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Adrenocortical Function in Acquired Immunodeficiency Syndrome^*

Department of Medicine, University of California San Francisco, California 94110

Address all correspondence and requests for reprints to: Dr. Edward G. Biglieri, Department of Medicine, University of California, Clinical Research Center, Building 100, Room 321, 1001 Potrero Avenue, San Francisco, California 94110.

Clinical features of adrenal steroid deficiency occur in patients with the acquired immunodeficiency syndrome (AIDS). To determine the frequency of aberrations in peripheral steroid levels in patients with AIDS and AIDS-related complex (ARC) we measured morning recumbent plasma cortisol, deoxycorticosterone, 18-hydroxydeoxycorticosterone (18-OHDOC), corticosterone, aldosterone, and 18-hydroxycorticosterone concentrations before and after administration of 0.25 mg ACTH (Cosyntropin) in 74 randomly selected hospitalized patients with AIDS and 19 patients with ARC. Basal (0800 h) cortisol levels in the AIDS patients were significantly higher (P < 0.01) than those in normal subjects, while other ACTH-dependent steroids of the 17-deoxypathway, deoxycorticosterone, corticosterone, and 18-OHDOC, were normal. These latter steroids increased subnormally in response to ACTH in patients with either AIDS (P < 0.001) or ARC (P < 0.005), but in ARC patients plasma 18-OHDOC levels were significantly higher than in those with AIDS (P < 0.001). Supraphysiological doses of ACTH were then administered for 3 consecutive days to 14 patients with AIDS and 9 with ARC, which confirmed and amplified the subnormal responses of these steroids in AIDS. The mean plasma cortisol response was reduced on the third day only in AIDS patients, whereas in the ARC patients the steroid responses were normal. Angiotensin III infusion and postural stimulation increased plasma aldosterone and 18-hydroxycorticosterone levels in AIDS and ARC patients. Defective stimulation of 18-OHDOC alone or in combination with defective stimulation of other 17-deoxysteroids can be a harbinger of subsequent impaired adrenal capacity in AIDS.

^* This work was supported in part by USPHS Research Grant AM-06415 from the NIADK, and in part from the Universitywide Task Force on AIDS, Yr 2. The studies were carried out in the General Clinical Research Center at San Francisco General Hospital (RR-00013).

Received January 9, 1987.

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