Abstract
Nontraumatic rhabdomyolysis has been associated with alcohol and drug abuse, seizures, strenuous exercise, muscle hypoperfusion, hyperthermia, electrolyte disturbances, diabetic coma, and hypothyroidism. Hyperthyroidism can be associated with several neuromuscular manifestations, such as thyrotoxic myopathy and thyrotoxic periodic paralysis, both associated with weakness and normal creatine phosphokinase levels. There have been only three reported cases of rhabdomyolysis as a result of thyrotoxicosis. We are reporting the fourth case of such association.
The patient is a 26-year-old black woman with history of hypertension. She presented to the clinic with blurred vision, headaches, palpitations, weight loss, weakness, and persistent high blood pressure. She was found to have exophthalmus, lid lag, and a symmetric, smooth, and diffuse goiter. Ptosis and diplopia were absent; neurologic examination findings was normal. The patient had positive TPO antibodies, elevated free T4 level, and low thyroid-stimulating hormone (TSH) level. Graves disease was diagnosed and propylthiouracil was prescribed. The patient then returned to the clinic 2 weeks later with weakness and myalgias. Her physical examination findings were unchanged except for mild muscle weakness. Laboratory evaluation showed normal electrolytes, normal renal function, and negative urine drug screening. Creatine phosphokinase was 1276 U/L. Her free T4 and T3 levels were elevated and TSH level was low. The patient was treated with aggressive oral fluid resuscitation. Propylthiouracil was continued and free T4 and T3 normalized along with creatine phosphokinase with resolution of symptoms.
Hyperthyroidism may, theoretically, cause rhabdomyolysis by means of increasing energy consumption associated with depletion of muscle energy stores and substrates. Our patient constitutes the fourth reported case of rhabdomyolysis associated with hyperthyroidism.
