Abstract: PUB259
A Case of Graves Disease Presenting as Hypokalemic Periodic Paralysis
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Kuruvada, Krishna Mohita, Montefiore Medical Center, New York, New York, United States
- Yunes, Milagros, Montefiore Medical Center, New York, New York, United States
Introduction
Thyrotoxic periodic paralysis(TPP) is a rare complication of hyperthyroidism and is a treatable form of hypokalemic periodic paralysis(HPP). While hereditary channelopathies primarily underlie HPP, acquired cases are seen with hyperthyroidism and tend to affect males more frequently. We describe a case of thyrotoxicosis that presented with severe hypokalemia and sudden onset paralysis.
Case Description
37-year-old male with no medical history presented with acute paralysis of upper and lower extremities. He had experienced severe muscle weakness and painful cramps intermittently over the past few months, worsened by exercise. He also noted weight loss, heat intolerance, and dry skin. Examination revealed thyromegaly, mild proptosis, power of 0/5 in upper and lower limbs, and hyporeflexia. Laboratory tests showed severe hypokalemia (< 2 mEq/L) and mild metabolic acidosis (pH 7.25, bicarbonate 16 mEq/L). The possibility of distal RTA was considered with the combination of hypokalemia and metabolic acidosis, however, thyroid studies were pursued as his exam findings were concerning for hyperthyroidism. Thyroid studies revealed low TSH (<0.05 µIU/mL), elevated free T4 (3 ng/dL), free T3 (>20 pg/mL), thyroid-stimulating immunoglobulin (326%), thyroid-binding inhibitor (34 IU/L), and thyroid peroxidase antibody (>1000 IU/mL). Ultrasound showed an enlarged, hypervascular and heterogeneous thyroid gland. These findings were consistent with Graves' thyrotoxicosis. The patient was started on potassium supplementation, methimazole 20 mg daily, and atenolol 50 mg twice daily with which his weakness improved. The resolution of symptoms with potassium replacement and treatment for Graves' disease suggests that severe hypokalemia in this patient represents a case of hypokalemic periodic paralysis caused by thyrotoxicosis.
Discussion
Thyroid hormone increases Na+/K+-ATPase activity on muscle membranes leading to intracellular potassium influx. Patients experience sudden, painless episodes of muscle weakness during periods of stress. Bulbar and respiratory muscles are minimally involved. Acute episodes are managed with potassium supplementation and treatment of hyperthyroidism. Beta blockers inhibit the Na+/K+-ATPase and can be used for symptom control. This case illustrates the importance of checking thyroid studies in patients with HPP as restoration of euthyroidism eliminates episodes.