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Rapid ACTH Test with Plasma Aldosterone Levels: Improved Diagnostic Discrimination

ROBERT G. DLUHY, M.D.; THEP HIMATHONGKAM, M.D.; and MARTIN GREENFIELD, M.D.
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Grant support: Supported in part by grant 9893, the John A. Hartford Foundation; and Public Health Service research grant AM-5100-14, the National Institute of Arthritis and Metabolic Diseases. The clinical studies, done in The Clinical Research Center, Peter Bent Brigham Hospital, were supported by grant 8-MO1-FR-31-06.

▸Requests for reprints should be addressed to Robert G. Dluhy, M.D., Endocrine-Metabolic Unit, Peter Bent Brigham Hospital, 721 Huntington Ave., Boston, MA 02115.


Boston, Massachusetts


Ann Intern Med. 1974;80(6):693-696. doi:10.7326/0003-4819-80-6-693
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Plasma cortisol and aldosterone levels were measured in 12 normal persons and in patients with primary and secondary adrenal hypofunction before and 30 minutes after intramuscular injection of 0.25 mg (25 units) α1-24-adrenocorticotrophin (Cortrosyn®). The basal cortisol levels of the normal persons ordinarily doubled; whereas their plasma aldosterone levels increased, on the average, 14 ng/100 ml above control (range, 4 to 29 ng/100 ml). Plasma cortisol levels failed to rise in steroid-treated, asthmatic patients, but their plasma aldosterone levels increased normally. Six patients with panhypopituitarism and five patients with primary adrenal insufficiency had abnormal plasma cortisol responses after ACTH administration. In contrast with patients with primary adrenal insufficiency whose plasma aldosterone levels failed to rise, all patients with panhypopituitarism had significant corticotrophin-stimulated aldosterone increments above the control level of 5 ng/100 ml or greater. Thus, the plasma aldosterone response after intramuscular ACTH administration can be useful in differential diagnosis when adrenal hypofunction is suggested by a subnormal cortisol response.

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