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Endocrine

Research Snapshot Theater: Endocrine, Adult III

(290) Hyporeflexia and Muscle Weakness: An Unusual Case Report of Thyrotoxic Periodic Paralysis

Tuesday, February 25, 2025
12:30pm – 1:30pm Eastern Time
Location: Connections Central - RST 14

    First Author(s)

  • EM

    Erica Marnet, MD (she/her/hers)

    Bridgeport, Connecticut, USA

    • Co-Author(s)

  • LG

    Lizda Guerrero Arroyo, MD

    Resident Physician
    Department of Medicine, Yale New Haven Health Bridgeport Hospital, United States

  • AD

    Armando Dominguez Diaz, MD

    Resident Physician
    Department of Medicine, Yale New Haven Health Bridgeport Hospital, United States

  • JK

    Jeffrey Kwon, MD

    Program Director, Pulmonary and Critical Care Medicine Fellowship
    Department of Pulmonary and Critical Care, Yale New Haven Health Bridgeport Hospital
    Bridgeport, Connecticut, United States

Introduction: Thyrotoxic periodic paralysis (TPP) is a non- familial form of hypokalemic periodic paralysis characterized by thyrotoxicosis (TT), hypokalemia and acute muscle paralysis. Often misdiagnosed as sporadic periodic paralysis, thyroid function tests are essential to establish the correct diagnosis. TPP predominantly affects males and Asian populations, with unknown incidence in the West, hence attentive high suspicion is key for its diagnosis.

Description: 20-year-old Hispanic male, with no relevant medical history was admitted with sudden bilateral lower extremity (BLE) weakness after consuming a high-carbohydrate meal, that progressed leading to a non-mechanical fall the following morning. For the last 2 years, he had 30-pound weight loss, and palpitations with tremors in the last 5 months. Family history remarkable for paternal hypothyroidism. On presentation, he had low-grade fever and sinus tachycardia. Physical exam revealed exophthalmos, diffuse painful thyromegaly, BLE weakness (2/5) and hyporeflexia. Chemistry was significant for hypokalemia (1.5mmol/L), hypomagnesemia, and hypophosphatemia. Urine potassium was 12mmol/L. Thyroid Stimulating Hormone (TSH) was undetectable, free thyroxine and triiodothyronine levels were elevated at 7.52 ng/dL and >651 ng/dL respectively. Anti-TSH receptor antibody was positive at 38 IU/L and thyroid-stimulating immunoglobulin index was 3.1. Thyroid ultrasound showed an enlarged, heterogeneous gland with “thyroid inferno” on doppler. After receiving propranolol, propylthiouracil (PTU) and hydrocortisone the patient demonstrated improvement in muscle strength within 12 hours. Electrolytes were repleted and normalized within 24 hours. PTU was replaced with methimazole, propranolol dose was reduced, and remaining therapies were discontinued. He had full recovery and was discharged on day 3.

Discussion: TPP is a rare complication of TT. The underlying mechanism thought to be due to overactivity of sodium-potassium-adenosine triphosphatase pump causing intracellular potassium shift. Achieving an euthyroid state is essential to correct electrolytes imbalances and propranolol has been shown to abort paralysis and prevent rebound hyperkalemia. Our case highlights the importance of early recognition and speedy recovery once adequate therapy is initiated.