Endocrine Abstracts

Amiodarone was first introduced in the 1960s and is now widely used to treat and prevent arrhythmias but it has a number of side effects, which include a perplexing array of thyroid effects. The latter stem from three features of the drug: its high iodine content, its ability to affect deiodination of T4 and its inhibition of T3 receptor binding. Around 3% of amiodarone-treated patients in areas with high iodine intake develop amiodarone-induced thyrotoxicosis (AIT), whereas this occurs in 12% of patients in areas of low iodine intake. There is a relative male preponderance, in contrast to other forms of thyrotoxicosis, reflecting the prevalence of ischaemic heart disease.

The first step in managing a patient with suspected AIT is to establish the diagnosis biochemically, often in the absence of any striking clinical features, and then to identify whether this is type 1 AIT secondary to exacerbation of underlying subclinical thyroid disease, or type 2 AIT, secondary to destructive thyroiditis. The distinction is usually made on clinical grounds, aided by colour-flow ultrasound. Markers such as serum IL-6 have not proved useful. Mixed forms of AIT exist and many cases of AIT type 2 are transient, exacerbating diagnostic problems. Patients with AIT type 1 usually respond to larger than normal doses of antithyroid drugs or potassium perchlorate. Clinical response can be delayed and the optimal use of these agents, alone or together, is still not entirely clear. Type 2 AIT frequently resolves spontaneously and maybe followed by a hypothyroid phase. More resistant cases require treatment with prednisolone. In both types of AIT, surgery is indicated when the response is slow and the patient’s clinical condition is parlous. Stopping amiodarone has little practical effect on either type of AIT, owing to the long half-life of the drug.