Endocrine Abstracts

Introduction: Amiodarone is a widely used antiarrhythmic drug for refractory atrial or ventricular tachyarrhythmias. Amiodarone-induced thyrotoxicosis (AIT) occurs in up to 6% of patients taking this medication in iodine-sufficient areas of the world and in up to 10% in iodine deficient areas. AIT can be divided into two types: type 1 is a form of iodine-induced hyperthyroidism whereas type 2 is a drug-induced destructive thyroiditis. Type 1 AIT tends to occur in patients with underlying thyroid autonomy in a nodular goitre, or Graves’ disease, while type 2 AIT appears as a result of direct damage or induction of apoptosis in thyrocytes by amiodarone.

Case report: A 69-year-old man admitted in Cardiology department for ventricular tachycardia (VT), presented a 3-week history of unintentional weight loss (10 kg), fatigue and lethargy. VT was diagnosed five years before and he started amiodarone. Thereafter, patient needed an implantable cardioverter defibrillator. He denied previous personal or familiar history of thyroid dysfunction. On examination, he presented tachycardia (120 bpm) and a small thyroid goitre. Thyroid function tests showed thyrotoxicosis (TSH 0.008 μU/ml, FT3 9.20 pg/ml, FT4 >7.76 ng/dl), negative TRAb (0.9 U/l) and positive anti-Tg antibody (486 U/ml). Given the previous medical history of amiodarone use, AIT was assumed. His cardiologist prescribed methimazole 20 mg qd, propranolol 40 mg tid and stopped amiodarone. However, significantly thyroid dysfunction persisted. An iodine uptake scan was not performed as patient had already been started on methimazole. Ultrasound revealed a heterogeneous and hyperechogenic thyroid gland, with a 1 cm nodule in the left lobe. At this point, methimazole dosage was increased to 30 mg qd and oral prednisolone 30 mg qd was co-administered. Approximatively 1 month later, biochemical re-evaluation showed TSH <0.005 μU/ml and FT4 >7.76 ng/dl. Given the severity of his presentation and lack of clinical or biochemical improvement, methimazole and prednisolone were increased to 50 mg (15+15+20) and 60 mg qd, respectively. His symptoms subsequently improved. Prednisolone was tapered and stopped while methimazole was progressively reduced to 20 mg qd. After 6 months, methimazole was stopped since thyroid function evolved to hypothyroidism. At the last visit, patient remains in subclinical hypothyroidism.

Conclusion: This patient presented severe AIT and needed administration of high dosage of both antithyroid medication and corticosteroids before improvement occurred. He presented features of both types of AIT, proving the diagnosis and management of this condition is sometimes challenging.