Neonatal thyroid function born to mothers living with long-term excessive iodine intake from drinking water

2014 ◽  
Vol 83 (3) ◽  
pp. 399-404 ◽  
Author(s):  
Wen Chen ◽  
Zhongna Sang ◽  
Long Tan ◽  
Shufen Zhang ◽  
Feng Dong ◽  
...  
2015 ◽  
Vol 11 (1) ◽  
pp. 43 ◽  
Author(s):  
Aleksey Vasil'evich Kiyaev ◽  
Nadezhda Mikhailovna Platonova ◽  
Fatima Magomedovna Abdulhabirova ◽  
Ekaterina Anatolyevna Troshina ◽  
Grigoriy Anatol'evich Gerasimov

2013 ◽  
Vol 67 (9) ◽  
pp. 961-965 ◽  
Author(s):  
S Lv ◽  
Y Wang ◽  
D Xu ◽  
S Rutherford ◽  
Z Chong ◽  
...  

2014 ◽  
Vol 18 (9) ◽  
pp. 1692-1697 ◽  
Author(s):  
Long Tan ◽  
Zhongna Sang ◽  
Jun Shen ◽  
Hua Liu ◽  
Wen Chen ◽  
...  

AbstractObjectiveTo explore (i) the prevalence of thyroid dysfunction in populations with adequate and excessive iodine intakes and (ii) the effect of iodine exposure on the prevalence of thyroid dysfunction.DesignCross-sectional study was conducted in Hebei in 2010. The population was classified as having adequate or excessive iodine intake according to the iodine concentration in drinking water. Demographic information was collected by questionnaire. Levels of serum thyroid hormones, thyroid autoantibodies and iodine in drinking water and urine were measured.SettingVillages with adequate or excessive drinking water iodine in Hebei Province, People’s Republic of China.SubjectsA total of 854 men and women aged 20–50 years who had lived in the surveyed areas for over 5 years, including 348 from the adequate iodine area (AIA) and 506 from the excessive iodine area (EIA).ResultsMedian urinary iodine concentration was 185 μg/l in AIA and 1152 μg/l in EIA. The prevalence of thyroid dysfunction in AIA was 10·3 %, which included 1·1 % with hypothyroidism and 8·1 % with subclinical hypothyroidism; and 20·6 % in EIA, which included 3·6 % with hypothyroidism and 13·6 % with subclinical hypothyroidism. The positive rates of thyroglobulin antibody were 16·1 % in AIA and 11·9 % in EIA; the positive rates of thyroperoxidase antibody were 20·7 % in AIA and 16·4 % in EIA.ConclusionsExcessive iodine intake may lead to increased prevalence of biochemical thyroid dysfunction, especially biochemical hypothyroidism. This is not related to an increase in prevalence of thyroid antibodies. Women are more susceptible to iodine excess.


2009 ◽  
Vol 94 (11) ◽  
pp. 4444-4447 ◽  
Author(s):  
Hye Rim Chung ◽  
Choong Ho Shin ◽  
Sei Won Yang ◽  
Chang Won Choi ◽  
Beyong Il Kim

Context: The dietary iodine intake of lactating women has been reported to be high in Korea. Objectives: The aim of this study was to assess iodine balance and to determine its relationship with thyroid function in preterm infants. Design: Thyroid functions of preterm infants born at 34 wk gestation or less were evaluated in the first (n = 31) and third (n = 19) weeks. Mothers’ breast milk (BM) and random urine samples of infants were taken on the same days for thyroid function tests. Results: Iodine concentrations in BM were very high (198–8484 μg/liter), and one third of the infants had an iodine intake of more than 100 μg/kg per day at the third week after birth (excessive iodine intake group). At that time, the levels of TSH were positively correlated with urinary iodine (r = 0.622; P = 0.004). The frequencies of subclinical hypothyroidism were high in the excessive iodine intake group at the third and sixth weeks. The estimated daily iodine intake at the third week (51.2 ± 45.5 vs. 149.0 ± 103.8 μg/kg per day; P = 0.033), urinary iodine at the third week (913.2 ± 1179.7 vs. 1651.3 ± 1135.2 μg/liter; P = 0.051), and estimated daily iodine intake at the sixth week (32.8 ± 35.5 vs. 92.1 ± 51.2 μg/kg per day; P = 0.032) were significantly higher in infants with subclinical hypothyroidism than in controls. Conclusions: Excessive iodine intake from BM contributed to subclinical hypothyroidism in these preterm Korean infants. An excessive amount of iodine in breast milk causes subclinical hypothyroidism in preterm infants.


2021 ◽  
pp. 1-30
Author(s):  
Ying Sun ◽  
Xin Du ◽  
Zhongyan Shan ◽  
Weiping Teng ◽  
Yaqiu Jiang

Abstract Iodine is an important element in thyroid hormone biosynthesis. Thyroid function is regulated by the hypothalamic-pituitary-thyroid axis (HPT). Excessive iodine leads to elevated thyroid stimulating hormone (TSH) levels, but the mechanism is not yet clear. Type 2 deiodinase (Dio2) is a selenium-containing protease that plays a vital role in thyroid function. The purpose of this study was to explore the role of hypothalamus Dio2 in regulating TSH increase caused by excessive iodine and to determine the effects of iodine excess on thyrotropin-releasing hormone (TRH) levels. Male Wistar rats were randomized into five groups and administered different iodine dosages (folds of physiological dose): normal iodine (NI), 3-fold iodine (3HI), 6-fold iodine (6HI), 10-fold iodine (10HI), and 50-fold iodine (50HI). Rats were euthanized at 4, 8, 12, or 24 weeks after iodine administration. Serum TRH, TSH, total thyroxine (TT4), and total triiodothyronine (TT3) were determined. Hypothalamus tissues were frozen and sectioned to evaluate expression of Dio2, Dio2 activity, and monocarboxylate transporter 8 (MCT8). Prolonged high iodine intake significantly increased TSH expression (p < 0.05), but did not affect TT3 and TT4 levels. Prolonged high iodine intake decreased serum TRH levels in the hypothalamus (p < 0.05). Dio2 expression and activity in the hypothalamus exhibited an increasing trend compared at each time point with increasing iodine intake (p < 0.05). Hypothalamic MCT8 expression was increased in rats with prolonged high iodine intake(p < 0.05). These results indicate that iodine excess affects the levels of Dio2, TRH, and MCT8 in the hypothalamus.


2019 ◽  
Vol 88 ◽  
pp. 134-135 ◽  
Author(s):  
Maria Ellfolk ◽  
Maija-Riitta Orden ◽  
Ulla Sankilampi ◽  
Heli Malm

2007 ◽  
Vol 156 (4) ◽  
pp. 403-408 ◽  
Author(s):  
Fan Yang ◽  
Zhongyan Shan ◽  
Xiaochun Teng ◽  
Yushu Li ◽  
Haixia Guan ◽  
...  

Objective: An increasing incidence of hyperthyroidism has been observed when iodine supplementation has been introduced to an iodine-deficient population. Moreover, the influence of chronic more than adequate or excessive iodine intake on the epidemiological features of hyperthyroidism has not been widely and thoroughly described. To investigate the influences of different iodine intake levels on the incidence of hyperthyroidism, we conducted a prospective community-based survey in three communities with mild-deficient, more than adequate (previously mild deficient iodine intake), and excessive iodine intake. Subjects and methods: In three rural Chinese communities, a total of 3761 unselected inhabitants aged above 13 years participated in the original investigation and 3018 of them received identical examinations after 5 years. Thyroid function, levels of thyroid peroxidase antibody (TPOAb), thyroglobulin antibody and urinary iodine excretion were measured and thyroid ultrasound examination was also performed. Results: In three communities, median urinary iodine excretion was 88, 214, and 634 μg/l (P<0.05) respectively. The cumulative incidence of hyperthyroidism was 1.4, 0.9, and 0.8% (P>0.05) respectively. Autoimmune hyperthyroidism was predominant in thyroid hyperfunction in all the three cohorts. Either positive TPOAb (>50 U/ml) or goiter in original healthy participants was associated with the occurrence of unsuspected hyperthyroidism in 5 years (logistic regression, OR=4.2 (95% CI 1.7–8.8) for positive TPOAb, OR=3.1 (95% CI 1.4–6.8) for goiter). Conclusion: Iodine supplementation may not induce an increase in hyperthyroidism in a previously mildly iodine-deficient population. Chronic iodine excess does not apparently increase the risk of autoimmune hyperthyroidism, suggesting that excessive iodine intake may not be an environmental factor involved in the occurrence of autoimmune hyperthyroidism.


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