Intensifying Iodine Deficiency Throughout Trimesters of Pregnancy in a Borderline Iodine-Sufficient Urban Area, Ankara, Turkey.

Iodine has long been recognized as an essential micronutrient for maternal thyroid function, as well as fetal growth and development during pregnancy. The current study aimed to evaluate thyroid hormone status, urinary iodine concentration (UIC), thyroid volume, and nodularity in pregnant women, throughout trimesters, in a borderline iodine sufficient, urban area with mandatory table salt iodization. Two-hundred-sixty-five pregnant women ranging from 17 to 45 years participated in this prospective longitudinal study. Thyroid function tests, thyroid volume, nodule growth, and UIC were recorded throughout the first, second, and third trimesters with no intervention. Median UIC was 96, 78, and 60 µg/L in the first, second, and third trimester of pregnancy, respectively (p < 0.001). Mean TSH values increased significantly (i.e. 0.65 mIU/ml, 1.1 mIU/ml, and 1.3 mIU/ml in the first, second, and third trimesters, respectively) (p < 0.001). Mean ± s.d. thyroid volume was significantly higher in the third trimester (14.72 ± 6.8 ml) compared with the first trimester (13.69 ± 5.31 ml) (p < 0.001). An intensifying iodine deficiency (ID) was reported throughout trimesters in this cohort of pregnant women from Ankara. A significant percentage of pregnant women from a borderline iodine sufficient, urban area in Turkey were iodine deficient during all trimesters, and the deficiency increased throughout the pregnancy. Pregnant women should receive iodine supplementation, besides consuming iodized salt in borderline iodine sufficient areas.

Iodine status of pregnant women in a metropolitan city which proved to be an iodine-sufficient area. Is mandatory salt iodisation enough for pregnant women?

The objective of this study was to assess the iodine status of pregnant women in a metropolitan city which was stated as iodine sufficient area after salt iodination program. This multicenter, cross-sectional study was carried out on 3543 pregnant women. Age, gestational weeks, smoking, consumption of iodized salt, dietary salt restriction, history of stillbirth, abortus and congenital malformations were questioned. Spot urine samples were analyzed for urine iodine concentration (UIC). The outcomes were: (a) median UIC in three trimesters of pregnancy and (b) frequency of ID among pregnant women. The median UIC was 73 µg/L. The median UIC was 77 µg/L (1-324), 73 µg/L (1-600) and 70 µg/L (1-1650) in three trimesters of pregnancy, respectively (p: 0.14). UIC <50 µg/L was observed in 36.6% (n: 1295) and UIC<150 µg/L was observed in 90.7% (n: 3214) of pregnant women. Only 1% (n: 34) of the pregnant women had UIC levels higher than 500 µg/L. This study showed that more than 90% of the pregnant women in this iodine-sufficient city are facing some degree of iodine deficiency during their pregnancy. A salt iodization program might be satisfactory for the non-pregnant population, but it seems to be insufficient for the pregnant population.

More than a decade of iodine prophylaxis is needed to eradicate goiter among school age children in a moderately iodine-deficient region.

BACKGROUND: There are many studies regarding the effect of iodine supplementation on goiter, but relatively few reports on the duration of iodine supplementation required to eradicate goiter in iodine-deficient regions. In the current study, we aimed to determine goiter prevalence as determined by sonographic methods, as it relates to changes in median urinary iodine concentrations (UIC) among school age children (SAC), ages 9-11. METHODS: This study was performed in Ankara, Turkey, before and 5-10 years after mandatory iodination of table salt. Three hundred to 400 SAC from the same primary schools were studied every year by measurement of UIC as part of Turkish Iodine Surveys. Sonographically determined thyroid volume of the SAC had been measured before the mandatory iodination in 1997 and 5-10 years afterward, in 2002 and 2007. The prevalence of goiter in children was evaluated using World Health Organization/International Council for the Control of Iodine Deficiency Disorders recommendations for age and sex. RESULTS: Moderate iodine deficiency was present in 1997 (median UIC, 25.5 microg/L), and it improved to mild iodine deficiency in 2001 (median UIC, 87 microg/L). Sufficient iodine intake (median UIC, 117 microg/L) was achieved by the year 2004. Goiter prevalence was 25% in 1997, 12.3% in 2001, and decreased to 1.3% in 2004. CONCLUSION: The time required to normalize the prevalence of goiter in SAC living in a moderately iodine-deficient environment was at least a decade. To achieve a goiter rate of less than 5% among SAC, it may require that, as a population, they were born and grew up under conditions of iodine sufficiency.

Thiocyanate overload and thyroid disease.

Thiocyanate [SCN-] is a complex anion which is a potent inhibitor of iodide transport. It is the detoxification product of cyanide and can easily be measured in body fluids. Consumption of naturally occurring goitrogens, certain environmental toxins and cigarette smoke can significantly increase SCN- concentrations to levels potentially capable of affecting the thyroid gland. Goiter endemics were reported to develop when the critical urinary iodine/ SCN- ratio decreases below 3 microg iodine per mg SCN-. Iodine supplementation completely reverses the goitrogenic influence of SCN-. SCN- is also generated from cigarette smoking as a detoxifying product of cyanide. During the past two decades many reports dealt with the possible effects of cigarette smoking on thyroid hormone synthesis, thyroid gland size and thyroid autoimmunity including infiltrative ophtalmopathy of Graves' disease. In this mini-review, issues regarding thiocyanate overload and thyroid disease will be summarized.

Twenty-four hour 17-hydroxyprogesterone response to adrenocorticotropine in adrenal incidentalomas: augmented response after adrenalectomy in two patients.

The current study aimed to investigate the midterm (24 hour) response of 17-hydroxyprogesterone (17-OHP) and dehydroepiandrosterone sulphate (DHEA-S) to synthetic high-dose adrenocorticotropin (ACTH) in adrenal incidentalomas (Al). Seventeen patients with Al and 40 age- and sex-matched controls received synthetic ACTH (tetracosactide, 1000 microg, IM). Plasma, 17-OHP and DHEA-S were collected in basal conditions and after 1, 4, 6, 8 and 24 hours. (HPA) axis was also evaluated using circadian serum cortisol, urinary free cortisol and over-night 2 mg dexamethasone suppression. Basal plasma 17-OHP levels did not differ among the groups. However, the increment in plasma 17-OHP in patients both in terms of peak [13.76 +/- 2.52, 4.77 +/- 0.30ng/ml, mean +/- S.E.M, p < 0.001] and area under the curve [190 +/- 46, 96.75 +/- 32 ng/ml/h, p < 0.001] were significantly higher than that of the controls. Stimulated 17OH-P levels never reached 9.1 ng/ml in controls. Sixty-five (11/17) % of the patients were found to have exaggerated response. Three of the patients were found to have subclinical Cushing's syndrome and interestingly, two augmented their 17-OHP response to ACTH after unilateral adrenalectomy and normalisation of their HPA axis. Basal DHEA-S levels of the patients were significantly lower [99.21 +/- 45, 230.18 +/- 34 microg/dl, p < 0.01] and stayed persistently lower than that of the controls. Evidence of a heterozygous 21 hydroxylase deficiency, as indicated by the exaggerated 17-OHP response to ACTH, has been widely reported in Al patients. However, to our knowledge to date there is no report on augmented 17-OHP response to ACTH after adrenalectomy. Possible reasons for the augmentation were discussed.