Skip to main content
ENDO 2026 Main banner

Thyroid Biology and Disease

SAT-388 - Thyrotoxic Periodic Paralysis in an Elderly Caucasian Woman with Delayed Neuromuscular Recovery

Saturday, June 13, 2026
9:30 AM - 4:30 PM CT
Location: ENDOExpo; Poster Floor
Disclosure(s):
SHAMSUN NAHAR, MD: No financial relationships to disclose


Introduction:
Thyrotoxic periodic paralysis (TPP) is a rare, potentially life-threatening complication of thyrotoxicosis, caused by thyroid hormone and adrenergically mediated potassium shift into cells. Though classically described in young Asian men, TPP is now also seen in non-Asians, females, and older patients, where diagnosis may be delayed due to subtle hyperthyroid symptoms.

Case Presentation:
A 74-year-old Caucasian woman with hypertension and depression experienced five months of worsening fatigue, tremor, insomnia, palpitations, heat intolerance, and an unintentional 17-lb weight loss. She was admitted to the hospital after developing sudden bilateral lower-extremity weakness and recurrent falls. Laboratory tests showed severe thyrotoxicosis (free T4 19.1 ng/dL, total T3 551 ng/dL, TSH < 0.01 mIU/L), hypokalemia (3.1 mmol/L), hypomagnesemia (1.2 mg/dL), and elevated NT-proBNP, which was consistent with acute diastolic heart failure. Initial treatment included intravenous potassium chloride (total 40 mEq over 24 hours) and magnesium sulfate (2 g IV), then oral potassium chloride 10 mEq daily and magnesium glycinate 500 mg daily. Antithyroid therapy with methimazole 20 mg daily was started, along with prednisone 20 mg daily for 30 days, and beta blocker (initially metoprolol succinate 50 mg orally once daily, later switched to propranolol 40 mg orally twice daily). Her serum potassium normalized within 24 hours, and thyroid hormone levels improved; however, she still experienced persistent lower-extremity weakness and continued to have falls for several weeks, even after laboratory correction. Neurologic assessment ruled out other neuromuscular causes. With continued control of thyrotoxicosis and after stopping corticosteroids, she gradually regained function without further episodes of paralysis.

Discussion:
This case demonstrates an uncommon presentation of TPP in an elderly Caucasian woman and underscores the importance of clinical awareness beyond classic demographic groups. In TPP, hypokalemia results from redistribution rather than depletion, so careful potassium replacement and use of nonselective beta-blockers are vital to prevent arrhythmias and rebound hyperkalemia. Importantly, neuromuscular recovery can lag behind normalization of electrolytes and thyroid function, especially in older patients with additional health issues and deconditioning.

Conclusion:
TPP should be included in the differential diagnosis for any patient with acute flaccid paralysis and hypokalemia in the context of thyrotoxicosis, regardless of age, sex, or ethnicity. Prompt diagnosis, carefully titrated electrolyte replacement, nonselective beta-blockade, and definitive management of hyperthyroidism are essential. Ongoing weakness after laboratory correction requires attention to fall risk and multidisciplinary care.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*