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Department of Medicine (K.B.M., P.P., K.S.K., M.M., N.A.G., G.I., A.G.V.), Division of Endocrinology, University of Patras Medical School, University Hospital, Patras GR-26500, Greece; and Institute of Child Health (C.M.), Athens 11527, Greece
Address all correspondence and requests for reprints to: Apostolos G. Vagenakis, Department of Internal Medicine, Division of Endocrinology, University of Patras Medical School, University Hospital, Patras GR-26500, Greece. E-mail: vag.inmd{at}med.upatras.gr.
The aim of the present study was to examine the effects of chronic iodide administration in pharmacological doses on thyroid function in children with a history of transient congenital hypothyroidism (TCH). We hypothesized that such children may carry a previously undisclosed intrinsic intrathyroidal defect, rendering them susceptible to TCH. We administered for this 6065 mg iodide daily for 60 d in 13 individuals with TCH (group A), 8 of their siblings (group B), 8 healthy controls (group C), and 11 normal adults (group D). Thyroid function was evaluated by measuring serum T3, T4, free T3, free T4, TSH, and thyroglobulin concentrations and autoantibodies against thyroid peroxidase and thyroglobulin at baseline at 15, 30, and 60 d during iodide administration, and 2 months after iodide withdrawal. Hyperthyrotropinemia greater than 4.2 mU/liter but not higher than 10 mU/liter with normal thyroid hormone concentrations was observed in one of the TCH group and in two of the group B siblings. During iodide administration, hyperthyrotropinemia was observed in 8 of 13 (62%) adolescents in group A, 4 of 7 (57%) in group B, and 6 of 8 (75%) in group C. None of the 11 adults (group D) developed hyperthyrotropinemia during iodide administration. Serum T4 and free T4 concentrations were decreased in all groups when compared with baseline values. The magnitude of the decrease of serum T4 was identical in all groups (0.70.8 µg/dl). Thyroid enlargement was observed in all subjects and was more pronounced in children. There were no cases of subclinical and/or overt hyperthyroidism. After iodine withdrawal, serum TSH decreased in all groups and returned to baseline levels, as well as the thyroid volume. In conclusion, the hypothalamic-pituitary-thyroid axis of adolescents with TCH responds to pharmacological doses of iodide similarly to that observed in normal children. The hyperthyrotropinemia observed in the adolescents exposed to iodides may reflect incipient transient hypothyroidism or simply a brisk TSH response to a small serum T4 decrease. Whatever the mechanism, chronic use of excessive quantities of iodide should be avoided until the end of puberty.
Abbreviations: anti-Tg, Autoantibodies against Tg; anti-TPO, autoantibodies against thyroid peroxidase; FT3, free T3; FT4, free T4; TCH, transient congenital hypothyroidism; Tg, thyroglobulin.
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