THE TEMPORARY NATURE OF THE INHIBITORY ACTION OF EXCESS IODIDE ON ORGANIC IODINE SYNTHESIS IN THE NORMAL THYROID<sup>1</sup>

Wolff, J.; Chaikoff, I.L.; Goldberg, R. C.; Meier, JJ

doi:10.1210/endo-45-5-504

Cited by 266 publications

(139 citation statements)

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“…The acute Wolff-Chaikoff effect (26,27) suggested that iodine-induced hypothyroidism, especially occurring in patients on amiodarone therapy, is caused by failure of the thyroid gland to escape from acute inhibition (28,29). However, the exact mechanism by which chronic high iodine intake induces hypothyroidism remains unclear.…”

Section: Discussionmentioning

confidence: 99%

More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels

Teng¹,

Shan²,

Chen

et al. 2011

European Journal of Endocrinology

152

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Objective: With the introduction of iodized salt worldwide, more and more people are exposed to more than adequate iodine intake levels with median urinary iodine excretion (MUI 200-300 mg/l) or excessive iodine intake levels (MUI O300 mg/l). The objective of this study was to explore the associations between more than adequate iodine intake levels and the development of thyroid diseases (e.g. thyroid dysfunction, thyroid autoimmunity, and thyroid structure) in two Chinese populations. Design: A population-based cross-sectional study was conducted in two areas in which people are exposed to different levels of iodine intake (Rongxing, MUI 261 mg/l; Chengshan, MUI 145 mg/l). A total of 3813 individuals were recruited by random sampling. Thyroid hormones, thyroid autoantibodies in serum, and iodine levels in urine were measured. B-mode ultrasonography of the thyroid was also performed for each participant. Results: The prevalence of subclinical hypothyroidism was significantly higher for subjects who live in Rongxing than those who live in Chengshan (5.03 vs 1.99%, P!0.001). The prevalence of positive anti-thyroid peroxidase antibody (TPOAb) and positive anti-thyroglobulin antibody (TgAb) was significantly higher for subjects in Rongxing than those in Chengshan (TPOAb: 10.64 vs 8.4%, PZ0.02; TgAb: 10.27 vs 7.93%, PZ0.01). The increase in thyroid antibodies was most pronounced in the high concentrations of TPOAb (TPOAb: R500 IU/ml) and low concentrations of TgAb (TgAb: 40-99 IU/ml) in Rongxing. Conclusions: More than adequate iodine intake could be a public health concern in terms of thyroid function and thyroid autoimmunity in the Chinese populations.European Journal of Endocrinology 164 943-950

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Section: Discussionmentioning

confidence: 99%

More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels

Teng¹,

Shan²,

Chen

et al. 2011

European Journal of Endocrinology

152

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“…This is also known as escape from the WolffChaikoff effect. 8,9 Unlike children and adults, the immature fetal and neonatal thyroid gland cannot decrease intracellular iodine transportation. The fetus therefore remains hypothyroid.…”

Section: Figurementioning

confidence: 99%

Maternal Iodine Exposure: A Case of Fetal Goiter and Neonatal Hearing Loss

et al. 2016

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A 27-year-old gravid 1 at 27 weeks 6 days with a history of hypothyroidism had an ultrasound that demonstrated a 3.9 × 3.2 × 3.3-cm well-circumscribed anterior neck mass, an extended fetal head, and polyhydramnios. Further characterization by magnetic resonance imaging (MRI) showed a fetal goiter. During her evaluation for the underlying cause of the fetal goiter, the patient revealed she was taking nutritional iodine supplements for treatment of her hypothyroidism. She was ingesting 62.5 times the recommended amount of daily iodine in pregnancy. The excessive iodine consumption caused suppression of the fetal thyroid hormone production, resulting in hypothyroidism and goiter formation. After the iodine supplement was discontinued, the fetal goiter decreased in size. At delivery, the airway was not compromised. The infant was found to have reversible hypothyroidism and bilateral hearing loss postnatally. This case illustrates the importance of examining for iatrogenic causes for fetal anomalies, especially in unregulated nutritional supplements.

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“…The effect has been postulated to be mediated by intermediate organic iodocompounds formed within the thyroid (2) as a result of high intrathyroidal iodide concentrations. After a period of 1±2 days, the thyroid adapts or escapes from this inhibition (3), and this is referred to as the escape from or adaptation to the acute Wolff± Chaikoff effect. We had proposed that the escape mechanism was due to a decrease in iodide transport from the plasma into the thyroid (4).…”

Section: Introductionmentioning

confidence: 99%

Regulation of the sodium iodide symporter by iodide in FRTL-5 cells

Eng

Cardona

Previti

et al. 2001

European Journal of Endocrinology

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Objective: The acute decrease in iodide organification in the thyroid in response to excess iodide is termed the acute Wolff±Chaikoff effect and normal organification resumes in spite of continued high plasma iodide concentrations (escape from the acute Wolff±Chaikoff effect). We have recently reported that large doses of iodide given to rats chronically decrease the sodium/iodide symporter (NIS) mRNA and protein, suggesting that escape is due to a decrease in NIS and subsequent iodide transport. We have now studied the effect of excess iodide on NIS in FRTL-5 cells to further explore the mechanisms whereby excess iodide decreases NIS. Design: FRTL-5 cells were employed and were incubated in the presence or absence of various concentrations of iodide. NIS mRNA and protein and the turnover of NIS were assessed. Methods: NIS mRNA was measured by Northern analysis, NIS protein by Western analysis and NIS turnover by pulse±chase labeling experiments. Results: Iodide (10 23 mol/l) had no effect on NIS mRNA in FRTL-5 cells at 24 and 48 h compared with cells cultured in the absence of iodide. However, excess iodide decreased NIS protein by 50% of control values at 24 h and by 70% at 48 h. This effect of iodide was dose dependent. Pulse±chase experiments demonstrated that there was no effect of iodide on new NIS protein synthesis and that the turnover of NIS protein in the presence of iodide was 27% faster than in the absence of added iodide. Conclusions: Excess iodide does not decrease NIS mRNA in FRTL-5 cells but does decrease NIS protein, suggesting that in this in vitro thyroid cell model iodide modulates NIS, at least in part, at a posttranscriptional level. This iodide-induced decrease in NIS protein appears to be due, at least partially, to an increase in NIS protein turnover.

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THE TEMPORARY NATURE OF THE INHIBITORY ACTION OF EXCESS IODIDE ON ORGANIC IODINE SYNTHESIS IN THE NORMAL THYROID¹

Cited by 266 publications

References 6 publications

More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels

More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels

Maternal Iodine Exposure: A Case of Fetal Goiter and Neonatal Hearing Loss

Regulation of the sodium iodide symporter by iodide in FRTL-5 cells

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THE TEMPORARY NATURE OF THE INHIBITORY ACTION OF EXCESS IODIDE ON ORGANIC IODINE SYNTHESIS IN THE NORMAL THYROID1

Cited by 266 publications

References 6 publications

More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels

More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels

Maternal Iodine Exposure: A Case of Fetal Goiter and Neonatal Hearing Loss

Regulation of the sodium iodide symporter by iodide in FRTL-5 cells

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THE TEMPORARY NATURE OF THE INHIBITORY ACTION OF EXCESS IODIDE ON ORGANIC IODINE SYNTHESIS IN THE NORMAL THYROID¹