MON-451 - Iodine-Induced Thyrotoxicosis Secondary to "Thyroid Support" Supplementation: A Case Report

Introduction:
Iodine-induced thyrotoxicosis, also known as the Jod–Basedow phenomenon, is a rare cause of thyrotoxicosis that typically occurs following exposure to high doses of exogenous iodine. Under normal conditions, excess iodine transiently suppresses thyroid hormone synthesis through the Wolff–Chaikoff effect. In some patients with underlying thyroid dysfunction, such as autoimmune thyroid disease or nodular goiter, this autoregulatory mechanism fails, resulting in the development of hyperthyroidism. While this phenomenon is most commonly associated with iodinated contrast media or amiodarone use, with the growing popularity of wellness spas, iodine-containing supplements are becoming a more prominent etiology.

Case Report:
A 41-year-old male with a history of obstructive sleep apnea and eosinophilic esophagitis presented to the emergency department with a three-week history of progressive morning headaches, heat intolerance with night sweats, and unintentional weight loss. He also endorsed palpitations, tremors, easy fatigability, and dyspnea with routine activities such as climbing stairs. Thyroid function testing revealed a TSH < 0.010 µIU/mL (reference range 0.40–4.0 µIU/mL), total T3 of 404 ng/dL (reference range 60–180 ng/dL), and free T4 of 3.82 ng/dL (reference range 0.71–1.51 ng/dL).

A detailed history revealed 7 months-long use of an over-the-counter “thyroid support” supplement (“Thyroid Px”) prescribed by a naturopathic provider at a wellness spa. The supplement contained 12 mg of iodine per serving, and the patient was instructed to take it twice daily, resulting in ingestion of 24 mg of iodine—approximately 160 times the recommended dietary allowance of 150 µg per day. The patient sought alternative care after frustration that pharmacotherapy was not initiated despite positive thyroid peroxidase antibodies (25.1 IU/mL; reference range < 6 IU/mL) in the setting of clinical and biochemical euthyroidism.

The supplement was discontinued, and the patient was started on atenolol 25 mg twice daily and methimazole 10 mg twice daily. Biweekly laboratory monitoring was initiated. At outpatient follow-up, his symptoms had improved, and free T4 had decreased to 2.46 ng/dL.

Conclusion:
This case underscores the importance of obtaining a thorough medication history, including over-the-counter supplements, in patients presenting with thyroid disease. As wellness culture and non–evidence-based medical advice proliferate on social media, clinicians should specifically inquire about iodine-containing supplements. Patients should be encouraged to provide product details so iodine exposure can be assessed. Supplements containing supraphysiologic iodine doses should be discontinued, and patients should be counseled on the potential risks and harms of excessive iodine intake.

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