An African American Man With Hyperthyroidism and Acute Paralysis

A 68-year-old African American man developed weakness in the legs that got progressively worse during the 2 days prior to the point that he became unable to walk. He fell at home, could not get up on his own, and was brought to the emergency room (ER). In the ER he was found to be severely weak and had a serum potassium level of 2.1 mEq/dL (normal, 3.5–5.1 mEq/dL); troponin level was increased, but cardiac workup was negative. The patient was loaded with IV potassium chloride under cardiac monitoring.

Past medical history included hyperthyroidism for which he was on methimazole 50 mg in the morning and 20 mg at night and atenolol with triamterene/hydrochlorothiazide for hypertension. He had a previous coronary angioplasty.

Family history was negative. The patient did not use drugs but used to smoke up until 1 year before. He did not drink alcohol.

Review of systems revealed no chest pains, shortness of breath, difficulty swallowing, or diplopia.

Examination the following day showed normal mentation and cranial nerves. There was minimal weakness of the proximal muscles of the legs, at about 5−/5. Gait was normal. Reflexes were trace in the legs and 1+ in the arms. Sensation to pinprick, touch, and vibration were normal. Coordination was normal. There was no myotonia.

The patient was observed and discharged home on potassium supplements of 20 mEq a day orally.

Discussion

This patient had thyrotoxic periodic paralysis, but in this case it was clearly secondary to hyperthyroidism. Secondary periodic paralysis could have many causes, and is similar to hypokalemic paralysis. This condition is more often described in the Japanese population, and 75% of cases occur in those of Asian extraction, but it has been reported in other populations, including African Americans.

The attacks are characterized by weakness with hyporeflexia, and thyrotoxicosis might appear simultaneously with the paralytic attacks in more than 80% of patients. The thyrotoxic signs could be mild.

Typically, attacks are characterized by proximal weakness that occurs after exercise or heavy meals. The hypokalemia is caused by insulin-induced entrance of potassium into muscle fibers. At the end of the attack, potassium is released from the muscle and might cause rebound hyperkalemia.

The relationship between periodic paralysis and the thyroid disorder is not clear, and the genetic defect in these patients is unknown.

Muscle biopsy shows nonspecific changes, but there could be vacuolization as in HypoPP. The EMG reveals myopathic motor units during attacks.

Acetazolamide is not efficient in preventing attacks and could even precipitate them, whereas propranolol is beneficial. Treatment of thyrotoxicosis is most important; low-carbohydrate and low-sodium diets and potassium supplements can sometimes help.

Summary

This patient with hyperthyroidism had an attack of weakness with hypokalemia; he was diagnosed with thyrotoxic paralysis.

Important Points

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Symptoms of thyrotoxic periodic paralysis are similar to those of HypoPP.
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Hypokalemic periodic paralysis and thyrotoxic periodic paralysis can present in any race.
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Management of an acute attack of paralysis in those with thyroid disease is similar to that used for those without thyroid disease.
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Attacks of muscle weakness in HypoPP are associated with the slow membrane depolarization, which is caused by insulin release lowering serum potassium levels.