Endocrine Abstracts

Background: Thyrotoxicosis is a well-known complication of amiodarone therapy. Three types of amiodarone-induced thyrotoxicosis (AIT) are recognized; type 1 AIT, type 2 AIT, and mixed/indefinite forms of AIT. Type 1 AIT is an iodine-induced hyperthyroidism that usually occurs in patients with pre-existing nodular goitre or latent Graves’ disease¹. We present a case of type 1 AIT associated with a transiently toxic solitary thyroid nodule, with hyperthyroidism resolving once amiodarone therapy was stopped.

Case Presentation: A 74-year-old lady with paroxysmal atrial fibrillation receiving long-term amiodarone therapy was referred because of biochemical thyrotoxicosis (free thyroxine: 30.1 pmol/l [reference range: 11.9-1 pmol/l], free triiodothyronine: 6.1 pmol/l [reference range: 3.5-6.1 pmol/l], and thyroid-stimulating hormone: 0.018 micIU/ml [reference range: 0.3-3.0 micIU/ml]). She complained of occasional episodes of palpitations and heat intolerance but was otherwise asymptomatic. Physical examination revealed a heart rate of 92 beats per minute with a blood pressure of 130/1 mmHg. There were no signs of thyroid eye disease, and no palpable thyroid nodules or goitre were appreciated. Investigations revealed a negative TSH-receptor antibody status, whilst a neck ultrasound showed a 1.1×0.1 cm hypoechoic nodule on the left thyroid lobe. Thyroid scintigraphy revealed a single focus of increased tracer uptake in the left thyroid lobe with no uptake in the rest of the thyroid gland suggesting a solitary toxic nodule. After consulting with the patient’s cardiologist, amiodarone was stopped, and carvedilol was prescribed instead. She was also commenced on carbimazole for type 1 AIT secondary to a solitary toxic thyroid nodule. The patient was reviewed at outpatients regularly and her carbimazole dose was titrated against her thyroid function. Follow-up neck ultrasound studies revealed stable findings. After twenty months, treatment with carbimazole was stopped. Six months following the cessation of carbimazole, she remained clinically and biochemically euthyroid.

Conclusions: This case is noteworthy for two main reasons; (i) the association between AIT and a solitary toxic thyroid nodule is rare¹, and (ii) following the cessation of amiodarone, the patient was eventually able to come off thionamide therapy as her hyperthyroidism resolved, highlighting the transient nature of this toxic thyroid nodule in the context of amiodarone use. Whilst mild AIT may subside in 20% of cases¹, usually patients with type 1 AIT end up requiring definitive treatment because of the underlying thyroid disorder.

Reference: 1. Brian SR, et al. Unusual case of amiodarone-induced thyrotoxicosis: "illicit" use of a technetium scan to diagnose a transiently toxic thyroid nodule. Endocr Pract. 2007Jul-Aug;13(4):413-6.