(289) How Low (K+)an You Go: A Case of Thyrotoxic Periodic Paralysis & Concomitant Renal Tubular Acidosis

Introduction: Thyrotoxicosis periodic paralysis (TPP) is a rare, dangerous complication of hyperthyroidism manifesting with recurrent episodes of muscle paralysis and hypokalemia. While well-studied in East-Asian patients, its incidence outside of this population is unknown. Additionally, distal renal tubular acidosis (RTA) is a rare complication of TPP.

Description: A 37-year-old Ghanaian male with no past medical history presented to the emergency department with bilateral lower extremity weakness, inability to walk and falls. Over the last year he had four episodes of sudden muscle weakness and self-resolving cramping with concurrent heat intolerance, weight loss, and diplopia. Vitals were notable for tachycardia and hypertension; physical exam was notable for reduced strength in the bilateral lower extremities and tremors in his hands on extension, as well as thyromegaly with a positive bruit. Labs showed K < 2 mEq/L, HbA1c 5.8%, free T4 3.0 ng/dL, TSH < 0.05 mlU/mL, and anti-TPO > 1000.0 IU/mL. Blood gas showed hypokalemic, hyperchloremic, non-anion gap metabolic acidosis, and urine studies demonstrated alkaline urine. He was admitted to the intensive care unit and started on propranolol/methimazole, continued to have tachycardia, undetectable TSH, and high FT4, and therapy was escalated to atenolol/increased methimazole. K, Mg, and Phos were repleted via central line, and he was started on bicarb tablets for suspected distal RTA. On hospital day 3, the patient was discharged with improved weakness, down-trending thyroid hormone levels, and close endocrine follow-up.

Discussion: Lower extremity weakness has a number of differentials including spinal cord pathologies, Guillain-Barre Syndrome and tick paralysis. It is important to have TPP in the differential as well, even in non-East-Asian patients, as it can be easily diagnosed and treated. Studies have suggested TPP is due to simultaneous derangements of the Na+/K+ ATPase and a specific potassium inward-rectifying channel (Kir2.6), leading to relative serum hypokalemia and paralysis. Urinary potassium wasting can occur in the event of a concomitant distal RTA (likely originating from autoimmunity) leading to total body potassium depletion. Treatment of TPP should focus on electrolyte repletion, symptomatic control, and antithyroid therapies.