Endocrine Abstracts (2009) 20 P307

Coincidence of primary hyperaldosteronism with thyrotoxic nodular goiter presenting as hypokalemic periodic paralysis: complicating or mimicking one another?

Inan Anaforoglu & Ekrem Algün

Department of Endocrinology; Trabzon Numune Training and Research Hospital, Trabzon, Turkey.

Thyrotoxicosis and primary hyperaldosteronism both cause hypokalemic periodic paralysis. A 51-year-old woman, with a history of 3 episodes of transient muscle weakness, was admitted to the emergency unit with complaint of the weakness of legs. Her medical history included hypertension for 10 years. A nodule approximately 3 cm in diameter was palpated in the left anterior neck. Decreased strength (2/5) and deep tendon reflexes in lower extremities symmetrically with normal sensory examination were detected. Initial laboratory findings were significant for a potassium of 1.5 mEq/l and sodium of 148 mmol/l. Thyroid function tests were compatible with primary hyperthyroidism with a hyperactive nodule in scintigraphy. The patient was prescribed propylthiouracil. Her potassium was replaced. She completely regained muscle strength. A diagnosis of thyrotoxic hypokalemic periodic paralysis was supposed. Nevertheless, a decrease in potassium level was observed in each time, immediately when replacement of potassium was stopped. A high level of aldosterone 51.6 ng/dl with supressed renin 0.2 ng/ml per hour, and the high ratio of aldosterone to renin (258) were compatible with the diagnosis of primary hyperaldosteronism. Plasma aldosteron was found to be 66.8 ng/dl after saline infusion test. Imaging of surrenal glands showed an adrenal mass on the left side. The diagnosis of hyperaldosteronism was supposed. Spironolactone, 200 mg/day, was started gradually. On the second week of therapy the patient became normokalemic without support of oral potassium perchloride. Spironolactone 200 mg/day and amlodipin 10 mg/day was enough to control her blood pressure. Whether thyrotoxicosis or hyperaldosteronism triggered hypokalemic periodic paralysis in this patient is a matter of debate. Two cases of thyrotoxicosis and primary aldosteronism complicating with hypokalemic periodic paralysis have been introduced to literature to date. In conclusion, adrenal function should be considered in a patient with hypertension and hypokalemia whatever the presentation of cases are.

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