Since Conn's description of the clinical features associated with primary aldosteronism in 1955,1 several other cases have been reported in the literature.2-12 This syndrome, which is the result of hypersecretion by the adrenal gland of the mineralocorticoid hormone aldosterone, is usually due to a functioning adrenocortical adenoma. In the few cases without adenoma, hyperplasia chiefly involving the zona fasciculata has been found,9 and hyperaldosteronism due to adrenocortical carcinoma with hepatic metastases has been reported.4 All patients were adults except one girl 6 aged 13, and one boy 12 aged 9 years.
The clinical syndrome originally described by Conn 1,13 consists essentially of polyuria and polydipsia, arterial hypertension, periodic weakness and "paralyses," paresthesiae, and intermittent tetany. These findings are associated with altered electrolyte metabo
lism manifested by metabolic alkalosis with hypokalemia and hypernatremia, and elevated potassium content of sweat, saliva, and urine, with low sweat, salivary, and