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T HE excessive production of androgenic steroids by the adrenal cortex in the adrenogenital syndrome due to adrenocortical hyperplasia and the clinical manifestations of this disordered function have been well documented (1). The basic derangement of adrenocortical function in this disease awaits precise clarification. Bartter et al. (2) suggested that the adrenal cortex was unable to synthesize readily glucogenic corticoids (compound F) so that the pituitary secreted excessive quantities of adrenocorticotropic hormone, which then over-stimulated the target organ in an attempt to attain a "normal" level of such steroids. This thesis would find support in the successful suppression of 17-ketosteroid secretion by the administration of cortisone according to Wilkins (1).In a preliminary report (3) it was indicated that the excretion of material measured as 3-alpha-20-alpha-pregnanediol (hereafter referred to as pregnanediol) was regularly high in the adrenogenital syndrome and that the levels fell following the institution of therapy with cortisone. Evidence was presented to show that the steroids so measured were in great part 3-alpha-17-alpha-20-alpha-pregnanetriol (hereafter referred to as pregnanetriol), and a simple screening procedure was described for its detection. The present studies were undertaken in order to shed more light on the fundamental causes of the derangement in hormonal synthesis in this condition. METHODSTwenty-four-hour collections of urine were preserved with toluene and stored at 4° C.