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

UNLABELLED

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.