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It has been ten years since Jerome W. Conn, MD, astounded hypertension researchers by suggesting that there were 3,000,000 cases of undiagnosed primary aldosteronism in the United States.1In conjunction with Drs. Rovner and Cohen, new criteria for the diagnosis of primary aldosteronism were defined and since that time the combination of hypokalemia, elevated aldosterone production, suppressed plasma renin activity, and normal glucocorticoid production has been the hallmark of classic primary aldosteronism.2This classic syndrome is generally associated with a large (greater than 1.5 cm in diameter) adrenal adenoma but may also be associated with bilateral adrenal hyperplasia. The removal of this abnormal adrenal tissue usually cures the hypertension and the associated manifestations of hyperaldosteronism. In 1965 and 1966, Conn et al3,4reported the first cases of normokalemic primary aldosteronism associated with smaller adrenal tumors (5 mm in diameter) and suggested that this represented an earlier phase
Clarence E. Grim (Sat,) studied this question.