Abstract
Amiodarone (Cordarone) has been proven to be useful in the management of atrial) fibrillation. However, because of a large iodine content, this drug is not used in this complication of thyrotoxicosis. We previously have observed a greater fall in serum T3 and T4 concentrations in hyperthyroid patients treated with amiodarone and methimazole than with methimazole alone. In the present study, we determined whether the addition of amiodarone to propylthiouracil (PTU) could improve the levels of circulating thyroid hormones in hyperthyroid patients, and we assessed the release of iodide from amiodarone by measuring the 24 h urinary iodine excretion. Twelve hyperthyroid patients were treated either with PTU, 600 mg daily for 10 days (group PTU), or with amiodarone (A), 1200 mg daily for 3 days in addition to PTU (group A-PTU). Basal serum T4, T3, and rT3 concentrations (mean ± SEM) were respectively 206 ± 13 nmol/L, 5.13 ± 0.8 nmol/L, and 81 ± 7 ng/dL for group PTU and 238 ± 39 nmol/L, 4.73 ± 1.06 nmol/L, and 84 ± 12 ng/dL for group A-PTU (NS). In group A-PTU, plasma amiodarone peaked on day 3 (mean ± SEM: 0.48 ± 0.11 mg/L), and urinary iodine reached 5.27 ± 1.28 mg/day on day 5. The fall in serum T3 and the increase in serum rT3 concentrations were significantly greater in group A-PTU than in group PTU (ANOVA, p < 0.05). In group A-PTU, the minimal serum T3 concentration was observed on day 5 of treatment (28 ±6% of the pretreatment values). The fall in serum T4 was not significantly greater in group A-PTU, but it became significant 1 day earlier than in group PTU. A significant decrease in heart rate was observed only in group A-PTU (ANOVA, p < 0.05). In conclusion, in our hyperthyroid patients, amiodarone in conjunction with PTU induced a greater fall in serum T3 concentrations than did PTU alone. In addition to the peripheral inhibition of T4 to T3 conversion by amiodarone, the iodide released by amiodarone presumably inhibited thyroid secretion.
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