Iodine kinetics and effectiveness of stable iodine prophylaxis after intake of radioactive iodine: a review.

Ingestion of potassium iodide (KI) offers effective protection against irradiation of the thyroid after accidental exposure to radioactive iodine. This prophylaxis aims at rapidly obtaining maximal thyroid protection without adverse effects. This article reviews studies on iodine kinetics in humans and on the efficacy of KI in protecting the thyroid. In adults with normal thyroid function, ingestion of 100 mg of iodide just before exposure to radioactive iodine blocks at least 95% of the thyroid dose. If exposure persists after iodide ingestion (100 mg), the percentage of averted dose may decrease significantly. Daily ingestion of a dose of 15 mg of KI would then maintain the thyroid blockade at a level above 90%. The efficacy of iodide and the occurrence of antithyroid effects also depend on external and individual factors such as dietary iodine intake, thyroid function, and age. The KI dosage regimen should be adjusted for age at exposure. For the fetus, the newborn, children, and adolescents, the risk of radiation-induced thyroid cancer in case of accidental exposure to radioactive iodine justifies KI prophylaxis, despite the risk of hypothyroidism, especially in newborns. For the elderly, the benefits of KI may be lower than the risk of iodine-induced hyperthyroidism.     

Variation in iodine handling during normal pregnancy.

Reports in the literature are divided on changes in thyroid volume and urinary iodine excretion (UI) during normal pregnancy. Reports from Ireland, an area of modest dietary iodine intake (median UI 70 microg/L) showed an increase in UI that rose to a median value of 135 microg/L in the first trimester (T1) and continued at 124 microg/L in the second (T2) and 122 microg/L in the third trimester (T3). In parallel with the increase in UI, mean ultrasound measured thyroid volume increased by a maximum of 47% over nonpregnant values in the third trimester (T3). Although these findings were consistent with studies in Cardiff, UK (median UI 73 microg/L), which also showed a pregnancy-associated rise in UI excretion (maximum 176 microg/L) accompanied by a 30% increase in median thyroid volume, they differed from findings in Sri Lanka (median UI 146 microg/L), a country in which a successful program of salt iodination has recently been implemented, which showed no significant changes in UI excretion (T3 maximum 154 microg/L) but did show a modest (20%) maximum increase in median thyroid volume at T3. Prospective studies on Irish subjects showed that median UI fell precipitously to nonpregnant control values (76 microg/L) at delivery. In addition, UI in neonates sampled at 3-days postdelivery showed that excretion was greater in breast-fed than in bottle fed infants. Differences in reported UI excretion patterns during pregnancy may may reflect the existence of a threshold above which increased renal clearance results in increased iodine loss but that is masked at higher iodine intakes. Assuming constant dietary iodine intake during pregnancy, any increased urine loss will inevitably lead to negative iodine balance and thyroid depletion. In these circumstances, increased thyroid volume may in part be a compensatory mechanism to allow for greater iodine storage.     

Excess iodine induces apoptosis in the thyroid of goitrogen-pretreated rats in vivo.

Previously, we observed that excess iodide rapidly suppressed the elevated ornithine decarboxylase activity in the thyroid of propylthiouracil (PTU)-pretreated rats. Excess iodide also induces involution of goitrous thyroids. These findings led us to study effects of excess iodide on apoptosis of rat thyroids. When given to PTU-pretreated rats, excess potassium iodide (KI) (13 mg/kg body weight, 10 mg as iodine) induced DNA fragmentation in the thyroid at the first 3 hours after its treatment. The percentage of DNA fragmentation was also maximal at 3 hours after KI treatment. In methimazole-pretreated rats, the kinetic of DNA fragmentation was nearly the same; apoptosis increased for the first 6 hours and then decreased at 12 hours after KI administration. Other iodinated compounds such as amiodarone and diiodotyrosine have also shown apoptosis-inducing activity, but their effect was observed later than KI. Iopanoic acid had no such effect. Apoptotic changes were also observed with the use of flow cytometry. PTU or methimazole alone had some stimulatory effect on thyroid apoptosis. Iodine effect was not observed in rats treated with either perchlorate or thiocyanate. These results suggest that excess iodine induces thyroid involution in goitrogen-treated rats at least partially by apoptosis.     

Short-term changes in maternal and neonatal urinary iodine excretion.

Investigation of maternal urinary iodine (UI) excretion in the immediate antenatal and early postpartum periods showed a precipitous fall in median values from 93 microg/L antenatally to 36 microg/L at delivery subsequently rising to 49 microg/L and 63 microg/L at days 3 and 10 postpartum respectively. The fate of ingested iodine not appearing in the maternal urine is unknown but measurement of UI in babies born to nursing mothers suggested transfer from the mother with median neonatal values of 117 and 159 microg/L being recorded at days 3 and 10. While maternal UI seemed to relatively unaffected by breast feeding, median UI from breast feeding babies (148 microg/L) was significantly greater than in those bottle feeding (50 microg/L). This was also reflected by the finding that no breast feeding baby had a UI values < 50 microg/L in comparison to 50% of bottle feeders. The depressed values in mothers and relatively high values in their infants could present a false picture and suggest the need to defer any investigations of iodine status at this time. The findings do however suggest a need for further investigations aimed at determining the fate of iodine ingested perinatally and its possible physiological significance in maintaining thyroid status in the mother and neonate.     

Selenium and goiter prevalence in borderline iodine sufficiency

DESIGN: Selenium (Se) is required for the biosynthesis of selenocysteine-containing proteins. Several selenoenzymes, e.g. glutathione peroxidases and thioredoxin reductases, are expressed in the thyroid. Selenoenzymes of the deiodinase family regulate the levels of thyroid hormones. For clinical investigators, it is difficult to determine the role of Se in the etiology of (nodular-)goiter, because there are considerable variations of Se concentrations in different populations as reflected by dietary habits, bioavailability of Se compounds, and racial differences. Moreover, most previous clinical trials which investigated the influence of Se on thyroid volume harbored a bias due to the coexistence of severe iodine deficiency in the study populations. METHODS: Therefore, we investigated the influence of Se on thyroid volume in an area with borderline iodine sufficiency. First, we investigated randomly selected probands for urinary iodine (UI) and creatinine excretion in spot urine samples and determined the prevalence of goiter and thyroid nodules by high-resolution ultrasonography. After this, we determined urinary Se excretion (USe) in probands with goiter as well as in matched probands without goiter. Adjustments between the two compared groups were made for age, gender, history of thyroid disorders, smoking, and UI excretion. RESULTS: The mean USe and UI rates of all 172 probands were 24 micro g Se/l or 27 micro g Se/g creatinine and 96 micro g I/l or 113 micro g I/g creatinine indicating borderline selenium (20-200 micro g/l) and iodine (100-200 micro g/l) sufficiency of the study population. Probands with goiter (n=89) showed significantly higher USe levels than probands with normal thyroid volume (n=83; P < 0.05). USe rates were not influenced by present smoking or pregnancy. CONCLUSIONS: In our investigation, USe was not an independent risk factor for the development of goiter. The higher USe in probands with goiter in comparison with probands with normal thyroid volume is most likely a coincidence. Se does not significantly influence thyroid volume in borderline iodine sufficiency because the iodine status is most likely the more important determinant.     

Assessment of goiter in an area of endemic iodine deficiency.

Urinary iodone (UI) excretion and sonographically measured thyroid volume were investigated in 195 subjects living in 6 separate villages in the Casamance region of southeastern Senegal, West Africa. A comparison of goiter prevalence using thyroid palpation and volume measurement and of iodine excretion expressed as micrograms per gram (microg/g) creatinine or micrograms per deciliter (microg/dl) urine was undertaken, and possible pathogenetic factors were investigated. Ultrasound measured thyroid volumes were above the recommended upper limit of the reference range for an area replete in iodine in 83.1% or females, 52.3% of males, and 80.0% of children aged 13 years or younger. Overall sensitivity and specificity for palpation compared to sonographically demonstrated thyroid enlargement was 51.7% and 91.5%, respectively. Thyroid enlargement was not associated with ethnic origin, thiocyanate ingestion, HLA DR/DQ phenotype frequency, or thyroid growth-stimulating immunoglobulin (TGI) positivity. Median UI was 32 microg/g creatinine with 65.0% having values consistent with iodine deficiency (< 50 microg/g). When results were expressed as micrograms per deciliter, the percentage having values consistent with iodine deficiency (< 5.0 microg/dl) increased to 95.7%. The findings suggest a primary role for iodine deficiency in goitrogenesis in the study population. They demonstrate that classification of the severity of the endemia in this or other study populations in areas of iodine deficiency is dependent on the methods used to determine goiter prevalence (palpation or ultrasound measured thyroid enlargement), or dietary iodine status (iodine excretion expressed as micrograms per gram creatinine or micrograms per deciliter urine).     

Recurrent iodine deficiency in Tasmania,Australia: a salutary lesson in sustainable iodine prophylaxis and its monitoring

Even mild iodine deficiency during early childhood and pregnancy has the potential to impair neurological development. Often considered a problem of developing nations, a number of industrialized countries are at risk of deficiency. Despite past success with intentional and unintentional iodine fortification, recurrence of deficiency is an ever-present risk. Tasmania, an island state of the Commonwealth of Australia, has a history of endemic iodine deficiency, which was successfully eliminated by iodine prophylaxis initiated in 1950. In this report we describe a formal assessment of iodine nutrition in the Tasmanian population, 50 yr after initiation of the prophylaxis program. The requirements and obstacles to achieving sustainable iodine prophylaxis in an otherwise affluent community are considered. A cross-sectional study was undertaken during the yr 2000. Urinary iodine excretion (UIE) and thyroid ultrasonography were assessed in a representative statewide sample of school-age children. Children (n = 225) aged 4 to 17 yr from throughout Tasmania were studied. The sample comprised 99 girls and 126 boys. The median UIE was 84 microg/liter (87 microg/liter for males and 81 microg/liter for females), with UIE 50 microg/liter or less in 20%. Based on age-specific World Health Organization/International Council for the Control of Iodine Deficiency Disorders normative data for thyroid volume, the prevalence of elevated thyroid volume was 5.3% for boys and 3.5% for girls. However, after correcting the World Health Organization/International Council for the Control of Iodine Deficiency Disorders reference data, the prevalence increased to 24.6% for boys and 20.7% for girls. No significant difference in the thyroid volumes was found between males and females in this study. These data confirm the recurrence of mild iodine deficiency in Tasmania. The failure of sustained iodine prophylaxis highlights the universal importance of persistent surveillance, use of sustainable measures, public awareness, and a specific legislative framework for managing ongoing iodine prophylaxis. Our findings also emphasize the importance of accurate reference data for assessment thyroid volume.     

Assessment of thyroid function and urinary and breast milk iodine concentrations in healthy newborns and their mothers in Tehran

OBJECTIVE: To measure breast milk iodine (MI) and urinary iodine (UI) concentrations in healthy newborns and their nursing mothers from an iodine-sufficient region to determine adequacy and to relate these parameters to thyroid function tests in mothers and infants. DESIGN: Cross-sectional. PATIENTS: Forty-eight healthy neonates of 37 to 42 weeks' gestation with normal cord blood TSH values and their mothers were recruited in Tehran, Iran. MEASUREMENTS: Serum thyroid function tests were performed, and maternal and infant urinary iodine excretion, and maternal MI concentration were measured. RESULTS: Neonatal age was 12.9 +/- 3.9 (mean +/- SD; range 7-30) days and maternal age was 25.8 +/- 5 years. Median (range) UI in neonates was 271 microg/l (57-800) and in mothers was 107 microg/l (20-710). Median (range) MI was 148 microg/l (45-750). Neonatal and maternal UI did not correlate with serum thyroid function tests. UI < 150, 150-230, and > 230 microg/l was found in 20, 12.5, and 67.5% of neonates and 79.1, 14, and 7% of mothers, respectively. MI was < 150, 150-180, and > 180 microg/l in 52.4, 11.9, and 35.7% of mothers, respectively. CONCLUSIONS: Among euthyroid neonates, UI was adequate despite low median maternal UI and MI concentrations. There were no significant correlations between UI or MI and thyroid function tests in the mothers and infants.     

Thyroid volume is associated with family history of thyroid disease in pregnant women with adequate iodine intake: a cross-sectional study in southern Brazil

Maternal euthyroidism is important for fetal neural development. For this reason, adequate iodine nutrition during pregnancy is an important public health objective and should be periodically revised. The objective of this study was to measure urinary iodine (UI) excretion and the factors associated with thyroid volume (TV), in a group of healthy pregnant women in southern Brazil, to evaluate iodine nutrition. The median UI of the 147 women was 224 microg/l (P25=164 microg/l and P75=286 microg/l). Serum levels of free T4 and thyroglobulin did not correlate with UI, but there was a weak inverse correlation between serum TSH levels and UI (r=-0.200; p=0.02). TV, calculated through ultrasound in 57 women, was significantly associated with family history of thyroid diseases (p=0.002) and BMI (p=0.03), but there was no association with UI, corrected or not for creatinine, serum free T4, TSH or thyroglobulin, current or past smoking, gestational age, parity or oral contraceptive. CONCLUSIONS: The healthy pregnant women studied had adequate iodine intake. In this situation, the main thyroid size determinants are probably genetic factors.     

Nuclear detonation, thyroid cancer and potassium iodide prophylaxis

The recent nuclear disaster at Japan has raised global concerns about effects of radioactive leakage in the environment, associated hazards, and how they can be prevented. In this article, we have tried to explain about the guidelines laid down by World Health Organization for a potassium iodide prophylaxis following a nuclear disaster, and its mechanism of action in preventing thyroid cancer. Data was collected mainly from the studies carried out during the Chernobyl disaster of Russia in 1986 and the hazardous effects especially on the thyroid gland were studied. It was seen that radioactive iodine leakage from the nuclear plants mainly affected the thyroid gland, and especially children were at a higher risk at developing the cancers. Potassium Iodide prophylaxis can be administered in order to prevent an increase in the incidence of thyroid cancers in the population of an area affected by a nuclear disaster. However, one has to be cautious while giving it, as using it without indication has its own risks.     

Thyroid ultrasound is the best prevalence indicator for assessment of iodine deficiency disorders: a study in rural/tribal schoolchildren from Gujarat (Western India)

OBJECTIVES: (i) To assess the severity of iodine deficiency disorders (IDD), (ii) to determine the aetiology of IDD in Gujarat, (iii) to identify the best prevalence indicator of IDD, and (iv) to compare thyroid volume (TV) results with the WHO International reference. METHODS: Five hundred and thirty schoolchildren (6-15 years) were studied from two districts (Baroda and Dang) and data were collected on dietary habits and parameters such as height, weight, thyroid size by palpation and ultrasonography, urinary iodine (UI), and blood thyroid stimulating hormone (TSH). Drinking water was analyzed for iodine content and food articles for goitrogens. RESULTS: In Gujarat children median UI (interquartile range)=56 (30-96)microg/l, mean TSH=1.71 +/- 2.10mU/l, goiter by palpatio n = 30%, and median TV = 27.8 (23-35)ml. Females had lower median UI (48 (27-82) microg/l) and higher mean TSH levels (2.0 +/- 2.5mU/l) than males. Applying the WHO ultrasonography reference to Gujarat children resulted in an enlarged TV-for-body surface area in almost 100% of subjects. Ninety-nine percent of females and 95% of males had enlarged TV-for-age. Three to eight times larger TV were seen in all subjects as compared with European children. Dang children were severely malnourished. Flavonoids like vitexin, glucosyl vitexin and apigenin were detected in pearl millet. Apigenin was never identified in pearl millet. Dang district water was lacking in iodine content. CONCLUSIONS: IDD is a severe public health problem in Gujarat. Baroda district is a new pocket of IDD. High amounts of dietary flavonoids in Baroda and Dang districts, and lack of iodine in Dang water, account for IDD. TV measurement by ultrasound is the best prevalence indicator of IDD.     

Goiter prevalence and urinary iodine concentration in slovenian adolescents.

Context: Slovenian school-age children are, as are more than half of European school-age children, still considered to be iodine deficient. In 1999, supplementation of salt was increased from 10 to 25 mg of KI/kg of salt. Objective: The objective of our study was to determine the success of this intervention. Design and Patients: Twelve hundred sixty-four girls (mean age +/- SD: 15.7 +/- 0.6 years) and 1200 boys (15.8 +/- 0.8 years) representing 10% of all 15-year-old Slovenian adolescents were studied. Thyroid size was estimated by clinical examination in all subjects and by ultrasound when enlarged thyroid was suspected. Thyroid volume was also determined by ultrasound in 108 random iodine-sufficient adolescents. In addition, urinary iodine concentration was determined in all subjects. Results: Enlarged thyroid was determined by clinical examination and ultrasound in 0.9% of all subjects. In randomly selected iodine-sufficient subjects, enlarged thyroid was determined in 4.6%. Median urinary iodine concentration for the population was 140 microg/L. In all regions it was greater than or equal to 100 microg/L. Values less than 50 microg/L were determined in 2.5% of all subjects. Conclusions: Slovenian adolescents are iodine sufficient and the prevalence of goiter is low, indicating that increased KI supplementation of salt in 1999 was successful.     

Urinary iodine levels and thyroid diseases in children; comparison between Nagasaki and Chernobyl.

We evaluated the incidence of childhood thyroid diseases and urinary iodine levels in Nagasaki, Japan and in Gomel, Belarus, which was greatly radio-contaminated by the Chernobyl accident, in order to obtain the comparative data of thyroid diseases between iodine-rich (Japan) and -deficient (Belarus) areas. In Nagasaki, the median level of urinary iodine, measured by ammonium persulfate digestion in microplate method, was 362.9 microg/L. In order to evaluate the geographical differences in Japan, other samples were collected in Hamamatsu and in South Kayabe, Hokkaido, where the median levels were 208.4 microg/L and 1015.5 microg/L, respectively. Furthermore, thyroid screening by ultrasound (US) in Nagasaki revealed only four cases that showed goiter (1.6%) and two cases (0.8%) that had cystic degeneration and single thyroid cyst. There was no evidence of thyroid nodule detected by US examination. In contrast, the median of urinary iodine level was 41.3 microg/L in Gomel. The incidences of goiter (13.6%) and echogenic abnormality (1.74%) in Gomel were much higher than in Nagasaki, suggesting the critical involvement of iodine deficiency in increased childhood thyroid abnormality around Chernobyl. Radioactive iodine released just after the Chernobyl accident may have influenced predominantly children residing in iodine-deficient areas. Our results suggest that management of thyroid screening for schoolchildren at ordinary times may be beneficial for monitoring the adverse effects of radioactive iodine from the standpoint of future prospective study.     

Thyroid autoimmunity in the current iodine environment.

Iodine is essential for thyroid function. Thyroid disorders related to iodine deficiency decreased progressively with the continuous iodine prophylaxis and the increased iodine intake. An adverse effect resulting from iodine prophylaxis may be the induction of thyroid autoimmunity. Although experiments performed in animal models suggest that iodine could initiate or exacerbate thyroid autoimmunity, the role of iodine in humans remains controversial. Several observational studies in areas with adequate or high iodine intake suggest that there is an increase in the incidence of thyroid autoimmune disease. Moreover, intervention studies suggest that increased iodine intake may enhance thyroid autoimmunity too. However, not all studies generated the same findings, probably because of genetic, racial, and environmental differences. It seems that autoimmune exacerbation is a transient phenomenon. Studies have shown that in persons presenting thyroid antibodies, the levels of these antibodies progressively decrease when the majority of them react against a nonspecific pattern of thyroglobulin (Tg) epitopes. However, in a small number of these persons, the anti-Tg antibodies are similar to those in patients with patent thyroid autoimmune disease, reacting against specific immunodominant Tg epitopes, and their levels persist. One possible attractive explanation is that enhanced iodine intake increases the antigenicity of Tg through the incorporation of iodine into its molecule and the formation of iodinated Tg epitopes or even the generation of noniodinated pathogenetic Tg epitopes that are normally cryptic.     

Thyroid volumes and urinary iodine in Swiss school children, 17 years after improved prophylaxis of iodine deficiency

Salt iodine content in Switzerland was raised from 7.5 to 15 mg per kg in 1980, and since then dietary iodine intake has been considered to be sufficient, even though a slight decrease due to imported food has recently been reported. The aim of this study was to establish normal values for thyroid volumes of school children who can be assumed to have had a sufficient iodine intake all their lifetime. Moreover. the present investigation was undertaken to verify that iodine sufficiency had been achieved equally in two regions each served by one of the two Swiss salt producers. Mean iodine concentration in urine spot samples from school children was 16.1 microg/dl, and it was identical in both the city of Lausanne (n=215) and the city of Solothurn (n=208). Thus it can be stated that in both cities (served by two different salt producers) iodine intake is equal and sufficient. Accordingly, thyroid volumes measured by ultrasound in school children aged 6 to 16 years were the same in both Lausanne (n=202) and Solothurn (n=207). Moreover, the age-adjusted median volumes at the 97th percentiles closely agree with and validate provisional international reference values recently proposed by the World Health Organisation and by the International Council for Control of Iodine Deficiency Disease.     

The impact of 25 years of iodine prophylaxis on the adult thyroid weight in Finland

The effect of iodine prophylaxis on endemic goiter was studied in an adult Finnish population by comparing autopsy records from 1959 and 1984. In the 1950's the iodine intake calculated both from urinary excretion of stable iodine and from food analysis data was 50-70 micrograms per day the intake being lower in the main endemic area in the eastern part of the country. The use of iodized salt raised these figures only by 15 micrograms per day. At the beginning of the 1980's the iodine intake calculated in the same way was around 300 micrograms per day all over the country. Initially 696 records from 1959 and 525 from 1984 were analyzed. Excluded were cases with primary or secondary malignant thyroid tumors, autopsies with incompletely recorded thyroid weight, and autopsies from patients submitted to pituitary or thyroid surgery or radiation therapy. Finally, 318 cases from 1959 and 478 from 1984 were accepted. A significant decrease in thyroid weight from a mean of 44 to a mean of 34 g was observed. The difference between the two populations was most marked in the age groups below 45 yr. In these age groups the mean thyroid weight was about 20-27 g which can be regarded as normal. In the age groups over 75 years there were no significant differences. These data indicate that the iodine prophylaxis gradually eradicates the endemic goiter in Finland but that it requires still some 25-35 yr before it has disappeared also in the oldest age groups.     

Hypertrophy and hyperplasia during goitre growth and involution in rats--separate bioeffects of TSH and iodine

Goitre growth was investigated in rats receiving a low iodine diet (less than 0.1 microgram iodine/g) and either 1 g/l KClO4 or 1 g/l propylthiouracil (PTU), or a combination of KClO4 or PTU with 50.82 nmol/1 T3 in tap water for 3 weeks. To investigate goitre involution, rats with iodine-deficient goitres were treated for 3 weeks either with T3 (0.5 microgram T3/day = 0.768 nmol/day), iodide (0.5 or 2.7 micrograms KI/day) or a combination of T3 with both iodide doses. Histology together with total DNA distinguished between hypertrophy and hyperplasia of the gland. During goitre growth there was highly significant correlation between goitre weight and TSH serum level (r = 0.93, P less than 0.001). Thyroid total DNA, however, was only weakly correlated to TSH but was inversely related to the degree of iodine deficiency. During goitre regression, TSH levels were normalized, histological signs of hypertrophy had disappeared, and thyroid weight was nearly normalized in all therapy groups. Total DNA, however, was normalized only with 2.7 micrograms KI/day (95 +/- 18 micrograms DNA/gland), and still elevated in all other groups. The highest DNA levels were found under T3 therapy (143 +/- 21 micrograms DNA/gland) and under 0.5 microgram KI/day (161 +/- 19 micrograms DNA/gland). Reduction of total DNA was independent of TSH, but followed replenishment of the iodine content of the glands. We conclude that TSH mainly induces hypertrophy, whereas thyroid hyperplasia is mainly regulated by the intracellular iodine content.     

不同碘水平对哺乳期母鼠和仔鼠的甲状腺功能及子代生长发育的影响

目的研究不同碘水平对哺乳期母鼠和仔鼠的甲状腺功能以及子代生长发育的影响。方法Wistar母鼠随机分为4组：重度缺碘组（SID）、轻度缺碘组（MiID）、正常碘组（NI）、碘过量组（ExI）。所有大鼠均食用缺碘饲料,饮水给予不同剂量的碘化钾,喂养3个月后交配,检测哺乳14d时母鼠及其仔鼠的尿碘、乳汁碘和血液甲状腺激素（TH）水平,观察仔鼠的体格发育和神经发育的情况,采用MIAS-2000图像分析系统测量生后10、14、20、25、28日龄仔鼠小脑外颗粒层（EGL）厚度。结果（1）母鼠及仔鼠尿碘、乳汁碘均随饮食碘供给量的增加而增加,其组间变化幅度以母鼠尿碘为最高、仔鼠尿碘次之、乳汁碘最低;（2）SID组母鼠血清TT4、TT3／TT4比值升高,仔鼠TT4降低,与NI组比较有统计学意义,而MiID和ExI组无论母鼠和仔鼠均与NI组无明显差异;（3）SID组仔鼠体格和神经发育明显落后于NI组,小脑EGL增殖和消退明显延迟;MiID和ExI组仔鼠的各项发育指标与NI组无明显差别。结论母亲重度缺碘会严重影响子代的生长发育和神经发育,但在轻度缺碘和碘过量（正常碘的30倍左右）时,通过母体的代偿作用可以保证子代正常的碘营养、甲状腺功能以及生长发育。     

T-2 mycotoxin intensifies iodine deficiency in mice fed low iodine diet

Mice were depleted of iodine and fed a 125I-labeled low iodine diet. After they developed isotopic equilibrium they were given T-2 mycotoxin, in doses 34% to 14% of LD50/day for 4 to 12 days. In all cases T-2 toxin caused loss of thyroid iodine from which the animals recovered when the T-2 toxin was stopped. When iodine intake was adequate, the T-2 toxin had no statistically significant effect on the thyroid iodine content. Since T-2 toxin is known to block the initiation of some protein synthesis, it may block thyroglobulin synthesis, and, in stimulated thyroids, limited hydrolysis may continue. Therefore, when the thyroids were stimulated and thyroglobulin was depleted, a blockade of thyroglobulin synthesis may have caused further depletion of thyroidal iodine.     

Iodine prophylaxis using iodized salt and risk of maternal thyroid failure in conditions of mild iodine deficiency

CONTEXT: Mild to moderate iodine deficiency during pregnancy can cause transient maternal hypothyroidism and impaired mental development of the progeny. These unfavorable effects are preventable by iodine supplementation. In Europe, however, less than 50% pregnant women receive iodine-containing supplements, thus representing dietary iodized salt the only carrier of iodine for most women in this life stage. OBJECTIVE/DESIGN: This longitudinal study is aimed to investigate the effects of long-term iodized salt consumption on maternal thyroid function during gestation. PARTICIPANTS/OUTCOME MEASURES: We prospectively evaluated thyroid function in 100 consecutive thyroperoxidase antibody-negative pregnant women from a mildly iodine-deficient area. Sixty-two women who had regularly used iodized salt for at least 2 yr prior to becoming pregnant and 38 who commenced iodized salt consumption upon becoming pregnant were classified as long-term (LT) and short-term (ST) iodine supplemented, respectively. RESULTS: Long-term iodized salt consumption resulted in a very low prevalence of maternal thyroid failure (MTF) in LT women. Conversely, short-term iodine prophylaxis does not seem to protect against the risk of MTF, the prevalence of which was almost 6-fold higher in ST than LT women (36.8% vs. 6.4%; chi(2) 14.7, P < 0.0005; relative risk 5.7, 95% confidence interval 2.03-16.08, P < 0.001). The relative risk reduction amounted to 82.5%, this measure indicating the extent to which long-term iodine prophylaxis using iodized salt would reduce the risk of MTF in ST women. CONCLUSIONS: Prolonged iodized salt significantly improves maternal thyroid economy and reduces the risk of maternal thyroid insufficiency during gestation, probably because of a nearly restoring intrathyroidal iodine stores.