Steroids and Thyrotoxicosis Precipitate Periodic Paralysis.

Thyrotoxic Periodic Paralysis (TPP) belongs to a group of muscle diseases called channelopathies, which present with painless generalized muscle weakness without exertion. TPP can be precipitated by a large carbohydrate meal, stress, strenuous exercise, alcohol, a high-salt diet, menstruation, and cold temperatures. Rarely, steroids such as dexamethasone can also precipitate a TPP attack. A 29-year-old Hispanic male, with a history of hyperthyroidism, presented to the emergency department with progressive weakness, predominantly in the lower extremities since morning. Earlier that day, the patient was seen in the same emergency department for difficulty in swallowing. He was diagnosed with uvulitis and received intramuscular dexamethasone and was discharged with amoxicillin for ten days. At home, he started to develop cramps in his lower extremities associated with paresthesias, which progressed to severe weakness to the point where he could not get out of bed. He returned to the hospital and revealed that he had suffered a similar episode following a steroid injection five years ago. He had not sought medical attention as it resolved spontaneously. He denied strenuous exercise, carbohydrate-rich meal, or alcohol ingestion. The patient had been noncompliant with atenolol and methimazole for the past month after losing his medical insurance. On examination, the patient appeared alert and calm. His vitals were significant for tachycardia of 123 beats per minute. Thyromegaly and tenderness were absent on examination of the neck. Muscle strength was 5/5 in the ankle dorsiflexors and ankle plantar flexors bilaterally, but the strength of the iliopsoas, quadriceps, and hamstrings was only 2/5 bilaterally. Deep tendon reflexes were diminished throughout to 1+. Laboratory findings were significant for profound hypokalemia, hypophosphatemia, low thyroid stimulating hormone, and elevated free T3 and T4 levels suggestive of hyperthyroidism. His electrolytes were replaced aggressively and his home medications were restarted. His electrolyte imbalance corrected and his symptoms resolved within a day and he was discharged home. The overwhelming majority of TPP cases reported are male patients, hence this case demonstrates the need to be aware of this complication while treating hyperthyroid male patients with steroids. Hyperthyroidism potentiates catecholamine-mediated Na/K ATPase transport of potassium into the cells. Glucocorticoids are used in the treatment of thyroid storm as it prevents the peripheral conversion of T4 to T3. Moreover, glucocorticoids increase glucose levels stimulating insulin release, which shifts potassium intracellularly accentuating muscle weakness. Although the incidence of glucocorticoids causing TPP is low and not many cases are documented, it is still an important condition to be aware of and can have major clinical implications. Clinicians should be aware of this small subset of hyperthyroidism patients where the use of glucocorticoids can precipitate paralysis.