Endocrine Abstracts

Introduction: Amiodarone is an effective drug for treating heart arrhythmias. High iodine content and specific metabolism of this drug, in 15-20% of patients lead to thyroid function disorder. Amiodarone induced thyrotoxicosis (AIT type 1 or type 2) usually occurs during the use of the drug, while it is rare after the drug cessation.

The aim: A case report of a patient with type 2 AIT that manifested after the cessation of short-term amiodarone treatment.

Case presentation: A 73-year-old patient was treated for atrial fibrillation with amiodarone for six months. Two months after the drug cessation, clinical manifestations of thyrotoxicosis (weight loss, sweating, tachycardia) occured. Laboratory tests showed overt thyrotoxicosis with normal antithyroid antibodies and high thyroglobuline (TSH 0.01 uIU/ml, fT4 45.4 pmol/l, fT3 10.8 pmol/l, antiTPO 6 IU/ml, antiTg 11 IU/ml, TSH-receptor antibodies 0.9 IU/l, thyroglobuline 232 ng/ml). Blood cell count and sedimentation rate were normal. The thyroid gland was painless, normal size, normoechogenic, with normal vascularisation and without nodal lesions. The patient was succesuflly treated with corticosteroids (at the beginning 60 mg/day with gradual drug suspension). After 10 weeks patient was euthyroid. One month later hypothyreosis occured, and levotyroxine substitution was started.

Conslusion: This case report showes a patient with type 2 AIT which occured two months after the cessation of short-term treatment with amiodarone. The elimination of amiodarone from the body is variable and iodine depot in the body can remain increased for up to 9 months after the drug is stopped. For this reason, it is necessary to monitor patients not only during amiodarone treatment, but also months after the suspension of the therapy.