FRI507 Thyrotoxic Periodic Paralysis: A Rare Occurrence Of Exogenous Thyroid Replacement

Disclosure: J. Case: None. D. Suravajjala: None. V. Eranki: None. Thyrotoxic periodic paralysis (TPP) occurs suddenly through excess thyroxine in tandem with insulin spurring an intracellular shift of potassium via increased activity of Na+/K+ ATPase pump leading to depletion of extracellular potassium with subsequent destabilization of cellular membranes and ensuing paralysis presenting with proximal muscle weakness of the legs. Common triggers involve vigorous exercise, infection, carbohydrate-rich meals, thyroiditis and graves' disease. Patients may be treated with IV potassium, non-selective beta blockers and treating the underlying cause. Exogenous thyroid hormone replacement causing iatrogenic hyperthyroidism as a cause of TPP is very rare. We present one such case below. A 61-year-old male with a history of primary hypothyroidism on thyroid replacement, atrial fibrillation, diabetes mellitus and hypertension, was admitted in September 2019 for lower extremity weakness at which time he was found with hypokalemia; he symptomatically improved following potassium replacement. He had a similar hospitalization in October, 2022 at which time he was found to have weakness alongside hypokalemia and hypomagnesemia, both of which were replaced with symptomatic improvement. He presented as an outpatient for follow up with likely etiology being TPP. Upon further review he had been taking both LT4 (Synthroid) 75mcg daily and T4/T3(Armour) 60mg daily; of note his TSH had been suppressed since 2019, three years prior to presentation. He was unsure why he had been on combination therapy. At our initial visit his labs were: TSH <0.005mIU/mL, free T4 1.38 ng/dL and T3 199 ng/dL. He was advised to stop all thyroid hormone replacement and experienced symptomatic improvement with normalization of potassium and magnesium. Repeat TFTs are pending for appropriate replacement dosing. Recognition of TPP and distinguishing from other etiologies of lower extremity weakness as well as other forms of periodic paralysis would aid in early resolution of an easily treatable, yet severe, condition given the implications of prolonged hypokalemia; earlier recognition of TPP in this patient as a sign of thyrotoxicosis may have prevented later hospitalizations and reduced risk of development of atrial fibrillation. This case also demonstrates the need for adequate monitoring and dosing of thyroid hormone supplement as well as potential complexities and risks of combination therapy in preventing an exogenously induced thyrotoxic state. Presentation: Friday, June 16, 2023