MON-466 - When A Stable Nodule Turns Toxic: Amiodarone-Induced Hyperthyroidism

Background:

Amiodarone is a commonly used antiarrhythmic with well-recognized effects on thyroid function. Amiodarone-induced thyrotoxicosis (AIT) is classically divided into iodine-induced hormone synthesis (Type 1) and destructive thyroiditis (Type 2); differentiation is often challenging in elderly patients with pre-existing nodular thyroid disease. Such patients are at increased risk of iodine-induced thyroid hormone excess, with prior studies suggesting that up to 10% develop Type 1 AIT. Early recognition is critical given the potential for cardiovascular complications.

Case:

An 80-year-old man with a longstanding 6 × 3 cm left thyroid lobe nodule presented with fatigue, palpitations, and orthostatic dizziness four weeks after starting amiodarone. He reported intermittent blurred vision and chronic dysphagia, unchanged from baseline. Laboratory evaluation showed suppressed TSH (0.19 μIU/mL) and elevated free T4 (2.18 ng/dL), representing an abrupt change from previously normal thyroid function. Imaging confirmed a stable thyroid mass with esophageal compression and no interval growth over several years. Methimazole was initiated due to concern for nodule-driven hyperthyroidism; however, the rapid biochemical shift, temporal relationship to amiodarone initiation, and nodular thyroid background supported a diagnosis of Type 1 AIT. The patient was managed with antithyroid therapy and close monitoring of thyroid function and cardiovascular status, with planned serial measurements of FT3 and FT4 and outpatient endocrinology follow-up.

Discussion:

This case illustrates how amiodarone can unmask functional autonomy in previously stable nodular thyroid disease, rapidly precipitating thyrotoxicosis. Nodular thyroid tissue may respond autonomously to the iodine load from amiodarone, even after years of radiographic stability. The abrupt biochemical change shortly after drug initiation favors Type 1 AIT over spontaneous toxic nodular progression. Distinguishing Type 1 from Type 2 or mixed AIT is critical, as management differs: antithyroid therapy is effective for Type 1, whereas destructive thyroiditis may require glucocorticoids. Early recognition and reassessment of etiology are essential to mitigate cardiovascular risk, particularly in older patients, where even modest hormone excess can precipitate arrhythmias or heart failure. Coordinated endocrinology–cardiology care with serial thyroid function monitoring is essential when initiating amiodarone in at-risk patients.

Conclusion:

Amiodarone can rapidly precipitate Type 1 thyrotoxicosis in patients with nodular thyroid disease despite long-term stability. Early recognition and prompt subtype-directed therapy are critical to reduce cardiovascular risk in this high-risk population.

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