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Amiodarone

A 64-year-old man has taken amiodarone for ten months for recurrent ventricular tachycardia after a myocardial infarction. He now reports fatigue, a 4 kg weight gain and cold intolerance. TSH is 14 mIU/L and free T4 is low. His arrhythmia has been well controlled and no alternative agent is considered safe for him. What is the most appropriate management?

Explanation

Key fact
Amiodarone-induced hypothyroidism does not require stopping the drug - add levothyroxine and carry on.

Continue amiodarone and start levothyroxine. The hypothyroid form is easily replaced, so an effective antiarrhythmic need not be sacrificed.

Why

Each 200 mg tablet releases roughly 75 mg of iodine, far above the daily requirement.

That iodine load causes a Wolff-Chaikoff block that some thyroids fail to escape from.

The result is a straightforward primary hypothyroidism: high TSH, low free T4.

Levothyroxine corrects it directly and the dose is titrated on TSH.

Amiodarone has a half-life of weeks to months, so stopping it would not help quickly anyway.

The two directions of amiodarone thyroid disease

HypothyroidismThyrotoxicosis type 1Thyrotoxicosis type 2
MechanismFailure to escape Wolff-ChaikoffIodine-induced excess synthesisDestructive thyroiditis
GlandOften pre-existing autoimmunityNodular or latent GravesNormal
Vascularity on Doppler-IncreasedAbsent
TreatmentLevothyroxineThionamideGlucocorticoid
Stop amiodarone?Not necessaryUsuallyOften can continue

Two ways an iodine load can go

A thyroid follicle receiving a shower of iodine dots from a tablet, with two arrows diverging to outcome boxes whose bars share a baseline: a short bar for hypothyroidism and a tall bar for thyrotoxicosis

Why not the others

Remember
Hypo: replace and continue. Hyper: think which type first. Only the thyrotoxic side forces a decision about the drug.

Go deeper

Baseline thyroid, liver and lung function plus a chest radiograph are checked before starting, then thyroid and liver function about six-monthly.

Other amiodarone toxicities to know: pulmonary fibrosis, corneal microdeposits, slate-grey photosensitive skin, hepatitis and optic neuropathy.

Its antiarrhythmic action is class III - potassium channel block prolonging phase 3 repolarisation - but it also has class I, II and IV activity.

Tripathi KD. Essentials of Medical Pharmacology, 9th ed. (Jaypee, 2024); Katzung's Basic & Clinical Pharmacology, 16th ed. (McGraw Hill, 2024).

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