Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2009) 20 P307

ECE2009 Poster Presentations Clinical case reports and clinical reports (61 abstracts)

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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