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Quantitative studies of iodine metabolism were carried out in iodide-treated hyperthyroid patients in order to observe the alterations of iodine metabolism which occur in response to clinical improvement and to the recurrence of symptoms. Twelve hyperthyroid patients were given 10 mg of iodide as KI t.i.d. and several thyroid function tests were performed at intervals of 2 weeks thereafter. Serum PBI and T3-resin sponge uptake decreased to the normal range within 2 weeks in all patients and these normal values continued until recurrence of thyrotoxicity. One, 2 and 24 hr thyroidal 131I uptakes decreased from 57.4 to 22.6%, from 68.0 to 24.4%, and from 75.1 to 19.9%, respectively, within 2 weeks of the iodide treatment. However, these values were considerably higher than those obtained from similarly treated euthyroid subjects (2.6, 2.5 and 3.4%, respectively). Thyroidal absolute iodine uptake (AIU), calculated from thyroidal clearance of 131I multiplied by serum inorganic 127I, increased about 3-fold during iodide treatment. Since thyroidal clearance of 131I was calculated from the increment in thyroidal 131I between 1 and 2 hr after 131I injection divided by serum 131I at the midpoint, AIU in the present experiment could be considered to represent the incorporation of iodine into organic components. It is very unlikely that all the increased AIU is stored in the thyroid. Therefore, the difference between the increased AIU and the decreased hormone secretion should reflect the release from the thyroid of nonhormonal iodine. Recurrence of thyrotoxicity during iodide treatment was observed in 6 patients, starting from 6 to 14 weeks after treatment was begun. At this time, serum PBIs increased into the hyperthyroid range, indicating that the hormone secretion had increased. However, thyroidal 131I uptake as well as thyroidal AIU did not change consistently in response to recurrence of thyrotoxicity. It appears, therefore, that, at least with chronic treatment, iodide does not decrease the total thyroidal iodine release, but decreases only hormone secretion and increases nonhormonal iodine secretion.
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Nagataki et al. (1970) studied this question.
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