17α-HYDROXYPROGESTERONE—A SALT-LOSING STEROID: RELATION TO CONGENITAL ADRENAL HYPERPLASIA

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Abstract
Sodium, chloride and potassium metabolic balance studies were performed on 3 “normal” subjects with intact adrenal function and 2 patients with adrenocortical insufficiency treated with desoxycorticosterone acetate (DCA) and cortisone acetate. During the period of daily oral administration of 500 mg. of noncsterified 17α-hydroxyprogesterone, there resulted an excessive loss of salt, significantly above control values in all “normal” subjects as well as in both patients with adrenal insufficiency receiving DCA concurrently. Changes in potassium excretion were variable. These changes in electrolytes promptly disappeared upon withdrawal of 17α-hydroxyprogesterone. No salt loss was produced during a four-day course of 17α-hydroxyprogesterone in 2 patients with adrenal insufficiency receiving no salt-retainer. The saluretic activity of 7α-hydroxyprogesterone appears to be dependent upon the presence of an adrenal salt-retaining steroid. Its mechanism of action is probably based on inhibition of the renal tubular effects of desoxycorticosterone and aldosterone. These observations are offered as an explanation for the active salt loss which often occurs in congenital adrenal hyperplasia, emphasizing the possible role of 17αhydroxyprogesterone as the adrenal principle involved.