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Department of Nuclear Medicine, The Royal Marsden Hospital Sutton, Surrey, United Kingdom
Department of Medicine, St. Helier Hospital Carshalton, Surrey SM5 1AA
Address all correspondence and requests for reprints to: R. H. Rao, M.D., Department of Endocrinology, University of Pittsburgh School of Medicine, Montefiore Hospital, 3459 Fifth Avenue, Pittsburgh, Pennsylvania 15213.
Iodine kinetic studies were performed serially in 15 patients taking 300 mg amiodarone/day for 6 months to assess the biological significance of the high iodine content of the drug. Urinary inorganic iodide excretion increased from 0.25 ± 0.03 (±SE) µmol/mmol creatinine before treatment to over 7/xmol/mmol during therapy. Thyroid iodide clearance fell from 5.93 ± 0.82 ml/min to less than 0.5 ml/min, while plasma inorganic iodide rose from 0.05 ± 0.01 µmol/liter to approximately 2.2 µmol/liter during treatment. Thyroid absolute iodide uptake rose from 16.3 ± 2.7 to 54.6 ± 5.7 nmol/h after 6 weeks of therapy (P < 0.001). Thereafter, it progressively declined, but it was still significantly elevated (32.0 ± 4.3 nmol/h) after 24 weeks (P < 0.01). The calculated daily excretion of inorganic iodide rose to over 80 µmol during the study, accounting for about 10% of amiodarone iodine. During this time, the patients all had the characteristic plasma thyroid hormone changes associated with amiodarone therapy, i.e. increased T4, free T4, and rT3 and decreased T3, while remaining clinically euthyroid.
The massive increase in available inorganic iodide during amiodarone treatment is probably responsible for the induction of both the hypothyroidism and the thyrotoxicosis that can occur in patients receiving the drug.
* This work was supported by a grant from Labaz-Sanofi (UK) Ltd.
Received June 6, 1985.
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