Angela M. Leung

Consequences of excess iodine

Iodine is a micronutrient that is essential for the production of thyroid hormones. The primary source of iodine is the diet via consumption of foods that have been fortified with iodine, including salt, dairy products and bread, or that are naturally abundant in the micronutrient, such as seafood. Recommended daily iodine intake is 150 µg in adults who are not pregnant or lactating. Ingestion of iodine or exposure above this threshold is generally well-tolerated. However, in certain susceptible individuals, including those with pre-existing thyroid disease, the elderly, fetuses and neonates, or patients with other risk factors, the risk of developing iodine-induced thyroid dysfunction might be increased. Hypothyroidism or hyperthyroidism as a result of supraphysiologic iodine exposure might be either subclinical or overt, and the source of the excess iodine might not be readily apparent.

Perchlorate and thiocyanate exposure and thyroid function in first-trimester pregnant women

CONTEXT Thyroid hormone, requiring adequate maternal iodine intake, is critical for fetal neurodevelopment. Perchlorate decreases thyroidal iodine uptake by competitively inhibiting the sodium/iodide symporter. It is unclear whether environmental perchlorate exposure adversely affects thyroid function in pregnant women. Thiocyanate, derived from foods and cigarette smoke, is a less potent competitive sodium/iodide symporter inhibitor than perchlorate. OBJECTIVE Our objective was to determine whether environmental perchlorate and/or thiocyanate exposure is associated with alterations in thyroid function in pregnancy. DESIGN AND SETTING We conducted a cross-sectional study at health centers in Cardiff, Wales, and Turin, Italy. PATIENTS During 2002-2006, 22,000 women at less than 16 wk gestation were enrolled in the Controlled Antenatal Thyroid Screening Study. Subsets of 261 hypothyroid/hypothyroxinemic and 526 euthyroid women from Turin and 374 hypothyroid/hypothyroxinemic and 480 euthyroid women from Cardiff were selected based on availability of stored urine samples and thyroid function data. MAIN OUTCOME MEASURES Urinary iodine, thiocyanate, and perchlorate and serum TSH, free T(4) (FT(4)), and thyroperoxidase antibody were measured. RESULTS Urinary iodine was low: median 98 microg/liter in Cardiff and 52 microg/liter in Turin. Urine perchlorate was detectable in all women. The median (range) urinary perchlorate concentration was 5 microg/liter (0.04-168 microg/liter) in Turin and 2 microg/liter (0.02-368 microg/liter) in Cardiff. There were no associations between urine perchlorate concentrations and serum TSH or FT(4) in the individual euthyroid or hypothyroid/hypothyroxinemic cohorts. In multivariable linear analyses, log perchlorate was not a predictor of serum FT(4) or TSH. CONCLUSIONS Low-level perchlorate exposure is ubiquitous but did not affect thyroid function in this cohort of iodine-deficient pregnant women.

Perchlorate, iodine and the thyroid

In pharmacologic doses, perchlorate inhibits thyroidal iodine uptake and subsequently decreases thyroid hormone production. Although pharmacologic doses may be used in the treatment of hyperthyroidism, recent literature has focussed on the detection of low levels of perchlorate in the environment, groundwater and foodstuffs and their potential adverse effects on human thyroid function. This is of particular concern to the developing foetus and infant, whose normal neurodevelopment depends on adequate iodine intake for the production of thyroid hormones. Further research is needed to clarify the potential health effects of low-level chronic environmental perchlorate exposure. The health impact of environmental perchlorate may be dependent upon adequate iodine intake and should be interpreted in combination with other environmental exposures that are also potential thyroidal endocrine disruptors.

Iodine-induced thyroid dysfunction.

Purpose of reviewTo summarize the mechanisms of iodine-induced hypothyroidism and hyperthyroidism, identify the risk factors for thyroid dysfunction following an iodine load, and summarize the major sources of excess iodine exposure. Recent findingsExcess iodine is generally well tolerated, but individuals with underlying thyroid disease or other risk factors may be susceptible to iodine-induced thyroid dysfunction following acute or chronic exposure. Sources of increased iodine exposure include the global public health efforts of iodine supplementation, the escalating use of iodinated contrast radiologic studies, amiodarone administration in vulnerable patients, excess seaweed consumption, and various miscellaneous sources. SummaryIodine-induced thyroid dysfunction may be subclinical or overt. Recognition of the association between iodine excess and iodine-induced hypothyroidism or hyperthyroidism is important in the differential diagnosis of patients who present without a known cause of thyroid dysfunction.

Iodine Status and Thyroid Function of Boston-Area Vegetarians and Vegans

CONTEXT Adequate dietary iodine is required for normal thyroid function. The iodine status and thyroid function of U.S. vegetarians and vegans have not been previously studied. Environmental perchlorate and thiocyanate (inhibitors of thyroid iodine uptake) exposures may adversely affect thyroid function. OBJECTIVE The objective of the study was to assess the iodine status and thyroid function of U.S. vegetarians (consume plant based products, eggs, milk; abstain from meat, poultry, fish, shellfish) and vegans (avoid all animal products) and whether these may be affected by environmental perchlorate and thiocyanate exposures. DESIGN AND SETTING This was a cross-sectional assessment of urinary iodine, perchlorate, and thiocyanate concentrations and serum thyroid function in Boston-area vegetarians and vegans. SUBJECTS One hundred forty-one subjects (78 vegetarians, 63 vegans) were recruited; one vegan was excluded. RESULTS Median urinary iodine concentration of vegans (78.5 μg/liter; range 6.8-964.7 μg/liter) was lower than vegetarians (147.0 μg/liter; range 9.3-778.6 μg/liter) (P < 0.01). Adjusted for cigarette smoking (confirmed by urinary cotinine levels) and thiocyanate-rich food consumption, median urinary thiocyanate concentration of vegans (630 μg/liter; range 108-3085 μg/liter) was higher than vegetarians (341 μg/liter; range 31-1963 μg/liter) (P < 0.01). There were no between-group differences in urinary perchlorate concentrations (P = 0.75), TSH (P = 0.46), and free T(4) (P = 0.77). Urinary iodine, perchlorate, and thiocyanate levels were not associated with TSH (P = 0.59) or free T(4) (P = 0.14), even when adjusted for multiple variables. CONCLUSIONS U.S. vegetarians are iodine sufficient. U.S. vegans may be at risk for low iodine intake, and vegan women of child-bearing age should supplement with 150 μg iodine daily. Environmental perchlorate and thiocyanate exposures are not associated with thyroid dysfunction in these groups.

Modified-Release Recombinant Human TSH (MRrhTSH) Augments the Effect of 131I Therapy in Benign Multinodular Goiter: Results from a Multicenter International, Randomized, Placebo-Controlled Study

BACKGROUND Recombinant human TSH (rhTSH) can be used to enhance (131)I therapy for shrinkage of multinodular goiter (MG). OBJECTIVE, DESIGN, AND SETTING The objective of the study was to compare the efficacy and safety of 0.01 and 0.03 mg modified-release (MR) rhTSH as an adjuvant to (131)I therapy, vs. (131)I alone, in a randomized, placebo-controlled, international, multicenter study. PATIENTS AND INTERVENTION Ninety-five patients (57.2 ± 9.6 yr old, 85% females, 83% Caucasians) with MG (median size 96.0, range 31.9-242.2 ml) were randomized to receive placebo (group A, n = 32), MRrhTSH 0.01 mg (group B, n = 30), or MRrhTSH 0.03 mg (group C, n = 33) 24 h before a calculated activity of (131)I. MAIN OUTCOME MEASURES The primary end point was a change in thyroid volume (by computerized tomography scan, at 6 months). Secondary end points were the smallest cross-sectional area of the trachea; thyroid function tests; Thyroid Quality of Life Questionnaire; electrocardiogram; and hyperthyroid symptom scale. RESULTS Thyroid volume decreased significantly in all groups. The reduction was comparable in groups A and B (23.1 ± 8.8 and 23.3 ± 16.5%, respectively; P = 0.95). In group C, the reduction (32.9 ± 20.7%) was more pronounced than in groups A (P = 0.03) and B. The smallest cross-sectional area of the trachea increased in all groups: 3.8 ± 2.9% in A, 4.8 ± 3.3% in B, and 10.2 ± 33.2% in C, with no significant difference among the groups. Goiter-related symptoms were effectively reduced and there were no major safety concerns. CONCLUSION In this dose-selection study, 0.03 mg MRrhTSH was the most efficacious dose as an adjuvant to (131)I therapy of MG. It was well tolerated and significantly augmented the effect of (131)I therapy in the short term. Larger studies with long-term follow-up are warranted.

Thyroid Testing during Pregnancy at an Academic Boston Area Medical Center

CONTEXT Gestational hypothyroidism leads to adverse obstetric outcomes and intellectual impairment in offspring. Pregnancy thyroid screening is controversial. OBJECTIVE Our objective was to determine thyroid function testing and thyroid dysfunction rates in pregnant women at Boston Medical Center (BMC). METHODS We retrospectively enrolled 1000 pregnant women aged 18-46 yr seen in BMCs Obstetrics/Gynecology (OB/GYN) or Family Medicine (FM) Clinics for their initial prenatal visit during 2008. Age, race, insurance, gestational age (GA), medical history (thyroid or other autoimmune disorders), obstetric history, and thyroid function tests were ascertained. RESULTS A total of 983 women were included (17 excluded for coding error). Median maternal age was 28 yr and GA 9.4 wk. Thyroid testing rates were similar in the 918 (93%) followed by OB/GYN and 65 (7%) followed by FM (84 vs. 86%). Thirty-nine women had previous thyroid disease, of whom 19 took thyroid medications. Four had type 1 diabetes, and nine had other autoimmune diseases. Serum TSH was obtained in 832 women (84.6%) at median GA 9.7 wk (range, 0.1-39.7). The majority were tested during their first trimester (65.5%). Of the 832 tested, 56 (6.7%) had trimester-specific elevated TSH, of whom nine had a previous history of thyroid disease, two had type 1 diabetes, and one had dyschromia. Based on current case-finding guidelines, 45 of 56 women (80.4%) with an elevated TSH in pregnancy might not have been tested. CONCLUSION BMC has a high rate of thyroid function testing in pregnancy. Targeted thyroid testing in only high-risk patients would have missed 80.4% of pregnant women with hypothyroidism.

Iodine nutrition in pregnancy and lactation.

Adequate iodine intake is required for the synthesis of thyroid hormones that are important for normal fetal and infant neurodevelopment. In this review, we discuss iodine physiology during pregnancy and lactation, methods to assess iodine sufficiency, the importance of adequate iodine nutrition, studies of iodine supplementation during pregnancy and lactation, the consequences of hypothyroidism during pregnancy, the current status of iodine nutrition in the United States, the global efforts toward achieving universal iodine sufficiency, and substances that may interfere with iodine use.

A Review: Radiographic Iodinated Contrast Media-Induced Thyroid Dysfunction

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.

History of U.S. Iodine Fortification and Supplementation

Iodine is a micronutrient required for thyroid hormone production. This review highlights the history of the discovery of iodine and its uses, discusses the sources of iodine nutrition, and summarizes the current recommendations for iodine intake with a focus on women of childbearing age.