Endocrine Abstracts

Background

Amiodarone is a widely-used anti arrhythmic medication. Amiodarone-induced hyperthyroidism (AIH) develops in 3% of amiodarone-treated patients. AIH is classified as type 1 or type 2. Type1 AIH occurs in patients with underlying thyroid condition while Type2 AIH is a result of amiodarone causing a subacute thyroiditis. Appropriate therapy for amiodarone-induced hyperthyroidism requires a careful diagnosis that may be difficult to achieve.

Aim

The aim of this study is to describe epidemiological, clinical and biological features of AIH, study the followed therapeutic strategies and report their clinical and biological outcomes.

Methods

We retrospectively analyzed the data of Tunisian patients affected with AIH from 1996 to 2020.

Findings

We reported data of 15 patients affected with AIH (5 men, 10 women), aged 54 years old on average, all from the Tunisian south. Type1 AIH was reported in 10 patients and type2 AIH in 5 patients, none of them was known to have a prior thyroid condition. Amiodarone was prescribed to treat atrial fibrillation in all patients with a dose of 200 mg daily, 5 days per week. Average symptoms onset term was 5.4 months for type1 AIH (0-24) and 16 months for type2 AIH (2-30). All patients exhibited clinical signs related to thyrotoxicosis. Most common symptoms were tremor, nervousness, palpitation, and sweating. No sign has shown to be statistically related to a AIH subtype except for exophthalmia which was seen only in patients with type1 AIH. Goiter was identified in all patients with type1 AIH but only in 2 patients with type2 AIH. Biologically, all patients had high FT4 and low TSH serum level except for one who had high TSH and FT4 serum level. Only 3 patients, all from type 1 AIH group, had serum antithyroid auto-antibodies. Scintigraphic imaging showed mild iodine fixation in type1 AIH group and absence of iodine fixation in type2 AIH group. While all patients were ordered to interrupt Amiodarone protocols, different antithyroid treatments were used for type1 AIH patients, 50% of them evolved to hypothyroidism. Patients with type2 AIH were followed up until euthyroidism was obtained (8 months on average).

Conclusion

Amiodarone-induced hyperthyroidism is a major adverse effect of Amiodarone. Careful history, physical examination, immunological tests and thyroid imaging are key to distinguish between AIH subtypes which is an important step for determining further management. Finally, we argue for the assessment of thyroid function before and while using Amiodarone.