Abstract:Iodine deficiency is recognised as a major preventable public-health worldwide problem. The aim of this study is to assess local reference values for thyroid volume, and give a snapshot of the epidemiology of goiter and iodine nutritional status of the Turin schoolchild population. Sonographic thyroid volume and median urinary iodine excretion were obtained in 1067 schoolchildren aged 11-15 yr resident in Turin for more than 5 yr to assess both goiter prevalence and iodine intake. All the subjects were asked t… Show more
“…Our patients were classified as iodine deficient, sufficient, or mixed group based on published UI excretion and endemic goiter prevalence (26)(27)(28)(29)(30)(31)(32). We are aware that this approach might be prone to a certain percentage of misclassification of patients (37)(38)(39). However, the alternative approach to using individual spot UI values is likely to be highly variable over time (40).…”
Objective: Differences in iodine intake could account for the variable prevalences reported for somatic TSH receptor (TSHR) mutations in toxic thyroid nodules (TTNs). However, this question has not been settled, since no study has yet determined the TSHR mutation prevalence in regions with different iodine supplies in the same population using the same methodology. Therefore, we studied the prevalence of somatic TSHR mutations in TTNs from patients living in iodine-deficient or -sufficient regions in Turkey. Design and methods: We screened 74 TTNs for somatic TSHR mutations. Exons 9 and 10 of the TSHR and 7 and 8 of the Gsa were screened by denaturing gradient gel electrophoresis. Determination of X-chromosome inactivation was used for clonality analysis. Results: TSHR mutations were identified in 52 (70.2%) of 74 TTNs. A Gsa mutation was identified in one TTN. Three new TSHR mutations were detected (A627V, I640K, I486N). No significant difference between frequencies of TSHR mutations in iodine deficient/sufficient regions was found. The frequency of non-random X-chromosome inactivation was similar in iodine-sufficient or -deficient regions and in TSHR mutation positive or negative hot nodules. Conclusions: These findings suggest that TTNs in iodine deficient/sufficient areas predominantly arise from aberrant growth of a single cell. Our results suggest that neither the prevalence of TSHR mutations nor that of monoclonal TTNs is related to iodine supply.European Journal of Endocrinology 155 535-545
“…Our patients were classified as iodine deficient, sufficient, or mixed group based on published UI excretion and endemic goiter prevalence (26)(27)(28)(29)(30)(31)(32). We are aware that this approach might be prone to a certain percentage of misclassification of patients (37)(38)(39). However, the alternative approach to using individual spot UI values is likely to be highly variable over time (40).…”
Objective: Differences in iodine intake could account for the variable prevalences reported for somatic TSH receptor (TSHR) mutations in toxic thyroid nodules (TTNs). However, this question has not been settled, since no study has yet determined the TSHR mutation prevalence in regions with different iodine supplies in the same population using the same methodology. Therefore, we studied the prevalence of somatic TSHR mutations in TTNs from patients living in iodine-deficient or -sufficient regions in Turkey. Design and methods: We screened 74 TTNs for somatic TSHR mutations. Exons 9 and 10 of the TSHR and 7 and 8 of the Gsa were screened by denaturing gradient gel electrophoresis. Determination of X-chromosome inactivation was used for clonality analysis. Results: TSHR mutations were identified in 52 (70.2%) of 74 TTNs. A Gsa mutation was identified in one TTN. Three new TSHR mutations were detected (A627V, I640K, I486N). No significant difference between frequencies of TSHR mutations in iodine deficient/sufficient regions was found. The frequency of non-random X-chromosome inactivation was similar in iodine-sufficient or -deficient regions and in TSHR mutation positive or negative hot nodules. Conclusions: These findings suggest that TTNs in iodine deficient/sufficient areas predominantly arise from aberrant growth of a single cell. Our results suggest that neither the prevalence of TSHR mutations nor that of monoclonal TTNs is related to iodine supply.European Journal of Endocrinology 155 535-545
“…Piemonte has been described as a moderately iodine-deficient region since the 1970s (42). However, over the years the Piemonte population has benefited from a silent iodine supplementation especially in rural/mountain areas (27,43) due to improved nutritional conditions, the presence of iodine residues remaining in milk from disinfectant agents (42) (iodophors) used in dairying, the increase in the use of industrially produced food, and to a widespread awareness among population of the risk of iodine-deficiency disorders. This has led to a condition of iodine sufficiency in this region (27,40).…”
Background: Mortality for thyroid cancer (TC) is low and has been decreasing worldwide; yet few population studies based on mortality have been conducted. Several nonradiation risk factors have been associated with TC, including residence in goiter-endemic areas (as an indicator of iodine deficiency). We used mortality data to perform a spatial-temporal analysis regarding TC in Italy and investigated the association between mortality and socioeconomic status and geographical features (residing in a mountainous area is a proxy for iodine deficiency). Methods: We analyzed data from Italy's National Mortality Database (1980Database ( -2009. To evaluate temporal trends in mortality the age-standardized death rate (ASR) was used; to identify geographic areas with excess deaths due to TC standardized mortality rates (SMR) were calculated. We also calculated the rate ratios (RR) of the ASR and the 95% CI by sex. We performed a cluster analysis to identify municipalities with major departures from expected mortality, both in the entire study period and in two separate periods to evaluate the spatial-temporal variability. Finally, we evaluated the association between mortality and index of deprivation and altitude.
The prevalence of goiter still remains high in some areas of Iran in spite of iodine supplementation. In the present study, we investigated the role of selenium (Se) deficiency in the etiology of goiter in Isfahan. Two thousand three hundred thirty-one schoolchildren were selected by multistage random sampling. Thyroid size was estimated in each child by inspection and palpation. Urinary iodine concentration (UIC) and plasma Se were measured. Overall, 32.9% of the 2,331 children had goiter. The median UIC was 19.55 microg/dl. Plasma Se was measured in 96 goitrous and 72 nongoitrous children. The mean +/- SD of plasma Se in goitrous and nongoitrous children was 66.86 +/- 21.82 and 76.67 +/- 23.33 microg/l, respectively (P = 0.006). Goitrous girls had lower plasma Se level than nongoitrous girls (65.62 +/- 21.64 vs. 76.51 +/- 22.61 microg/dl, P = 0.02). Goitrous boys had lower plasma Se level than nongoitrous boys (68.45 +/- 22.21 vs. 76.91 +/- 24.76 microg/l, P = 0.14). The prevalence of Se deficiency was significantly higher in goitrous boys and girls than nongoitrous children. Se deficiency is among the contributors of goiter in Isfahan goitrous schoolchildren. However, the role of other micronutrient deficiencies or goitrogens should be investigated in this region.
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