Abstract

Abstract Disclosure: A. Akofu: None. S.A. Brietzke: None. N. Sheung: None. A. Uddin: None. N. Akabogu: None. S. Dejhansathit: None. F. marium: None. Grave’s disease is due to autoantibodies activating TSH receptors, driving downstream effects of iodine organification, iodotyrosine coupling, and release of T4 and T3 from intracellular stores. Severe thyrotoxicosis is traditionally treated with high dose thionamides to block thyroid hormone synthesis, iodides to slow iodine transport and block thyroid hormone release (collectively known as the Wolff-Chaikoff effect), and beta-blockers to slow heart rate and relieve tremulousness. We report the case of a health-conscious patient who had taken OTC iodide for years, and whose thyrotoxic condition abruptly worsened with discontinuation of his iodide supplement. A 67-year-old man was found in a delirious state wandering in the woods and was taken to the hospital ED. He had afib with RVR and evidence of high-output CHF. Diffuse goiter twice normal size was obvious on exam, and he was tremulous and diaphoretic. Serum TSH was <0.005 mcU/ml, with FT4 > 7.77 ng/dl and FT3 7.8 pg/ml. Initial treatment was metoprolol 25 mg TID, propylthiouracil (PTU) 300 mg TID, cholestyramine 4g BID and Lugol’s iodine 10 drops TID. Encephalopathy resolved after 2 days and FT4 decreased to 3.72 ng/dl after 8 days. Cholestyramine and Lugol’s iodine were thus discontinued. 2 days later, FT4 further declined to 2.75 ng/dl and he was switched from PTU to methimazole 30 mg twice daily. After 3 days, FT4 had increased to 5.17 ng/dl, and in response methimazole was increased to 40 mg TID. 3 days later FT4 increased further to 6.43 ng/dl, prompting a switch from methimazole back to PTU 300 mg TID. Because of further increase in FT4 and FT3, cholestyramine and Lugol's iodine were resumed. 3 days later, FT4 had declined from > 7.7 to 5.4 ng/dl, and he was discharged with plan to perform thyroidectomy once FT4 and FT3 reached nearly normal levels. Near the end of his hospitalization, he divulged that he had taken iodide drops for “thyroid health” for many years independent of medical advice, but hadn’t taken it for several days during the period of being lost in the woods prior to admission. Possible explanations for resistance of thyrotoxicosis to aggressive prescribed treatment include medication non-adherence, drug malabsorption, hyperaccelerated drug metabolism, anti-drug antibodies and antagonism of thionamide action by excessive intrathyroidal iodine. In this case, we hypothesize that his use of iodide serendipitously attenuated severity of Graves disease, by giving him a prolonged Wolf-Chaikoff effect. Discontinuation of iodide over a matter of days allowed reversal of this phenomenon and prevented control of his hyperthyroid condition until the deliberate restoration of the Wolf-Chaikoff effect with therapeutically prescribed Lugol’s solution. Whenever response to usual hyperthyroidism treatment is ineffective or paradoxical, as in this case patients should be specifically queried regarding use of OTC iodine preparations. Presentation Date: Saturday, June 17, 2023

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