URINARY METABOLITES OF CORTISOL IN ADRENAL INSUFFICIENCY AND IN PITUITARY EUNUCHOIDISM

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Abstract
PREVIOUS to the development of the highly specific replacement therapy now available for the treatment of Addison's disease, the average life expectancy of such patients was about one and a half years (1). Nevertheless, patients with the classical signs and symptoms of the condition were observed who survived for much longer periods of time. On clinical grounds it appeared that in such patients a small remnant of functioning adrenal tissue sufficed to provide the small quantity of adrenal hormones necessary to permit survival, although often in a condition of semi-invalidism. The diagnosis of Addison's disease, even when beyond doubt on clinical grounds, cannot always be confirmed by characteristic changes in the levels of serum electrolytes, nor in the urinary excretion of steroids derived from the secretions of the adrenal cortex. In such cases the patient may have a small amount of functioning adrenocortical tissue and, if untreated, may later pass into a dangerous state of acute adrenal insufficiency either because of the increased adrenal hormone requirements associated with an incidental infection, or because of the final destruction or atrophy of all the adrenal cortex. With the ready availability of cortisone for the treatment of adrenal insufficiency, the diagnosis in such cases is most important. Laidlaw and associates (2) referred to 7 patients with definite clinical evidence of Addison's disease whose urinary excretion of 17- hydroxycorticoids (as estimated by the method of Reddy, Jenkins and Thorn (3)) was within the normal range. The urines of 5 of these patients were subsequently shown by paper chromatography to contain tetrahydrocortisone and tetrahydrocortisol after glucuronidase hydrolysis.