PharmacologyTier 1Medical Sciences concept

Amiodarone-induced thyroid dysfunction (type 1 vs type 2 thyrotoxicosis, hypothyroidism)

Core concept

Amiodarone is ~37% iodine by weight and structurally resembles thyroxine -- causes both hypothyroidism and thyrotoxicosis, with thyrotoxicosis split into type 1 and type 2 by mechanism
Type 1: iodine-induced excess hormone synthesis in an abnormal thyroid (underlying nodular goitre/latent Graves') -- essentially Jod-Basedow phenomenon
Type 2: destructive thyroiditis releasing preformed hormone from an otherwise normal gland -- inflammatory, not synthetic

Feature	Type 1	Type 2
Underlying gland	Abnormal (nodular/latent Graves')	Normal
Mechanism	inc synthesis (iodine excess)	Destructive thyroiditis
Colour-flow Doppler US	Increased vascularity	Reduced/absent vascularity
Treatment	Thionamides (methimazole) +/- perchlorate, consider stopping amiodarone	Corticosteroids; amiodarone often continued
Hypothyroidism	Also occurs (Wolff-Chaikoff effect failing to escape) -- managed with levothyroxine, amiodarone usually continued

Mixed/indeterminate forms are common in practice -- may need combined thionamide + steroid therapy when type cannot be clearly distinguished
Trap: reflexively stopping amiodarone in all amiodarone-induced thyrotoxicosis -- appropriate in type 1 (ongoing iodine substrate) but usually unnecessary in type 2, and amiodarone's long half-life (weeks) means stopping it does not produce rapid clinical benefit anyway
Baseline TFTs (and periodic monitoring) required before/during amiodarone given its high rate of thyroid dysfunction

Amiodarone hypothyroidism is far more common than thyrotoxicosis overall, especially in iodine-replete populations
Long amiodarone half-life (weeks-months, due to extensive tissue/fat storage) means thyroid effects can persist long after cessation
Jod-Basedow (iodine-induced hyperthyroidism) also occurs with iodinated contrast media -- same type 1 mechanism, different iodine source

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