Towards an animal model of amiodarone-induced thyroid dysfunction.
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In 7 patients with hyperthyroidism and 9 patients with hypothyroidism both thve before treatment and after a period of normal thyroid function of at least one year duration. As far as conduction velocity and relative refractory period are concerned there was no difference between hyperthyroid patients and normal persons, whereas in cases of hypothyroidism before treatment the conduction velocity was shown to be significantly reduced; moreover a prolonged relative refractory period and a decline in amplitude of the nerve action potential were found. These alterations of peripheral nerve function, interpreted as evidence of neuropathy, proved to be reversible when the thyroid function returned to normal.
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The purpose of this study was to review the epidemiological aspects and the characteristics of the thyroid disfunction produced by amiodarone in Catalonia, an area with type I endemic goiter. For this purpose, three groups of patients have been studied: 1) 102 patients with prolonged amiodarone treatment, out of whom 6 (5.9%) presented hyperthyroidism, and 2 (1.9%) hypothyroidism. 2) 909 patients with hyperthyroidism of any origin out of which 42 (4.6%) were produced by amiodarone. 3) 203 patients presenting primary hypothyroidism of any origin out of which 11 (3.8%) were induced by amiodarone. Out of the 48 patients with amiodarone induced hyperthyroidism, 16 presented multinodular goiter, 2 toxic thyroid goiter and 7 Graves Basedow disease. Thyroid uptake of 131I was studied in 10 cases being normal or increased in six of them, all with a underlaying thyroid pathology. Out of the 13 patients with amiodarone induced hypothyroidism, 3 presented diffuse goiter; thyroid uptake of 131I was studied in 5 patients, being normal or increased in 4 cases, 2 of which with thyroid pathology. Amiodarone administration very often produces thyroid disfunction, specially hyperthyroidism. These patients with hyperfunctional thyroids usually present underlying thyroid pathologies in which thyroid uptake of 131I are frequently not suppressed as well as in those patients in whide amiodarone induced hypothyroidism.
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