SAT-390 Thyrotoxic Periodic Paralysis: An Overlooked Diagnosis in Acute Muscle Weakness

Abstract Disclosure: F.O. Asemota: None. W. Lahens: None. R. Blanco: None. A. Torijano: None. M.A. Hashim: None. A. Sajan: None. Introduction: Thyrotoxic periodic paralysis (TPP) is a rare, reversible, potentially life-threatening disorder seen in patients with thyrotoxicosis. We present a case of TPP in an otherwise asymptomatic patient without known thyroid disease. Case: A 37-year-old Hispanic male with no significant past medical history presented with progressive bilateral lower extremity weakness for 24 hours. There were no known precipitating events, exacerbating, or alleviating factors. His initial vital signs were normal. On the physical exam, he had proximal muscle weakness of bilateral lower extremities. Initial labs showed a mildly decreased potassium level of 3.4 mEq/L [3.5-5.3], low thyroid stimulating hormone (TSH) level of <0.01 IU/mL [0.45-5.33] and high free thyroxine (FT4) level of 214.9 ug/L [6 - 12 ug/L]. Thyroid ultrasound demonstrated a diffusely heterogeneous and hypervascular gland. Autoantibody testing revealed elevated thyrotropin receptor antibody level of 14.60 IU/L [0.00-1.75] which confirmed the diagnosis of Graves’ disease. Discussion: TPP is characterized by acute, transient episodes of muscle weakness typically associated with hypokalemia in thyrotoxicosis. TPP can be caused by any of the etiologies of thyrotoxicosis. Most patients present with TPP after the onset of hyperthyroidism symptoms. It is typically seen in young Asian or Hispanic men in the second, third or fourth decade of life. TPP episodes are generally precipitated by strenuous exercise, high carbohydrate intake and stress. It is understood to be caused by increased activity of the sodium-potassium-ATPase transporter activity on skeletal muscle which increases intracellular potassium levels leading to extracellular hypokalemia, paradoxical depolarization, which causes inactivation of Na+ channels and muscle paralysis. Our patient, who did not have any hyperthyroid symptoms, had an episode of TPP without any precipitating factors. He was treated with potassium chloride supplementation and methimazole. He had marked improvement in his neurological symptoms once hypokalemia resolved and was able to ambulate without assistance. He was subsequently discharged with an ambulatory follow-up appointment. Conclusion: TPP remains a diagnostic dilemma in otherwise asymptomatic patients like ours without a known history of thyroid disorder as it can be confusing for hypokalemic periodic paralysis or stroke. As most patients with TPP have signs of hyperthyroidism, this case illustrates the need to maintain a high index of suspicion for TPP among those without hyperthyroid symptoms presenting with acute paralysis episodes and hypokalemia. Presentation: Saturday, July 12, 2025