SUN-519 Hypokalemic Periodic Paralysis

Abstract

Background:Hypokalemic periodic paralysis is a rare disorder associated most often with a genetic defect in electrolyte channels, which can also occur in the setting of thyrotoxicosis. The presenting state in the acquired form has a low potassium, low TSH, high free T4 or high T3. It is more common in men, and in the Asian population with an approximate incidence of 2%. Symptoms can last from hours to days and are often precipitated by stress, exercise, and/or high carbohydrate intake. It is believed that the excess thyroid hormone creates an increased catabolic state which drives potassium inward and hyperpolarizes the muscle membrane to create a paralytic state. Case:A 23 year old African American male presented with chest discomfort and palpitations. TSH was <0.01 μU/mL (normal 0.530 - 6.340) with a free T4 of 3.31 ng/dL (normal 0.60–1.60). EKG showed ventricular conduction delay and he was sent home on propranolol 20mg daily and methimazole 5mg three times daily. He returned 5 days later with worsening palpitations and now new onset weakness. He was found to have a potassium of 1.4 mmol/L (normal 3.5–5.1) and magnesium of 1.2 mg/dL (normal 1.6–2.5). EKG showed normal sinus rhythm at a rate of 97, prolonged QT at 524msec (normal 330–470 msec), with repeat EKG 20 minutes later showing atrial tachycardia with a rate of 114 (normal 60–100). He was not able to move anything beyond his head, other than minor upper extremity hand movements, and could not sit up in bed. His potassium was initially repleted with eight doses of 10mEq KCl given q1h. His paralysis significantly improved within the first 4hrs, and was completely resolved by the next morning. Additional lab workup revealed thyroid stimulating antibody level of 13.00% (normal 0.0–0.55). He was discharged on methimazole 10mg twice daily and propranolol 10mg twice daily with instruction to follow up closely with his primary care physician and endocrinology. Conclusion:This patient presented with acute onset of weakness and palpitations in the setting of hyperthyroidism from Graves’ disease and hypokalemia consistent with thyrotoxic periodic paralysis. The physiology behind the presentation is not clear, but the current hypothesis is that depolarization of the neuromuscular junction leads to a tonic state from hyper-polarization. Thyroid hormone increases the metabolic demand, which along with an increase in sympathetic tone drives the sodium-potassium ATPase activity into overdrive, thus decreasing extracellular potassium. Thyrotoxic periodic paralysis is rare presentation, but should be considered for any patient that presents potassium abnormalities and symptoms of thyrotoxicosis.