SAT-602 Thyrotoxic Periodic Paralysis Precipitated by Glucocorticoid Injection

Background: Thyrotoxic periodic paralysis (TPP) is a rare manifestation of hypokalemia that is driven by thyrotoxicosis. TPP is associated with any etiology of thyrotoxicosis, though Graves’ disease is the most common. Some of the provoking factors for these episodes are a high carbohydrate meal, rest after heavy exercise, fasting, stress, alcohol intake, and pulse steroid therapy. Clinical Case: A 48-year-old man presented with acute-onset lower extremity paralysis. He had been in his usual state of health until two days prior to admission when he developed a streptococcal throat infection. He was given IM injections of 80mg methylprednisolone and 1g ceftriaxone in an urgent care clinic and discharged. Soon after discharge, he developed progressively worsening bilateral lower extremity soreness and weakness resulting in a fall. He was taken to the hospital by EMS, where he was found to have bilateral lower extremity paresis. He was anxious, mildly tachycardic, and had a non-tender, 25-gram diffuse goiter. No thyroid nodules were palpated nor did the patient exhibit cervical lymphadenopathy. Lid lag, a fine tremor, and onycholysis were also detected. Basic metabolic panel revealed a serum potassium of 2.3 mmol/L (ref: 3.5-5.1 mmol/L). An ECG was normal. He was given 60 mEq of oral potassium chloride and started on propranolol 10mg TID and reported symptomatic improvement within several hours. During hospitalization, the patient remained asymptomatic and his serum potassium remained normal. Thyroid function testing revealed an undetectable TSH, a Free T4 of 4.41 ng/dL (ref: 0.61-1.18 ng/dL), and a Free T3 of 10.29 pg/mL (ref: 2.5-3.9 pg/mL). Radionucleotide uptake scan of the thyroid showed diffusely increased uptake (81%) with no nodules, consistent with Graves’ disease. Thyrotropin receptor antibody and Thyroid stimulating immunoglobulin levels were elevated. He underwent successful radioactive iodine ablation. Serial laboratory testing was done and within six weeks the patient became hypothyroid. He is now treated with levothyroxine for post-ablative hypothyroidism. A literature search reveals case reports implicating steroids in the precipitation of TPP. Corticosteroids, along with thyroid hormone, increase the activity of sodium-potassium ATPase channels in skeletal muscle. Steroids also lead to hyperglycemia and subsequent increased insulin release that causes an intracellular shift of potassium. Conclusion: Though rare, TPP is important to recognize, as failure to treat underlying hyperthyroidism can lead to repeated episodes of hypokalemia and paralysis. This case highlights TPP precipitated by pulse glucocorticoid injection, described rarely in the literature. The potential of glucocorticoids to precipitate paralysis should be recognized when considering steroid treatment for other medical conditions in hyperthyroid patients.