Iodized salt consumption maintains euthyroidism in iodine-deficient hypothyroid subjects
- PMID: 12847995
- DOI: 10.1024/0300-9831.73.3.187
Iodized salt consumption maintains euthyroidism in iodine-deficient hypothyroid subjects
Abstract
Following previous reports of impaired physical and intellectual growth, hearing deficit, hypothyroidism, and hyperendemic goiter in Kiga, and the administration of iodized oil injection, this study was conducted to evaluate whether or not the effect of the injection could be sustained by iodized salt supplementation. In 1989, one mL of iodized oil solution containing 480 mg of iodine was injected in 198 schoolchildren aged 8 to 14 years. Four years later, in 1993, iodized salt consumption was begun and has since been continued. Serum thyroid hormones, RT3 uptake and thyroid-stimulating hormone (TSH) were measured before, and three, four, and six years after intervention (1989, 1992, 1993, and 1995). Assessment of urinary iodine was performed by the Foss method at the same intervals mentioned above. Prior to the injection, 94% had grade 2 goiters; four years after injection, 26% and 41% had grades 2 and 1 respectively, and 30% had no goiter (p < 0.001). Two years after the introduction of iodized salt consumption, 5 and 39% had grades 2 and 1 goiter, and 56% were not goiterous. Urinary iodine was 11.4 +/- 19.8 micrograms/L before intervention, and was increased to 93 +/- 66 and 92 +/- 34 micrograms/L, three and four years, respectively, after intervention. Two years after iodized salt consumption it was 161 +/- 34 micrograms/L. Mean serum T4 was 5.0 +/- 2.0, 9.6 +/- 2.0, 9.6 +/- 2.0 and 9.2 +/- 1.5 micrograms/dL; serum TSH was 20.3 +/- 22.8, 2.1 +/- 1.9, 2.5 +/- 1.6 and 2.9 +/- 1.7 mU/L; before and three, four, and six years after the beginning of the study. All children were euthyroid after three, four, and six years of study. Findings show the benefits of iodized oil administration in decreasing goiter size and in reversing abnormal thyroid function. These effects are sustained by iodized salt consumption in schoolchildren who had been previously hypothyroid due to iodine deficiency.
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