Endocrine Abstracts

Introduction

Amiodarone is a drug commonly used for the treatment of refractory atrial or ventricular arrhythmias. In 20% of patients, amiodarone may cause subclinical or clinically overt hypothyroidism or hyperthyroidism. The high iodine exposure caused by amiodarone treatment interferes with thyroid autoregulation. Two underlying mechanisms are considered to be involved in the pathogenesis of amiodarone-induced thyrotoxicosis (AIT). AIT1 is more common in patients with underlying Graves’ disease or nodular goiter and results in excessive synthesis of thyroid hormones due to the high iodine intake by amiodarone. In AIT2, a destruction of thyroid follicles due to amiodarone toxicity (subacute and destructive thyroiditis) is observed leading to uncontrolled thyroid hormone release. Also mixed forms are described. We present the patient with amiodarone-induced thyrotoxicosis developed in two years after amiodarone therapy initiation.

Case description

We examined 15-year-old girl whose arrhythmia in the form of a ventricular extrasystole was first diagnosed at the age of 10 (2015) during a preventive examination. A cardioverter-defibrillator was implanted in 2018 and Amiodarone therapy was initiated. Her current Amiodarone dose is 500 mg per day. She regularly underwent examinations and only the thyroid volume increase was noted by ultrasound while hormonal examination always showed euthyroidism. In December 2020 (2.5 years after initiation of amiodarone therapy) patient began to complain of increased heart rate. Hormonal analysis identified a decrease in thyroid-stimulating hormone level (0.0001 uIU/ml; N: 0.35–5.5 ulU/ml) and a pronounced increase in free-thyroxine (fT4) (52.11 pmol/l; N: 11.5–22.7 pmol/l) and free-triiodothyronine (fT3) (7.35 pmol/l; N: 3.5–6.5 pmol/l) levels. Therapy with Prednisolone was initiated at a starting dose of 30 mg per day. Two weeks after the start of therapy, it was possible to achieve the decreasing of fT4 (18.49 pmol/l; N: 10.1–17.9 pmol/l) and fT3 levels (3.5 pmol/l; N: 2.8–6.3 pmol/l). Also, according to the results of ultrasound of the thyroid gland, a decrease in the volume to 14.2 ml was noted (from 21 ml initially). The girl was consulted by cardiologists, the cancellation of therapy was started. We continue to monitor her condition.

Conclusion

Amiodarone-induced thyroid dysfunction is usually atypical; therefore, monitoring of thyroid status before, during, and after Amiodarone treatment is demanded. AIT could significantly deteriorate the clinical status of children with complex cardiac diseases. Early and proper diagnose of AIT allows the introduction of immediate and appropriate treatment considering the cardiac condition of the young patient.