Inhibition of Thyroidal Iodine Release by Estrogens in Patients with Hyperthyroidism*

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Abstract
The effects of pharmacological doses (25 mg daily, orally) of the estrogen Dienoestrol on thyroidal iodine release of patients with untreated hyperthyroidism were examined. Thyroidal release was assessed by measuring the urinary radioiodide derived from deiodination of endogenously labeled [125I]T4 and the exogenously administered[131I]T4.The ratio of 125I to 131I in urine was plotted on semilogarithmic paper and depicted a slope which reflected thyroidal release. Estrogeninduced a sharp decline of the progressively rising slope in five of the six patients. The slope value for the whole group was 0.153 ± 0.103 in the control phase and 0.013 ± 0.032 during estrogen treatment (P < 0.025). The contribution of iodide recirculation to this effect was evaluated in four hyperthyroid patients who did not receive estrogens. Their mean 7¬day control slope was 0.167 ± 0.086. During days 14¬21, the time period correspondingto the estrogenic phase of the treated group and during which the probable effects of iodide recycling might become noticeable, the slope value declined slightly to 0.130 ± 0.069 (P = NS). All patients had undetectable levels of serum TSH during both the control and estrogenic phases. Estrogen decreasedthe fractional turnover of T4 from 18.5% to 13.8‰/day (P < 0.01), the distribution space from 10.6 to 10.1 liters (P = NS), and the MCR from 1.96 to 1.40 liters/day (P < 0.005). Serum T4 increased from 22.9 to 25.0 jug/100 ml (P < 0.05), whereas absolute T4 disposal fell from 438 to 343 fig/day (P < 0.005). The data suggest that in addition to its effects on the peripheral metabolism of T4, estrogen treatment in the dose used in this study partly inhibited the thyroidal secretion of patients with hyperthyroidism.