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The most common form of the congenital adrenal hyperplasia syndrome is caused by an inefficient enzymatic hydroxylation of the adrenal steroids at the 21 position (1-4). The symptoms of this disease can be explained by a deficiency in cortisol secretion resulting in an increased ACTH output and an overproduction of androgens and cortisol precursors by the hyperplastic adrenals (5, 6). About a third of these patients manifest a marked tendency to sodium loss and potassium retention (7). The pathogenesis of this phenomenon has not yet been fully understood, and three major hypotheses have been advanced. The first was suggested by Crigler, Silverman, and Wilkins (8), who observed an increase in sodium diuresis in patients treated with ACTH (1, 9), as well as a decreasing requirement for desoxycorticosterone acetate (DOCA) when they were treated with cortisone or corticosterone (8). These authors interpreted their results as suggesting the secretion of sodium-losing hormones by the patients' adrenals. Earlier, Darrow (10) had noted that patients with congenital adrenal hyperplasia and salt loss required amounts of DOCA or salt, or both, which were larger than those needed by Addisonian patients. Barnett and

the journal of clinical investigation/the journal of clinical investigation

Aldosterone Secretion Rate in Congenital Adrenal Hyperplasia. A Discussion of the Theories on the Pathogenesis of the Salt-losing Form of the Syndrome*