Amiodarone-induced thyrotoxicosis type 2 (AIT-2) is managed differently from type 1 (AIT-1). The distinction and treatment of AIT-2 is:
- A AIT-2 is due to excess iodine stimulating synthesis; treated with carbimazole/PTU
- B AIT-2 is due to autonomous nodule activation; treated with radioiodine therapy
- C AIT-2 is a destructive thyroiditis releasing preformed hormone from amiodarone-damaged follicles; treated with glucocorticoids ✓
- D AIT-2 cannot be distinguished from AIT-1 and both require combined antithyroid + glucocorticoid therapy always
Explanation
Amiodarone (contains 37% iodine by weight) causes two types of thyrotoxicosis: AIT-1 occurs in iodine-deficient patients with underlying thyroid pathology (Graves, multinodular goiter) — excess iodine drives synthesis (Jod-Basedow effect), treated with thionamides ± potassium perchlorate. AIT-2 is a destructive thyroiditis caused by amiodarone's direct cytotoxic effect on follicular cells releasing preformed T3/T4; it responds to glucocorticoids (prednisolone 40 mg/day), not antithyroids (since synthesis is not increased). Mixed forms exist. Color-flow Doppler sonography (absent/reduced vascularity in type 2 vs. normal/increased in type 1) helps distinguish them.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.