Synopsis
Detect and phenotype thyroid dysfunction caused by amiodarone or lithium, coordinate essential-drug decisions and treat hypo- or hyperthyroidism without causing cardiac or psychiatric harm.
- Check thyroid function before amiodarone, every six months during treatment and for several months after discontinuation, as MHRA advises; its long tissue half-life makes late effects biologically plausible.
- Amiodarone can cause hypothyroidism or thyrotoxicosis. High iodine exposure and inhibition of T4-to-T3 conversion also produce predictable early laboratory changes that are not automatically disease.
- Type 1 amiodarone-induced thyrotoxicosis reflects increased synthesis, often in Graves' or nodular thyroid disease; type 2 is destructive thyroiditis. Mixed or indeterminate forms are common in practice.
Key red flags
Underlying nodular goitre or Graves' disease, thyroid vascularity and positive relevant antibodies can support iodine-driven increased synthesis. The distinction is probabilistic and may not be clean.
Investigation priorities
Confirm persistent dysfunction and characterise its biochemical direction and severity.
Management branches
Persistent overt biochemical hypothyroidism during or after amiodarone exposure.
- Confirm persistence, symptoms and baseline pattern; check adrenal risk if severe central features are possible and review all amiodarone toxicities.
- Discuss amiodarone indication with cardiology. It can often continue while levothyroxine is introduced cautiously, especially in ischaemic or arrhythmic heart disease.
Key medicines
LevothyroxineStart cautiously and titrate in older adults or those with ischaemic and rhythm disease; otherwise follow BNF replacement principles and serial tests.
Carbimazole for synthesis-predominant AITHigh iodine exposure may require a specialist-selected regimen and close biochemical review; prescribe only with endocrinology oversight.