Endocrine Abstracts

Introduction: Amiodarone-induced thyrotoxicosis(AIT) is a condition fraught with difficulties from the diagnostic and therapeutic standpoints. It can be developed precociously or years after the beginning amiodarone uptake and after its suspension. AIT is subdivided in three different forms. Type 1 is developed in subjects with underlying thyroid disease, being caused by an exacerbation by iodine load of thyroid autonomous function. Type 2 is a form of destructive thyroiditis and the majority of the cases is developed in normal thyroid glands. Mixed forms of AIT may also be observed.

Case report: Man, 60 years-old, revealing history of tetralogy of Fallot surgically corrected and atrial fibrillation since 2005, under therapeutic with amiodarone(200 mg/day), digoxin and hypocoagulation therapy since diagnosis. He was hospitalized due to a bradyarrhythmia, submitted to a definitive pacemaker implant, suspended amiodarone therapy and started the study for future heart transplant. He re-started atrial fibrillation and amiodarone was reintroduced(400 mg/day). Six days after, thyroid function test results were compatible with thyrotoxicosis(TSH−0.01 UI/ml; FT₄−1.88 ng/dl;FT₃-1.82 pg/ml) with negative antithyroid antibodies and TSH receptor antibodies. The colour flow Doppler sonography showed a normal thyroid gland with normal vascularity and the 24-h thyroid radioactive iodine uptake value was 1%. Results obtained from complementary clinical examinations point out evidences of ATI type 2. Nevertheless, due to the non-normalised thyroid function controlled by hydrocortisone, the patient started combination treatment with propiciltiouracil(100 mg/day) and prednisolone. This therapy was effective in reducing the serum concentration of thyroid hormones.

Discussion: The type of AIT could not be assessed in most of the reported cases.