Clinical pharmacology and therapeutics for MRCP Part 2

A 68-year-old woman on long-term amiodarone for atrial fibrillation presents with weight loss, tremor and palpitations. TSH is suppressed and free T4 elevated. Colour flow Doppler of the thyroid shows ABSENT vascularity, and interleukin-6 is raised. There is no goitre and no antibodies. What is the most appropriate treatment?

1. Immediate total thyroidectomy Reserved for severe, refractory disease where the cardiac condition cannot tolerate ongoing thyrotoxicosis. Not first line.
2. Simply stopping amiodarone and observing Insufficient alone. Amiodarone has a half-life of many weeks, so stopping it produces no useful short-term change, and the decision to stop must also weigh the arrhythmia it is controlling.
3. Oral corticosteroids correct Correct. This is amiodarone-induced thyrotoxicosis type 2: a destructive thyroiditis releasing preformed hormone, characterised by absent vascularity on Doppler and raised inflammatory markers. It responds to corticosteroids, not to thionamides.
4. Carbimazole Wrong for type 2. Thionamides treat type 1, where excess iodine drives increased synthesis in an abnormal gland with preserved or increased vascularity. Here there is no overproduction to block.
5. Radioiodine ablation Wrong. The iodine load from amiodarone saturates the gland, so uptake is negligible and radioiodine will not work.

The point: Amiodarone thyrotoxicosis: type 1 is iodine-induced overproduction in an abnormal gland, increased vascularity, treat with carbimazole. Type 2 is destructive thyroiditis, absent vascularity, treat with steroids. Mixed pictures are treated with both. Amiodarone also causes hypothyroidism, pulmonary fibrosis, hepatitis and corneal deposits.

Source: ETA guidelines for the management of amiodarone-associated thyroid dysfunction European Thyroid Association · tier 2, specialty society or college