Iodine-induced Hyperthyroidism Research Articles

Nationwide trends in surgery and radioiodine treatment for benign thyroid disease during iodization of salt

Iodization of salt was introduced in Denmark in 1998 because of mild-to-moderate iodine deficiency (ID). The aim of this study was to analyze the utilization rate of surgery and radioiodine therapy for benign thyroid disorders before and after the introduction of iodization, and to study a possible association between the changes and the raised iodine intake. A nationwide register study. Information on operations and radioiodine treatments for benign thyroid disorders was extracted from nationwide registers in the years 1990 to 2007. Treatment rates are presented for surgery and for radioiodine separately, and as a combined rate, both nationwide and split by the regions of prior mild and moderate ID. A total of 65 605 treatments were identified: 26 456 operations and 39 149 radioiodine treatments. In the first years of iodization (1998-2000; rate ratio 2000/1997), the combined treatment rate increased with 2.5% (95% confidence interval (CI): -1.8-7.1). Split by prior ID level, the increase was seen in the region of moderate ID, but a decrease was seen in the region of mild ID. After 2000, the combined rate decreased, and ended up being 11.1% (95% CI: 7.1-15.0) lower in 2007 than before iodization (rate ratio 2007/1997). The changes were primarily due to changes in the use of radioiodine therapy as the surgery rates remained almost constant. Iodization seemed to be associated with a temporary increase in the utilization rate of surgery and radioiodine therapy in the region of prior moderate ID, probably as a result of treatment of iodine-induced hyperthyroidism, but the rates ended up being lower than before iodization.

High Prevalence of Side Effects After Recombinant Human Thyrotropin–Stimulated Radioiodine Treatment with 30 mCi in Patients with Multinodular Goiter and Subclinical/Clinical Hyperthyroidism

Treatment of multinodular goiters (MNGs) is highly controversial. Radioiodine (RAI) therapy is a nonsurgical alternative for the elderly who decline surgery. Recently, recombinant human thyrotropin (rhTSH) has been used to augment RAI uptake and distribution. In this study, we determined the outcome of 30 mCi RAI preceded by rhTSH (0.1 mg) in euthyroid (EU) and hyperthyroid (subclinical/clinical) patients with large MNGs. This was a prospective cohort study. Forty-two patients (age, 43-80 years) with MNGs were treated with 30 mCi RAI after stimulation with 0.1 mg of rhTSH. Patients were divided into three groups, according to thyroid function: EU (n = 18), subclinically hyperthyroid (SC-H, n = 18), and clinically hyperthyroid (C-H, n = 6). All patients underwent a 90-day low-iodine diet before treatment, and those with clinical hyperthyroidism received methimazole 10 mg daily for 30 days. Serum TSH, free thyroxine (FT4), total triiodothyronine (TT3), and thyroglobulin were measured at baseline and at 24, 48, 72, 168 hours, and 1, 3, 6, 9, 12, 18, 24, and 36 months after therapy. Thyroid volume was assessed by computed tomography at baseline and every 6 months. Patients had high iodine urinary excretion (308 +/- 108 microg I/L) at baseline. TSH levels at baseline were within the normal range (1.5 +/- 0.7 microU/mL) in the EU group and suppressed (<0.3 microU/mL) in the SC-H and C-H groups. After rhTSH, serum TSH peaked at 24 hours reaching 12.4 +/- 5.85 microU/mL. After RAI administration, patients in both hyperthyroid groups had a higher increase in FT4 and TT3 compared with those in the EU group (p < 0.001). Thyroglobulin levels increased equally in all three groups until day 7. Thyroid volume decreased significantly in all patients. Side effects were more common in the SC-H and C-H groups (31.4% and 60.4%, respectively) compared with EU patients (17.8%). Permanent hypothyroidism was more prevalent in the EU group (50%) compared with the SC-H (11%) and C-H (16.6%) groups. Patients with MNG may have subclinical and clinical nonautoimmune iodine-induced hyperthyroidism. Despite a low-iodine diet and therapy with methimazole, hyperthyroid patients have a significantly higher increase in FT4 and TT3 levels after RAI ablation. This can lead to important side effects related mostly to the cardiac system. We strongly advise that patients with SC-H and C-H be adequately treated with methimazole and low-iodine diet aiming to normalize their hyperthyroid condition before rhTSH-stimulated treatment with RAI.

Iodine status in a Sherpa community in a village of the Khumbu region of Nepal

To assess the iodine status of Sherpa residents living in Kunde village, Khumbu region, Nepal. Prevalence of goitre was determined by palpation. Urinary iodine concentrations (UIC) were determined in casual morning samples, and thyroid-stimulating hormone (TSH) in finger-prick blood samples on filter paper. Dietary and demographic data were obtained via questionnaire, and selected foods analysed for iodine. Khumbu region is an area of low soil iodine in Nepal, where the prevalence of goitre was greater than 90% in the 1960s prior to iodine intervention. Two hundred and fifteen of 219 permanent residents of Kunde were studied. Overall prevalence of goitre was 31% (Grade 1 goitre, 27.0%; Grade 2, 4.2%). When adjusted to a world population, goitre prevalence was 27% (95% CI 23, 32%); Grade 2 goitre prevalence was 2.8% (95% CI 1.0, 4.6%). Median UIC was 97 microg/l, but only 75 microg/l in women of childbearing age. Thirty per cent had UIC < 50 microg/l and 52% had UIC < 100 microg/l, while 31% of children aged <14 years had UIC > 300 microg/l. Ten per cent of participants had TSH concentrations >5 microU/ml. The prevalence of severe iodine deficiency has decreased since the 1960s, but mild iodine deficiency persists, particularly in women of childbearing age. The consumption of high-iodine uncooked instant noodles and flavour sachets by school-aged children contributed to their low prevalence of goitre and excessive UIC values. This finding may obscure a more severe iodine deficiency in the population, while increasing the risk of iodine-induced hyperthyroidism in children. Ongoing monitoring is essential.

Thyroidectomy in iodine induced thyrotoxic storm

Between January 1996 and September 1997 we treated 4 patients with iodine-induced thyrotoxic storm (2 females, 2 men; age 54-77 years). Iodine contamination was due to iodine-containing contrast media in 3 patients and iodine-containing disinfectant in 1 patient. Thyroid storm with tachycardia, hypertension, sweating, tremor, weight loss and coma occured 3-10 weeks after iodine contamination. These symptoms were accompanied by raised fT4- and fT3-values. All 4 patients were initially treated with antithyroid drugs for 7 days, whereas 2 patients with coronary artery disease, demonstrated by coronary angio-graphy, were treated with antithyroid drugs for 2 weeks. Because of unsuccessful antithyroid drug treatment, all 4 patients underwent subtotal thyroidectomy. There were no perioperative complications. We conclude that early thyroidectomy is the appropriate treatment for iodine-induced thyrotoxicosis even in patients with severe accompanying diseases.

Iodine nutrition in Brazil: where do we stand?

Brazilian legislation, since 1955, failed to achieve its objectives because the issue was not properly addressed: iodized salt was only available in endemic areas, at a low amount of 10 mg Iodine/kg salt. Lack of surveillance and cooperation were common errors. From 1982 to 1992, the INAN distributed potassium iodate to the industry free of charge, but it was abolished in 1991. Only four years later (1995) was a new law enacted effective in determining that all salt for human use should be iodized at levels established by the Health Authorities. During the period comprising 1998 to 2004, excessive iodination of salt (40 to 100 mg/kg) could lead to an increased prevalence of chronic autoimmune thyroiditis and iodine-induced hyperthyroidism. In 2003, the content of iodine/kg of salt was lowered to 20 to 60 mg I/kg salt. A national survey of schoolchildren is currently underway and will indicate the changes required for adequate iodine in salt for human use.

Association of Iodine Fortification with Incident Use of Antithyroid Medication—A Danish Nationwide Study

Iodine-induced hyperthyroidism has been reported in the early phases of almost all iodine fortification programs, depending on prior iodine intake in the population, the amount of fortification, and the rate of change. The aim of the study was to monitor the effect of the Danish iodine fortification program on incidence of hyperthyroidism as measured by the incident use of antithyroid medication. We conducted a register study. Using the unique identification number of all Danes, we linked data from the Register of Medicinal Product Statistics and the Civil Registration register on an individual level. All dispensing of antithyroid medication from 1995 to 2007 was studied. The place of residency was used to divide patients into mildly and moderately iodine-deficient groups. We measured the incident use of antithyroid medication. In the region with moderate iodine deficiency, the number of incident users of antithyroid medication increased 46% in the first 4 yr of iodine fortification. The use increased the most among the youngest age group (younger than 40 yr) and the oldest age group (older than 75 yr). In the mildly iodine-deficient region, the number of incident users increased only 18%, and only in the youngest age groups (below 40 and 40-59 yr). After 4 yr of fortification, the incidence rates started to fall and reached baseline, for most groups, 6 yr after onset of fortification. This study shows that iodine fortification induced a temporary, modest increase in the incidence of hyperthyroidism as measured by use of antithyroid medication. A new steady state has not yet evolved.

Preoperative therapeutic plasma exchange in patients with thyrotoxicosis

The purpose of this report was to determine the effectiveness of therapeutic plasma exchange (TPE) in preoperative preparation of patients with thyrotoxicosis scheduled for either thyroid or nonthyroid surgery. We retrospectively reviewed 11 patients with thyrotoxicosis and those who prepared surgery with plasmapheresis between 1999 and 2008 at our institution. Ten patients underwent thyroid surgery and one patient was operated for femur fracture during antithyroid drug treatment. The indications for plasmapheresis in all patients with severe thyrotoxicosis were poor response to medical treatment (seven patients), agronulocytosis due to antithyroid drugs (three patients), iodine-induced thyrotoxicosis (Jodd Basedow effect in one patient), and rapid preparation for urgent orthopedic operation (one patient). After TPE, we observed a marked decrease in free thyroxin (FT3) and free triiodothyronin (FT4) levels; however, the decline in the biochemical values were not statically significant (P > 0.62, P > 0.15). Although both FT3 and FT4 levels remained above the normal limits in two of 11 patients, the signs and symptoms of thyrotoxicosis improved in all patients and no thyroid storm observed during the perioperative period. TPE can be considered a safe and effective alternative to prepare patients with thyrotoxicosis for surgery when drug treatment fails or is contraindicated and when emergency surgery is required.

Diffuse Non-toxic Goitre Therapy with Iodine Alone or with Combination of Iodine and Levothyroxine

Aim: to assess the efficacy and tolerability of low-dose iodine therapy compared with the combination of iodine and levothyroxine in endemic goitre patients. Methods: 12-month prospective study was performed, in which 81 patients were randomized on two groups: Group 1 (n = 40) - KI (200 micrograms/day) and Group 2 (n = 41) - KI (100 mcg/day) + L-T4 (1.0 mcg/kg). Thyroid volume, TSH and Anti-TPO-Ab levels were evaluated at baseline, at 8 month of the treatment and at 12 month (4 month after the cessation of the therapy). Results: the significant decreasing of thyroid volumes was found in group 1 at 8 month compared with baseline (20.5 ml at baseline and 16,4 ml at 8 month р &lt; 0.001). After the therapy cessation the further benefit of a sustained effect was demonstrated (16.4 ml at 8 month and 16.1 ml at 12 month, р = 0.31). Iodine-induced hypo- and hyperthyroidism were not observed. High Anti-TPO-Ab level was found in one of 31 patients (3%). In group 2 significant difference between thyroid volumes was found at 8 month compared with baseline (20,5 ml at baseline and 16.2 ml at 8 month р &lt; 0.001). The sustained effect was revealed at least 4 month after the therapy cessation (16.2 ml at 8 month and 16.1 ml at 12 month, р = 0.77). One man had iodine-induced subclinical hyperthyroidism. Anti-TPO-Ab was not detected in this group. No significant difference between thyroid volume decreasing, TSH and Anti-TPO-Ab levels in two comparable groups was observed. Conclusion: KI alone (200 mcg/day) or the combination of L-T4 (1.0 mcg/kg) and KI (100 mcg/day) are equally effective and tolerable for endemic goitre therapy.

Amiodarone-induced thyrotoxicosis: something new to refine the initial diagnosis?

Amiodarone-induced thyrotoxicosis (AIT) is a clinical condition fraught with difficulties and uncertainties both from the diagnostic and therapeutic standpoints (1). Diagnosis and treatment are closely linked, because the diagnostic problems may affect the therapeutic approach and lead to suboptimal treatment and delayed resolution of dysfunction. This, in turn, is risky for the AIT patient, who generally has underlying heart abnormalities (arrhythmias, heart failure) for which prompt restoration and stable maintenance of euthyroidism represent fundamental actions (1). Indeed, AIT is associated with increased mortality, particularly in elderly patients with markedly impaired left ventricular function (2). Thus, at variance with amiodarone-induced hypothyroidism (3), AIT poses relevant and urgent therapeutic problems. What is difficult in AIT is not to diagnose the thyrotoxic state, but the pathophysiologic mechanism(s) underpinning it. Traditionally, although schematically, two main forms of AIT are distinguished (4). Type 1 AIT is a classical form of iodine-induced thyrotoxicosis associated with true hyperthyroidism; thyroid hyperfunction is triggered by the iodine load, and the thyroid gland generally is intrinsically abnormal owing to latent autonomy due to thyroid nodular or autoimmune disease. Type 2 AIT is a form of destructive thyroiditis caused by iodine or, more likely, amiodarone or its metabolite, desethylamiodarone; most cases develop in normal thyroid glands, although a small, diffuse or nodular goiter may sometimes be present. AIT may occur at any time during amiodarone therapy and even long after amiodarone withdrawal (1). Clinical presentation of the two forms does not differ (1). A relevant proportion (about 20%) of patients with type 2 AIT develop hypothyroidism in the long run (5). Type 1 AIT is treated with thionamides with or without potassium perchlorate, but it often is resistant to therapy because of the large intrathyroidal iodine stores (1); on the contrary, type 2 AIT is managed with oral glucocorticoids (6), but the time required to normalize thyroid status may vary depending mainly on thyroid volume and severity of baseline thyrotoxicosis (7).

Thyroid and the environment: exposure to excessive nutritional iodine increases the prevalence of thyroid disorders in São Paulo, Brazil

To evaluate the prevalence of chronic autoimmune thyroiditis (CAT) and iodine-induced hypothyroidism, hyperthyroidism (overt and subclinical), and goiter in a population exposed to excessive iodine intake for 5 years (table salt iodine concentrations: 40-100 mg/kg salt). Design This was a population-based, cross-sectional study with 1085 participants randomly selected from a metropolitan area in São Paulo, Brazil, and conducted during the first semester of 2004. Thyroid ultrasound examination was performed in all participants and samples of urine and blood were collected from each subject. Serum levels of thyroid-stimulating hormone, free thyroxine, and anti-thyroid peroxidase (TPO) antibodies, urinary iodine concentration, thyroid volume, and thyroid echogenicity were evaluated. We also analyzed table salt iodine concentrations. At the time the study was conducted, table salt iodine concentrations were within the new official limits (20-60 mg/kg salt). Nevertheless, in 45.6% of the participants, urinary iodine excretion was excessive (above 300 microg/l) and, in 14.1%, it was higher than 400 microg/l. The prevalence of CAT (including atrophic thyroiditis) was 16.9% (183/1085), women were more affected than men (21.5 vs 9.1% respectively, P=0.02). Hypothyroidism was detected in 8.0% (87/1085) of the population with CAT. Hyperthyroidism was diagnosed in 3.3% of the individuals (36/1085) and goiter was identified in 3.1% (34/1085). Five years of excessive iodine intake by the Brazilian population may have increased the prevalence of CAT and hypothyroidism in subjects genetically predisposed to thyroid autoimmune diseases. Appropriate screening for early detection of thyroid dysfunction may be considered during excessive nutritional iodine intake.

Empfehlungen zur Prophylaxe der Nebenwirkungen bei intravasaler Applikation jodhaltiger Kontrastmittel

Iodinated contrast media are widely used in computed tomography and angiography. Adverse reactions such as contrast-medium induced nephropathy (CIN), anaphylactoid reactions and iodine-induced thyrotoxicosis are associated with intravasal administration of contrast agents. Iodinated contrast agents are generately considered to be safe, but in rare cases they can cause severe life threatening situations. In this review we present an overview about the incidence, pathways, and risk factors of adverse reactions. Simple schemes including hydration protocols for prevention of CIN, medication for prophylaxis of iodine-induced thyrotoxicosis with thyreostatics and anaphylactoid reactions with histamine antagonists and corticosteroids are suggested.

Cardiovascular assessment of hyperthyroid patients with multinodular goiter before and after radioiodine treatment preceded by stimulation with recombinant human TSH

Treatment of large multinodular goiter (MNG) with radioiodine preceded by recombinant human thyrotropin (0.1 mg rhTSH) has been shown to be a safe alternative for patients with comorbidities that preclude surgery. However, the increase in serum thyroid hormones that follows both treatments may be harmful for some patients, particularly those with underlying cardiovascular disease. In this study, we evaluated cardiac parameters (clinical, ECG, 24-h Holter, Doppler echocardiogram, treadmill stress test) in 27 of 42 patients (ages 42-80 years) with large MNGs who were treated with rhTSH before receiving 30 mCi radioiodine therapy. At baseline, 18 patients had subclinical and six patients had overt iodine-induced hyperthyroidism. All patients had a transient surge in serum levels of free T4 and total T3 into the hyperthyroid range after therapy. However, repeated cardiac evaluation did not show significant changes as compared with baseline evaluation. In conclusion, rhTSH stimulated RAI treatment of MNG did not affect structural and functional parameters of the heart, despite transient high-serum levels of thyroid hormones.

Clinical Studies of Exposure to Perchlorate in the United States

Perchlorate is a competitive inhibitor of the sodium/iodine symporter, decreasing the active transport of iodine into the thyroid. It was used as an antithyroid drug in the treatment of hyperthyroidism in the 1950s and 1960s but was discontinued because of the occasional occurrence of aplastic anemia. More recently, lower doses of perchlorate have been used successfully in the treatment of iodine-induced hyperthyroidism. There has been concern that naturally occurring perchlorate and industrial contamination of water supplies with perchlorate might pose a health hazard by inducing or aggravating underlying thyroid dysfunction. In a series of studies in normal volunteers, administration of perchlorate from 2 weeks to 6 months and in perchlorate production workers exposed intermittently to high levels of perchlorate for years, no abnormalities of circulating thyroid hormones, thyroid-stimulating hormone, thyroglobulin, or ultrasound evaluation of thyroid structure were observed even though the thyroid (123)I uptake was decreased in some studies. Further studies of the effects of perchlorate on thyroid function in normal volunteers will now be difficult to carry out due to the adverse publicity that perchlorate and the studies on its effect have received.

Proportion of type 1 and type 2 amiodarone‐induced thyrotoxicosis has changed over a 27‐year period in Italy

Two main forms of amiodarone-induced thyrotoxicosis (AIT) exist. Type 1 AIT is a form of iodine-induced hyperthyroidism. Its management is complex and includes thionamides, potassium perchlorate and, occasionally, thyroidectomy. Type 2 AIT is a destructive thyroiditis, responds to glucocorticoids, and usually does not require further thyroid treatment once euthyroidism has been restored. To assess retrospectively the prevalence and relative proportion of type 1 and type 2 AIT over a 27-year period at a tertiary referral centre in Italy. Consecutive AIT patients (n = 215) seen at the department of endocrinology of the University of Pisa between 1980 and 2006. Type 1 AIT constituted the most frequent AIT form (60%) during the first years covered by this study. The annual mean number of type 1 AIT patients was 3.6 at the beginning of the study period, and 2.5 during the later years. In contrast, the mean annual number of new cases of type 2 AIT progressively increased from 2.4 to 12.5. Likewise, the proportion of type 2 AIT increased in a significant linear manner (P < 0.0001), currently accounting for 89% of AIT cases. Type 2 AIT patients showed a male preponderance, higher serum FT4/FT3 ratio (P < 0.002), lower 3-h and 24-h thyroidal radioactive iodine uptake values (P < 0.0001), and received a higher cumulative dose of amiodarone (P < 0.0001) than type 1 AIT patients. Over a 27-year period, the epidemiology of AIT changed, as the prevalence of type 2 AIT progressively increased and that of type 1 remained constant. Thus, under most circumstances, endocrinologists nowadays deal with type 2 AIT, which is a destructive thyroiditis, generally treated successfully with glucocorticoids. Although no additional treatment is usually required after the destructive process subsides, periodic assessment of thyroid function is warranted, because of the occurrence of hypothyroidism (up to 17%) during long-term follow-up of these patients.

Nutritional Epidemiology and Thyroid Hormone Metabolism

Severe iodine deficiency was the main cause of endemic goiter and cretinism. Most of the previously iodine-deficient areas are now supplemented, mainly with iodized salt. The geographical distribution of severe endemic areas has been progressively reduced, and at present, approximately 200 million people living in remote places are still at risk of severe iodine deficiency. International public health programs should be focused first on reaching these populations, and second on auditing and monitoring the operational work of supplementation programs. This second point is essential to prevent iodine-induced hyperthyroidism or interruptions of iodine supplement distribution, which could be catastrophic for the fetus and the young infant. Echography brings a complementary tool to clinical assessment of goiter by palpation. Inductively coupled plasma-mass spectrometry brings at least a definitive gold standard for iodine measurement and thyroid hormone measurement. Thiocyanate overload has been clearly documented as a goitrogen in Central Africa, and when associated with selenium deficiency, it may be included as risk factor for endemic myxedematous cretinism. Variable exposure to different environmental risk factors is likely the explanation of the variable distribution of two types of endemic cretinism (neurological and myxedematous), and the clinical overlap of the pathogeny of both syndromes is more important than previously described. It is possible that Kashin-Beck osteoarthropathy is another evanescent endemic disease that will disappear with the correction of iodine deficiency.

Gadolinium as an Alternative Contrast Agent During Cardiac Catheterization in Patient with Iodine-induced Hyperthyroidism

We report the first case of a male patient with iodine-induced hyperthyroidism and unstable angina pectoris in whom a diagnostic cardiac catheterization with gadolinium as contrast agent was chosen. The patient was hospitalized with an iodine-induced hyperthyroidism after angioplasty using an iodinated contrast agent. He presented with a continuous arrhythmia and unstable angina pectoris. A repeated cardiac catheterization using iodinated contrast agent was contraindicated. This case report shows that gadolinium is a useful alternative contrast agent for cardiac intervention in patients with iodine-induced hyperthyroidism.

Iodine-induced thyrotoxicosis after ingestion of kelp-containing tea

Iodine-induced thyrotoxicosis after ingestion of kelp-containing tea

Iodine-Induced Thyrotoxicosis after Ingestion of Kelp-Containing Tea

Iodine-Induced Thyrotoxicosis after Ingestion of Kelp-Containing Tea

Drug-Induced Thyrotoxic Periodic Paralysis

To report a case of iodine-induced (Jod-Basedow) hyperthyroidism leading to thyrotoxic periodic paralysis (TPP). A 64-year-old white male, one day status-post-cardiac catheterization, presented to the local emergency department with profound weakness of his extremities and an inability to stand on his own. Pertinent laboratory test results included a potassium level of 3.0 mEq/L. Treatments of oral and intravenous potassium supplementation resulted in his complete recovery. Two days later he was diagnosed with hyperthyroidism and subsequently treated with nadolol 40 mg daily and methimazole 20 mg daily. At time of writing, the patient remained euthyroid, receiving no antithyroid medications. There had been no further reports of paralysis in the 6 years since his original presentation. The Naranjo probability scale indicated a probable relationship between the patient's episode of TPP and his exposure to the iodinated contrast dye. TPP is an uncommon manifestation in white patients with hyperthyroidism. Iodine-induced TPP is even more rare, with only 2 such cases reported as of November 2, 2005. In this case, Jod-Basedow hyperthyroidism was induced by the iodine-containing dye that the patient received during cardiac catheterization. Soon after the dye was administered, he developed TPP. Clinicians should be aware not only of potential causes of drug-induced thyroid disease, but also of the potential for drug-induced hyperthyroidism leading to TPP. The diagnosis of TPP should be considered in patients presenting with acute onset of extremity weakness or paralysis and hypokalemia. Quick diagnosis and prompt treatment of TPP can prevent life-threatening complications of this treatable and curable disorder.

Urinary Iodine Concentration of Pregnant Women and Female Adolescents as an Indicator of Excessive Iodine Intake in Sri Lanka

Mild deficiencies and excesses of iodine have deleterious effects in both females and males. The iodine status of the population after implementation of the universal salt iodization program in Sri Lanka is not known. This cross-sectional study was carried out to assess the iodine status of pregnant women and female adolescents, with urinary iodine concentration used as the measure of outcome. The participants were 100 women in the first trimester of pregnancy and 99 female adolescents in Kuliyapitiya, Kurunegala District, North-Western Province, Sri Lanka. The urinary iodine concentration was measured in a casual urine sample from each subject. The iodate contents of salt samples collected from households of the adolescents participating in the study were also measured. The median urinary iodine concentration of 185.0 microg/L and the prevalence of values under 50 microg/L of only 1% among the pregnant women indicate adequate iodine intake and optimal iodine nutrition. The median urinary iodine concentration (213.1 microg/L) among female adolescents indicates a more than adequate iodine intake and a risk of iodine-induced hyperthyroidism. Approximately 8% and 4% of the adolescents and pregnant women, respectively, had urinary iodine concentrations in the range of mild iodine deficiency (51 to 100 microg/L). More than half of the adolescents (56%) and 39% of the pregnant women had urinary iodine concentrations higher than optimal. The median iodine content in salt samples was 12.7 ppm. Only 20.2% of the samples were adequately iodized, and 10.1% of the samples had very high iodine levels. Female adolescents and pregnant women had no iodine deficiency, but a considerable proportion of them, especially female adolescents, were at risk for iodine-induced hyperthyroidism. There is thus a need for proper monitoring of the salt iodization program to achieve acceptable iodine status.