnosed with Graves' disease should be counseled regarding the impact of treatment options on a potential pregnancy. Although the absolute risk is small, antithyroid medications can have teratogenic effects. Propylthiouracil appears to have less severe teratogenicity compared to methimazole and is therefore favored during the first trimester if a medication is needed. Women should be advised to delay pregnancy for at least 6 months following radioactive iodine to minimize potential adverse effects from radiation and ensure normal thyroid hormone levels prior to conception. As thyroid hormone is critical for normal fetal development, hypothyroidism is associated with adverse obstetric and child neurodevelopmental outcomes. Women with overt hypothyroidism should be treated with levothyroxine (LT4) to a thyrotropin (thyroid-stimulating hormone; TSH) goal of <2.5 mIU/L. There is mounting evidence for associations of maternal hypothyroxinemia and subclinical hypothyroidism with pregnancy loss, preterm labor, and lower scores on child cognitive assessment. Although there is minimal risk of LT4 treatment to keep TSH within the pregnancy-specific reference range, treatment of mild maternal thyroid hypofunction remains controversial, given the lack of clinical trials showing improved outcomes with LT4 treatment., (© The Author(s) 2020. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Objective: This study aims to evaluate the association of serum iodine concentration (SIC) with urinary iodine concentration (UIC) and thyroid function in pregnant women, as well as to provide the reference range of SIC of pregnant women in iodine-sufficiency area., Methods: Pregnant women were enrolled in the Department of Obstetrics, Tanggu Maternity Hospital, Tianjin from March 2016 to May 2017. Fasting venous blood and spot urine samples were collected. Serum free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH), thyroglobulin (Tg), thyroid peroxidase antibody (TPOAb), thyroglobulin antibody (TgAb), UIC and SIC were measured., Results: One thousand and ninety-nine participants were included in this study. The median UIC was 156 μg/L. The median SIC was 108 μg/L, and the 95% reference interval for SIC was 65.6-164.7 μg/L. SIC was positively correlated with UIC (r = 0.12, P < 0.001), FT3 (r = 0.23, P < 0.001), and FT4 (r = 0.50, P < 0.001) and was inversely correlated with TSH (r = -0.14, P < 0.001). Pregnant women with a SIC < 79.9 μg/L had a higher risk of hypothyroxinemia compared to those with higher SIC (OR = 2.44, 95% CI: 1.31-4.75). Those having SIC > 138.5 μg/L were more likely to have thyrotoxicosis than those with lower SIC values (OR = 13.52, 95% CI: 4.21-43.36)., Conclusions: Serum iodine level is associated with UIC and thyroid function in pregnant women. Low SIC was associated with increased risk for iodine deficiency and hypothyroxinemia, while high SIC was related to excess and thyrotoxicosis., (© 2019 John Wiley & Sons Ltd.)

Understanding of changes in thyroid function and the consequences of thyroid disease during pregnancy has rapidly grown in the past two decades, and revised American Thyroid Association guidelines on this topic were published in 2017. This Review explores the association between thyroid autoimmunity and complications during and after pregnancy. Thyroid autoimmunity refers to the presence of antibodies to thyroperoxidase or thyroglobulin, or thyroid-stimulating hormone receptor antibodies (TRAbs), or a combination of these, and is present in up to 18% of pregnant women. Thyroid antibodies in pregnant women with normal functioning thyroids (ie, euthyroid) have been associated with several complications, including miscarriage and premature delivery. Treatments to improve pregnancy outcomes are being studied. Whether thyroid antibodies are associated with infertility and assisted reproductive technology outcomes is unclear; although, treatment with low doses of levothyroxine, which is usually used to treat hypothyroidism, can be considered in such situations. Additionally, thyroid antibodies have been associated with other neonatal and maternal complications. All these associations require confirmation in larger prospective studies, and their pathogenic mechanisms need to be better understood. Post-partum thyroiditis is substantially more frequent in women who have thyroid antibodies during pregnancy than in those who do not have thyroid antibodies; however, whether treatment can prevent post-partum thyroiditis in women who are or have been antibody positive is unknown. Finally, TRAbs cross the placenta from the mother to the fetus and can cause fetal or neonatal hyperthyroidism. Therefore, women who are positive for TRAbs during pregnancy should be monitored., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Background: The American Thyroid Association (ATA) is continually striving to improve the quality of its publications. The ATA Guidelines Policies and Procedures Task Force was active during 2017. It recently recommended convening a formal standing committee to review and update policies and procedures for the development of clinical practice guidelines (CPGs) and Statements on an ongoing basis., Objective: This statement reviews the history of official ATA publications and discusses the challenges and findings identified by the Task Force. We also wish to present our "work in progress" and propose future directions for the new ATA Guidelines and Statements Committee (ATA GSC)., Methods: Our Task Force reviewed the publication record of the ATA with respect to CPGs. We also reviewed existing ATA policies for CPGs and other official statements, examined policies of other organizations, solicited input from external experts and organizations, and convened five conference calls and two in-person meetings., Results: The ATA has a rich history of developing official publications that have been influential based on download and citation records as well as changes in practice trends. Key future issues to be further addressed by the ATA GSC include the following: (i) striving to improve the methodologic rigor of development of CPGs while balancing considerations of feasibility and timeliness and the role of transparently communicated expert opinion; (ii) formalizing a framework and process for development of new Statements; (iii) increasing stringency and transparency of management of competing interests of individuals being considered for CPG/Statement panel membership; (iv) encouraging consideration of equity and diversity in CPG/Statement development group composition; (v) increasing relevant stakeholder representation (including patient representatives) in development of CPGs/Statements; and (vi) expanding future guideline implementation strategies., Conclusions: As shown by the completed literature search, the ATA has a long history of producing CPGs and Statements with global impact on informing clinical management, education, and research in thyroid diseases. The ATA remains committed to a process of continual improvement of its publications and to meeting stakeholder information needs. Based on the work of our Task Force, we have identified many elements that are needed to achieve this goal and areas of challenge for our new committee.

Background: Thyroid disease in pregnancy is a common clinical problem. Since the guidelines for the management of these disorders by the American Thyroid Association (ATA) were first published in 2011, significant clinical and scientific advances have occurred in the field. The aim of these guidelines is to inform clinicians, patients, researchers, and health policy makers on published evidence relating to the diagnosis and management of thyroid disease in women during pregnancy, preconception, and the postpartum period., Methods: The specific clinical questions addressed in these guidelines were based on prior versions of the guidelines, stakeholder input, and input of task force members. Task force panel members were educated on knowledge synthesis methods, including electronic database searching, review and selection of relevant citations, and critical appraisal of selected studies. Published English language articles were eligible for inclusion. The American College of Physicians Guideline Grading System was used for critical appraisal of evidence and grading strength of recommendations. The guideline task force had complete editorial independence from the ATA. Competing interests of guideline task force members were regularly updated, managed, and communicated to the ATA and task force members., Results: The revised guidelines for the management of thyroid disease in pregnancy include recommendations regarding the interpretation of thyroid function tests in pregnancy, iodine nutrition, thyroid autoantibodies and pregnancy complications, thyroid considerations in infertile women, hypothyroidism in pregnancy, thyrotoxicosis in pregnancy, thyroid nodules and cancer in pregnant women, fetal and neonatal considerations, thyroid disease and lactation, screening for thyroid dysfunction in pregnancy, and directions for future research., Conclusions: We have developed evidence-based recommendations to inform clinical decision-making in the management of thyroid disease in pregnant and postpartum women. While all care must be individualized, such recommendations provide, in our opinion, optimal care paradigms for patients with these disorders.

An awareness of the gestational changes to thyroid physiology and the impact of uncontrolled thyroid disease on pregnancy and infant outcome is essential for the successful management of hypothyroidism and hyperthyroidism. This review summarizes strategies for the management of thyroid disease in pregnancy and post partum, and it highlights areas where there is still a lack of consensus., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Context: Thyroid hormone production is dependent on adequate iodine intake. Excess iodine is generally well-tolerated, but thyroid dysfunction can occur in susceptible individuals after excess iodine exposure. Radiological iodinated contrast media represent an increasingly common source of excess iodine., Objective: This review will discuss the thyroidal response after acute exposure to excess iodine; contrast iodine-induced thyroid dysfunction; risks of iodine-induced thyroid dysfunction in vulnerable populations, such as the fetus, neonate, and patients with impaired renal function; and recommendations for the assessment and treatment of contrast iodine-induced thyroid dysfunction., Methods: Data for this review were identified by searching PubMed, Google Scholar, and references from relevant articles from 1948 to 2014., Conclusions: With the increase in the use of computed tomography scans in the United States, there is increasing risk of contrast-induced thyroid dysfunction. Patients at risk of developing iodine-induced thyroid dysfunction should be closely monitored after receiving iodinated contrast media and should be treated as needed.

Purpose of Review: This review will present a general overview of the sources, human studies, and proposed regulatory action regarding environmental perchlorate exposure., Recent Findings: Some recent studies have reported significant associations between urinary perchlorate concentrations, thyroid dysfunction, and decreased infant intelligence quotient in groups who would be particularly susceptible to perchlorate effects. An update regarding the recently proposed regulatory actions and potential costs surrounding amelioration of perchlorate contamination is provided., Summary: The potential adverse thyroidal effects of environmental perchlorate exposure remain controversial, and further research is needed to further define its relationship to human health among pregnant and lactating women and their infants.

C-reactive protein (CRP) levels have not been routinely used to diagnose thyroid disease, although many thyroid conditions involve inflammation. This study was intended to determine whether CRP levels could differentiate between inflammatory and noninflammatory thyroid conditions, especially between type II inflammatory amiodarone-induced thyrotoxicosis (AIT) and type I iodine-induced AIT. Serum high-sensitivity CRP levels were measured in 100 euthyroid controls (7 taking amiodarone) and 353 patients with one of the following thyroid conditions: AIT, subacute thyroiditis, toxic diffuse goiter, nodular goiter, Hashimoto's thyroiditis, shortterm hypothyroidism, or postpartum thyroiditis. No patients with nontoxic multinodular goiter (n = 34), toxic nodular goiter (n = 23), or toxic diffuse goiter, either untreated (n = 49) or euthyroid while taking methimazole (n = 33), had positive CRP levels (>10 mg/L). The occurrence of positive CRP levels among patients with Hashimoto's thyroiditis (n = 35), short-term hypothyroidism (n = 38), and postpartum thyroiditis (n = 70) did not differ significantly from controls. The occurrence of positive CRP values did not differ significantly between patients with type I and type II AIT and controls. Six of 7 patients (86%) with untreated subacute thyroiditis had positive CRP levels (p < 0.00001). These results indicate that there is only a limited role for measurement of CRP levels in the diagnosis of thyroid diseases other than subacute thyroiditis.

A cross-sectional survey of 102 Peace Corps volunteers in Niger, West Africa, in 1998 had previously demonstrated a high rate of thyroid dysfunction and goiter attributable to excess iodine from their water filters. The Peace Corps volunteers were followed-up a mean of 30 wk after they ceased using iodine-based water filtration systems. Goiter was present in 44% of subjects during excess iodine ingestion and in 30% after removal of excess iodine. Mean serum iodine decreased from 293 micro g/liter during excess iodine ingestion to 84 micro g/liter after cessation of excess iodine. Mean total serum T(4) values increased from 100.4 to 113.3 nmol/liter (7.8 to 8.8 micro g/dl). Mean serum free T(4) increased from 32.2 to 34.7 pmol/liter (2.5 to 2.7 ng/dl). Mean serum TSH decreased from 4.9 to 1.8 mU/liter. Mean serum thyroid peroxidase antibody levels decreased from 33,000 to 22,000 IU/liter (33 to 22 IU/ml). We found that during prolonged excess iodine exposure there were marked increases in serum total iodine concentrations, and the prevalence of goiter, elevated serum TSH values, and elevated serum thyroid peroxidase antibody values increased. The prevalence of all abnormalities decreased after removal of excess iodine from the drinking water system.

Autism spectrum disorder (ASD), with its high economic and societal costs, is a growing public health concern whose prevalence has risen steadily over the last two decades. Although actual increased incidence versus improved diagnosis remains controversial, the increased prevalence of ASD suggests non-inherited factors as likely contributors. There is increasing epidemiologic evidence that abnormal maternal thyroid function during pregnancy is associated with increased risk of child ASD and other neurodevelopmental disorders. Prenatal exposure to endocrine-disrupting chemicals such as per- and polyfluoroalkyl substances (PFAS) is known to disrupt thyroid function and can affect early brain development; thus, thyroid dysfunction is hypothesized to mediate this relationship. The concept of a potential pathway from prenatal PFAS exposure through thyroid dysfunction to ASD etiology is not new; however, the extant literature on this topic is scant. The aim of this review is to evaluate and summarize reports with regard to potential mechanisms in this pathway.

Background: We aimed to assess the long-term effects of the transition in iodine status on the incidence of thyroid disorders over 20 years of follow-up. Methods: The original prospective cohort study, started in 1999 (n = 3761), classified three regions in north China based on iodine status (insufficient iodine, more than adequate iodine, and excessive iodine, respectively) for 5 years. Subsequently, participants were followed for up to another 15 years to assess the long-term effects of shifts to adequate iodine on the incidence of thyroid disorders. Panshan transitioned from insufficient to adequate iodine, and Huanghua transitioned from excessive to more than adequate iodine. Both regions were compared with Zhangwu, in which iodine status changed from more than adequate to adequate iodine (from 214 to 167.2 μg/L). A cluster sampling method was used to select participants in the three regions. Participants completed questionnaires and underwent thyroid ultrasonography. Urinary iodine concentrations (UICs), serum thyroid hormone concentration, and thyroid antibodies were measured. Results: When the iodine status changed from insufficient to adequate (with the median UIC increasing from 88 to 141.9 μg/L), the incidence density of subclinical hyperthyroidism, positive thyroperoxidase antibody, positive thyroglobulin antibody (TgAb), and goiter decreased significantly (p < 0.05 for all). Additionally, the cumulative incidence of subclinical hypothyroidism was significantly lower compared with the region where the iodine status changed from being more than adequate to adequate (1.9% vs. 6.0%, p < 0.001). When the iodine status changed from excessive to more than adequate (median UIC from 634 to 266.7 μg/L), a significant decrease in the incidence density of subclinical hyperthyroidism, positive thyroid antibodies, positive TgAb, and goiter (p < 0.05 for all) were also found. However, an increase in thyroid nodule incidence density (17.26 vs. 28.25 per 1000 person-years, p < 0.001) was seen. Conclusions: The incidence of thyroid disorders (except for thyroid nodules) stabilized or decreased among adults in the three communities from year 5 to year 15 of follow-up. Appropriate iodine fortification is safe and effective over the long term. Restoring urinary iodine to appropriate levels reduces population risk for thyroid disorders. [ABSTRACT FROM AUTHOR]

Autism spectrum disorder (ASD), with its high economic and societal costs, is a growing public health concern whose prevalence has risen steadily over the last two decades. Although actual increased incidence versus improved diagnosis remains controversial, the increased prevalence of ASD suggests non-inherited factors as likely contributors. There is increasing epidemiologic evidence that abnormal maternal thyroid function during pregnancy is associated with increased risk of child ASD and other neurodevelopmental disorders. Prenatal exposure to endocrine-disrupting chemicals such as per- and polyfluoroalkyl substances (PFAS) is known to disrupt thyroid function and can affect early brain development; thus, thyroid dysfunction is hypothesized to mediate this relationship. The concept of a potential pathway from prenatal PFAS exposure through thyroid dysfunction to ASD etiology is not new; however, the extant literature on this topic is scant. The aim of this review is to evaluate and summarize reports with regard to potential mechanisms in this pathway. [ABSTRACT FROM AUTHOR]

Both hyperthyroidism and hypothyroidism can have adverse effects in pregnancy. The most common causes of thyrotoxicosis in pregnancy are gestational transient thyrotoxicosis and Graves' disease. It is important to distinguish between these entities as treatment options differ. Women of reproductive age who are diagnosed with Graves' disease should be counseled regarding the impact of treatment options on a potential pregnancy. Although the absolute risk is small, antithyroid medications can have teratogenic effects. Propylthiouracil appears to have less severe teratogenicity compared to methimazole and is therefore favored during the first trimester if a medication is needed. Women should be advised to delay pregnancy for at least 6 months following radioactive iodine to minimize potential adverse effects from radiation and ensure normal thyroid hormone levels prior to conception. As thyroid hormone is critical for normal fetal development, hypothyroidism is associated with adverse obstetric and child neurodevelopmental outcomes. Women with overt hypothyroidism should be treated with levothyroxine (LT4) to a thyrotropin (thyroid-stimulating hormone; TSH) goal of <2.5 mIU/L. There is mounting evidence for associations of maternal hypothyroxinemia and subclinical hypothyroidism with pregnancy loss, preterm labor, and lower scores on child cognitive assessment. Although there is minimal risk of LT4 treatment to keep TSH within the pregnancy-specific reference range, treatment of mild maternal thyroid hypofunction remains controversial, given the lack of clinical trials showing improved outcomes with LT4 treatment. [ABSTRACT FROM AUTHOR]

Observational cohort studies have demonstrated that gestational subclinical hypothyroidism is associated with adverse obstetric outcomes, although the evidence demonstrating a benefit of LT4 treatment in subclinical hypothyroidism during pregnancy is limited. Overt hypothyroidism in pregnancy is known to be associated with adverse obstetric and child developmental effects, and there is universal agreement that it requires treatment with levothyroxine (LT4). [Extracted from the article]

Background: Thyroid hormone acts on the heart and peripheral vasculature in multiple ways. Even in patients with subclinical hypo- or hyperthyroidism, subclinical alterations in left ventricular (LV) structure and function may be associated with important clinical effects. Our objective was to determine whether thyroid function is related to echocardiographic indices of LV structure and function. Methods: Cross-sectional association of serum thyroid-stimulating hormone (TSH) with two-dimensionalguided M-mode echo LV dimensions and function. Participants were 1376 Framingham Heart Study participants (61% women, mean age 69 years) who attended a routine examination 1979-1981. We excluded participants with myocardial infarction or heart failure, renal insufficiency, and missing data, and those using thyroid hormone or antithyroid medications. Serum TSH was measured 1977-1979. The following echocardiographic measurements were analyzed both as continuous variables and dichotomized at the top quintile: LV end-diastolic dimensions, LV wall thickness, LV mass, LV fractional shortening (an indicator of systolic function), and left atrial diameter. Sex-specific multiple regression models were adjusted for age, height, weight, blood pressure, heart rate, total to high-density lipoprotein cholesterol ratio, and the presence of diabetes, hypertension treatment, and valve disease. Results: In multivariable linear models, log-TSH was not related to LV mass, LV wall thickness, or left atrial size in either sex, or to LV systolic function in men. Log-TSH had a borderline inverse association with fractional shortening ( p=0.06) in women. In multivariable logistic models, women with TSH <0.5mU/L (n=81) had a greater odds of being in the highest quintile of fractional shortening compared to euthyroid subjects (odds ratio 2.2, 95% confidence interval 1.3-3.8, p=0.01). Conclusions: In our moderate-sized community-based sample, TSH concentration was not associated with LV structure in either sex, but was inversely related to LV contractility, consistent with the known inotropic effects of thyroid hormone. [ABSTRACT FROM AUTHOR]

Thyroid dysfunction is common, especially among women over the age of 50. In caring for peri- and post-menopausal women, it is important to recognize the changing clinical manifestations of thyroid disease with age. Postmenopausal women are at increased risk of both osteoporosis and cardiovascular disease, and untreated thyroid disease may exacerbate these risks. Screening for thyroid dysfunction in asymptomatic individuals is controversial, but aggressive case-finding should be pursued, especially in older women. Women with overt thyroid dysfunction should be treated. Therapy for women with subclinical thyroid dysfunction is more controversial, although women with levels of thyroid stimulating hormone(TSH) ≥10 mU/L should be treated, and treatment may be considered in symptomatic women with subclinical hypothyroidism and TSH values <10 mU/L, and in women with subclinical hyperthyroidism who have TSH values consistently <0.1 mU/L. In women who are treated with thyroxine, careful dose titration and monitoring are required in order to prevent the adverse consequences of iatrogenic subclinical hyperthyroidism or hypothyroidism. Finally, caution is required in diagnosing and treating thyroid dysfunction in women who are taking oral estrogens or selective estrogen receptor modulators. [ABSTRACT FROM AUTHOR]

Abstract: Subclinical hyperthyroidism is defined as normal serum free thyroxine (T4) and triiodothyronine (T3) concentrations and persistently suppressed thyroid stimulating hormone (TSH) concentrations. The most common cause of subclinical hyperthyroidism is the use of suppressive doses of L-thyroxine for treatment of hypothyroidism or, less commonly, diffuse nontoxic goiter or thyroid carcinoma (exogenous subclinical hyperthyroidism). Endogenous subclinical hyperthyroidism may be caused by a variety of thyroid disorders that result in overproduction and release of thyroid hormones from the gland with normal/high 24-hour thyroid radioiodine uptake or by inflammation in the thyroid resulting in release of excess thyroid hormones and low 24-hour thyroid radioiodine uptake. Several groups have investigated whether persistent endogenous or exogenous subclinical hyperthyroidism, like overt hyperthyroidism, causes symptoms, adverse effects on the cardiovascular and the skeletal systems, and increased mortality, whether endogenous subclinical hyperthyroidism evolves to overt thyrotoxicosis, and whether or not it should be treated. The present report reviews the most important and recent studies of subclinical hyperthyroidism and attempts to draw conclusions based upon the literature and the authors’ experience. [Copyright &y& Elsevier]

The author discusses the findings of a report by C. M. Rhee et al. which examined associations between exposure to iodinated radiologic contrast media and development of incident thyroid dysfunction. He indicates that iodine-induced hypothyroidism resulted from a failure to escape from the acute Wolff-Chaikoff effect. He suggests that patients who are unable to tolerate thyroid dysfunction may be good candidates for monitoring thyroid function after iodine exposure.

The article discusses research which found that excessive iodine exposure during pregnancy might also be harmful to maternal thyroid health and suggests a lower limit for maternal iodine intake than that presently advised by the World Health Organization (WHO). The deficiency is associated with adverse neurodevelopmental outcomes in offspring.

The article focuses on the use of universal salt iodization (USI) by the American Thyroid Association for sustainable global elimination of iodine deficiency disorders (IDD). Topics discussed include the use of salt for iodine fortification in human consumption salt, adverse health effects with IDD such as goiter and cretinism; and iodized salt quality monitoring for ensuring safety and efficacy with USI programs.

The article focuses on treating iodine deficiency while pregnancy and also discusses the methods to avoid complications due to maternal hypothyroidism on fetal and neonatal neurodevelopment. It reports that in the U.S. all pregnant and lactating women are taking a diet supplement with 150 microgram iodine as recommended by the American Thyroid Organization.

The article focuses on the Lewis E. Braverman Distinguished Award Lectureship. It notes that the award was introduced by Doctor E. Chester Ridgway at the 81st Annual Meeting of the American Thyroid Association (ATA) in the U.S. on October 29, 2011. It also mentions that the award has been developed to honor the contribution of Doctor Lewis E. Braverman to ATA.

A letter to the editor is presented in response to the article "Pemberton's sign," by R. Salvatori and S. Basaria from the March 25, 2004 issue.

Presents an article to review the diagnosis and treatment of the different types of common thyroid disorders. Mechanisms of autoimmune thyroid destruction such as genetic susceptibility and environmental factors; Clinical and biochemical changes in thyroid diseases; Types of thyroid diseases such as Hashimoto's thyroiditis, painless sporadic thyroiditis, suppurative thyroiditis and others.