9-α-FLUOROHYDROCORTISONE-INDUCED HYPER TENSION IN A MALE INFANT WITH ADRENOGENITALISM, AND IN 6 ADULTS WITH ADDISON'S DISEASE

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Abstract
IN 1954, Fried and Sabo (1) reported that substitution of a fluorine atom in the 9-alpha position of the hydrocortisone molecule produced a marked potentiation of glucocorticoid effects; Borman et al. (2) reported a corresponding mineralocorticoid enhancement. This new compound, 9-α-fluorohydrocortisone, promised to become of major importance in antiphlogistic and maintenance adrenocortical therapy. In the course of time, it has become apparent that the potentiations observed are unequal; salt and water effects are enhanced more than anti-inflammatory effects, and consequently fluid retention as an undesirable side-effect is likely to occur at any dosage level producing a satisfactory antiphlogistic response. Thus Boland and Headley soon observed the occurrence of edema in patients with rheumatoid arthritis under treatment with 9-α-fluorohydrocortisone. This complication occurred in 12 out of 13 patients; in 6 of the 12 slight to moderate elevation of blood pressure also developed (3). Though unsuitable for anti-inflammatory therapy, it seemed likely that the new compound might still prove valuable in the maintenance therapy of hypoadrenal patients. In an early report, Goldfien et al. indicated that 9-α-fluorohydrocortisone is satisfactory for this purpose but implied that, in order to avoid fluid retention, the dose must be kept so low that a small amount of cortisone is also necessary to restore a feeling of well-being. They also mentioned a patient with the adrenogenital syndrome in whom 2 mg. daily proved to be effective in suppressing corticotropin secretion without producing any side-effects (4).