Amiodarone-induced thyroid dysfunction in cardiac patients from areas with iodine deficiency

Abstract

Amiodarone via iodine excess can determine thyroid dysfunction.

Aim: to assess thyroid dysfunction in patients treated with amiodarone, according to previous daily iodine intake.

Material and methods: 63 patients treated with amiodarone were assessed. 11 of 63 were resident in a moderate iodine deficient area. Thyroid stimulating hormone (TSH), free and total thyroxine (T4) and total triiodothyronine (T3) were measured. Thyroid ultrasonography, color flow Doppler sonography (CFDS), radioiodine uptake (RAIU) at 2 and 24 hours were also performed.

Results: Amiodarone-induced thyrotoxicosis developed in 31 patients (49.2%); 17 patients (27%) remained euthyroid. Patients from iodine deficient areas developed more frequent hyperthyroidism (91% vs. 40.4%), at significant lower cumulative doses of amiodarone, and never hypothyroidism. Overt hyperthyroidism prevails (29/31 patients). Frequency of amiodarone-induced thyrotoxicosis type I was 19% (12/63), type II 12.7% (8/63), and of mixed forms 17.5% (11/63), without significant differences between the two geographical areas. There are no peculiar features of amiodarone-induced thyrotoxicosis versus common hyperthyroidism, but there is a tendency at recurrence of tachyarrhythmias at lower levels of T3 than in common hyperthyroidism. Amiodarone-induced hypothyroidism developed in 15 patients (23.8%) and none was from iodine deficient areas, but almost half show high levels of antithyroid peroxidase antibodies (ATPO). Subclinical hypothyroidism prevails (11/15 patients).

Conclusion: a predictor for amiodarone-induced thyroid dysfunction is iodine deficiency in nutrition.