SAT-410 Thyrotoxic Periodic Paralysis Presenting As Acute Lower Extremity Weakness In A Previously Healthy Young Male

Abstract Disclosure: S. Abusharar: None. K.S. Manglani: None. W. Kuenstner: None. M.B. Sharma: None. Background: Thyrotoxic periodic paralysis (TPP) is a rare but potentially life-threatening complication of hyperthyroidism, characterized by acute hypokalemia-induced muscle weakness. Sometimes it can be the first presentation of hyperthyroidism. Although it is more commonly reported in Asian populations, early recognition across diverse demographics is essential to prevent severe morbidity. Case Presentation: A 26-year-old previously healthy Hispanic male presented with sudden-onset bilateral lower extremity weakness upon awakening, following a large carbohydrate-rich meal the night prior. He denied sensory deficits, bowel/bladder dysfunction, or preceding gastrointestinal symptoms. Examination revealed tachycardia and hyporeflexia and weakness of lower extremities without sensory impairment. Initial labs showed profound hypokalemia of (K⁺ 1.7 mmol/L; ref 3.5-5.0) and suppressed TSH (<0.008 mIU/L; ref 0.4-4.0), elevated free T4 (2.88 ng/dL; ref 0.8-1.8) and free T3 (7.74 pg/mL; ref 2.3-4.2). TT3 was on the upper border of normal (174.9 ref 60-180.0 ng/dL). EKG demonstrated an accelerated junctional rhythm with prolonged QTc 657 ms (ref >460 ms). Further evaluation revealed positive thyroid-stimulating immunoglobulins, and thyroid ultrasound demonstrated a mildly heterogeneous gland without nodules or hypervascularity, consistent with early Graves' disease. The patient was started on methimazole, propranolol and aggressive potassium repletion with clinical improvement. Discussion: TPP results from a sudden intracellular potassium shift triggered by thyrotoxicosis and potentiated by insulin and adrenergic stimulation. Although rare in non-Asian populations, it must be considered in any patient presenting with painless paralysis and hypokalemia. Management focuses on cautious potassium repletion, beta-adrenergic blockade, and definitive treatment of the underlying thyroid dysfunction. Conclusion: Early recognition of TPP, even in atypical demographics, is critical to prevent potentially fatal complications such as cardiac arrhythmias. Awareness of this condition among diverse populations remains essential. Presentation: Saturday, July 12, 2025

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Journal
Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.2323
Primary Topic
Ion channel regulation and function
Type
article
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article

SAT-410 Thyrotoxic Periodic Paralysis Presenting As Acute Lower Extremity Weakness In A Previously Healthy Young Male

William Kuenstner, Meeta B Sharma, Kajol Manglani, Shahed Abusharar
Journal of the Endocrine Society
Ion channel regulation and function
article

SAT-410 Thyrotoxic Periodic Paralysis Presenting As Acute Lower Extremity Weakness In A Previously Healthy Young Male

William Kuenstner, Meeta B Sharma, Kajol Manglani, Shahed Abusharar
article en

Abstract

Abstract Disclosure: S. Abusharar: None. K.S. Manglani: None. W. Kuenstner: None. M.B. Sharma: None. Background: Thyrotoxic periodic paralysis (TPP) is a rare but potentially life-threatening complication of hyperthyroidism, characterized by acute hypokalemia-induced muscle weakness. Sometimes it can be the first presentation of hyperthyroidism. Although it is more commonly reported in Asian populations, early recognition across diverse demographics is essential to prevent severe morbidity. Case Presentation: A 26-year-old previously healthy Hispanic male presented with sudden-onset bilateral lower extremity weakness upon awakening, following a large carbohydrate-rich meal the night prior. He denied sensory deficits, bowel/bladder dysfunction, or preceding gastrointestinal symptoms. Examination revealed tachycardia and hyporeflexia and weakness of lower extremities without sensory impairment. Initial labs showed profound hypokalemia of (K⁺ 1.7 mmol/L; ref 3.5-5.0) and suppressed TSH (<0.008 mIU/L; ref 0.4-4.0), elevated free T4 (2.88 ng/dL; ref 0.8-1.8) and free T3 (7.74 pg/mL; ref 2.3-4.2). TT3 was on the upper border of normal (174.9 ref 60-180.0 ng/dL). EKG demonstrated an accelerated junctional rhythm with prolonged QTc 657 ms (ref >460 ms). Further evaluation revealed positive thyroid-stimulating immunoglobulins, and thyroid ultrasound demonstrated a mildly heterogeneous gland without nodules or hypervascularity, consistent with early Graves' disease. The patient was started on methimazole, propranolol and aggressive potassium repletion with clinical improvement. Discussion: TPP results from a sudden intracellular potassium shift triggered by thyrotoxicosis and potentiated by insulin and adrenergic stimulation. Although rare in non-Asian populations, it must be considered in any patient presenting with painless paralysis and hypokalemia. Management focuses on cautious potassium repletion, beta-adrenergic blockade, and definitive treatment of the underlying thyroid dysfunction. Conclusion: Early recognition of TPP, even in atypical demographics, is critical to prevent potentially fatal complications such as cardiac arrhythmias. Awareness of this condition among diverse populations remains essential. Presentation: Saturday, July 12, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
Anne Arundel Medical Center (US), Washington Hospital (US), MedStar Health (US)
Openalex Percentile: Top 73%
Ion channel regulation and function
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