SUN-410 - Iodine-Induced Thyrotoxicosis in A Normal Thyroid Gland

Background
Iodine-induced thyrotoxicosis classically occurs in individuals with underlying thyroid pathology such as multinodular goiter or latent Graves’ disease. The thyroid normally maintains hormonal stability during iodine excess through autoregulatory mechanisms; however, sustained exposure to supraphysiologic iodine doses may overwhelm these safeguards and precipitate thyroid dysfunction even in individuals without known thyroid disease. The increasing use of high-dose iodine supplements in alternative medicine practices raises concern for underrecognized iodine-related endocrine complications.
Case Presentation
A 63-year-old man with Parkinson’s disease and no prior thyroid pathology presented with three months of unintentional weight loss, tremor, anxiety, palpitations, progressive weakness, and newly diagnosed atrial fibrillation. Prior thyroid testing demonstrated normal thyroid function and negative thyroid autoantibodies. He reported chronic iodine supplementation prescribed by an alternative medicine provider, initially 12.5 mg daily for approximately 18 months, followed by escalation to a compounded iodine preparation providing >300–450 mg daily. Approximately three months after dose escalation, he developed symptoms prompting endocrine referral. Laboratory evaluation revealed severe thyrotoxicosis with free T4 7.4 ng/dL and undetectable TSH < 0.01 mIU/L. Ultrasonography demonstrated a normal-sized gland with homogeneous echotexture, no nodules, and no increased vascularity. All iodine-containing supplements were discontinued, and methimazole was initiated with gradual biochemical improvement. After inadvertent reintroduction of high-dose iodine while on methimazole, the patient developed overt biochemical hypothyroidism, necessitating cessation of antithyroid therapy. Thyroid function subsequently normalized following withdrawal of both iodine and methimazole.
Discussion & Conclusion
This case illustrates that prolonged ingestion of extreme iodine doses can disrupt thyroid autoregulation and cause severe thyrotoxicosis followed by transient hypothyroidism, even in patients without underlying thyroid disease. Symptoms may appear weeks to months after exposure, and thyroid function may fluctuate during recovery. The patient’s iodine intake exceeded the recommended daily allowance by several thousand-fold. The subsequent transient hypothyroidism likely reflects combined inhibitory effects of excess iodine and antithyroid therapy, consistent with a prolonged Wolff–Chaikoff effect. These findings highlight the delayed and biphasic nature of iodine-induced thyroid dysfunction. Clinicians should actively inquire about over the counter & holistic products, be cognizant for the potential for delayed thyroid dysfunction and counsel patients regarding the risks of excessive iodine exposure.

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