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Journal of Clinical Endocrinology & Metabolism, Vol 59, 893-898, Copyright © 1984 by Endocrine Society

ARTICLES

Short and long term effects of radioiodine treatment on the iodine content of the thyroid gland

M Schlumberger, P Fragu, C Hill, C Parmentier and M Tubiana

Thyroid iodine content (TIC) was measured in nine patients with hyperthyroid Graves' disease for 5-26 months after treatment with 131I (100-125 muCi/g tissue). In all patients, TIC decreased; in eight patients it became undetectable within 5 +/- 3 (SD) months. This fall was parallel to those of serum T3 and T4 levels and was not prevented by the administration of large doses of stable iodine. In four patients, this decrease was irreversible and they became clinically hypothyroid. In the five other patients, it was partly reversible: the secondary increase of TIC was parallel to those of serum T3 and T4 and to a decrease in TSH levels. These data suggest that during the months after 131I treatment, determination of TIC may help to distinguish transient from irreversible hypothyroidism. The late effects of 131I were studied in 38 patients who had been treated for hyperthyroid Graves' disease from 1.5-22 yr previously. The 16 patients who, at the time of examination, were euthyroid with normal serum TSH levels (less than 8 microU/ml) had a TIC [3.2 +/- 3 (SD) mg] significantly lower than that of 10 euthyroid patients previously treated only with antithyroid drug therapy (16.7 +/- 8.2 mg). A significant negative correlation was found between log basal TSH and log TIC (r = 0.61, P less than 0.001) and a positive correlation between log T4 and log TIC (r = 0.56, P less than 0.002). The T3/T4 ratio in patients with undetectable TIC (19.9 +/- 7.9) was higher than that of the other patients (14.6 +/- 3.2) (P = 0.02, Wilcoxon test). This hormonal profile was not modified by iodide supplementation, which increased TIC only transiently. The turnover of thyroid iodine was accelerated, which appeared to be the consequence of a small thyroid functional mass and of hyperstimulation by TSH.




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