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Abstract: TH-PO375

Newly Diagnosed Graves Disease in a Young Patient with Lower Extremity Weakness

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Richardson, Trey Howard, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Leong, Russell, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Grantham, Connor J., Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • El Shamy, Osama, Vanderbilt University Medical Center, Nashville, Tennessee, United States

Group or Team Name

  • Vanderbilt Nephrology.

The differential diagnosis for myositis and myopathy is broad and includes medication side effects, auto-immune myositis, infectious myositis, neuromuscular junction disease, metabolic diseases, and electrolyte abnormalities.

Case Description

A 32-year-old male with osteoarthritis presents to the emergency department with acute lower extremity weakness that developed over the course of the day. He had a similar episode 3 months ago that self-resolved, however on this occasion, the weakness progressed to lower extremity paralysis, prompting his presentation. His labs were notable for a potassium of 2.2 mEq/dL, an undetectable TSH, total T3 of 311 (high), and a T4 of 1.6 (high). Thyroid receptor antibodies were elevated to 21.3. He was diagnosed with thyrotoxic periodic paralysis (TPP) due to Graves disease. His potassium was repleted, and he was started on methimazole with rapid improvement in his symptoms.


TPP is a skeletal muscle channelopathy associated with hyperthyroidism - most often secondary to Graves disease. Besides hypokalemia, differentiating factors from other forms of periodic paralysis include elevated T4, low T3, hypophosphatemia, hypomagnesemia, and often presents after the second decade of life. Thyrotoxicosis increases the activity and transcription of the Na-K ATPase, enhances sensitivity to catecholamines, and inhibits potassium leak channels leading to intracellular potassium shifts. This leads to cellular hyperpolarization and subsequent paralysis. Treatment of TPP should be directed at correcting hypokalemia. Those treated with intravenous potassium tend to recover more quickly than those receiving oral supplementation. Lifestyle modifications such as avoiding heavy exercise, high-carbohydrate meals, and alcohol are crucial. Definitive treatment is achieved by restoring euthyroidism either through medications, radioactive iodine ablation, or surgery. It is vital to maintain a high index of suspicion of TPP in patients presenting with hypokalemia and abrupt paralysis.