HYPOTHALAMIC-PITUITARY-ADRENAL FUNCTION IN NON-AIDS PATIENTS WITH ADVANCED HIV-INFECTION

Authors
Citation
St. Azar et Jc. Melby, HYPOTHALAMIC-PITUITARY-ADRENAL FUNCTION IN NON-AIDS PATIENTS WITH ADVANCED HIV-INFECTION, The American journal of the medical sciences, 305(5), 1993, pp. 321-325
Citations number
37
Categorie Soggetti
Medicine, General & Internal
ISSN journal
00029629
Volume
305
Issue
5
Year of publication
1993
Pages
321 - 325
Database
ISI
SICI code
0002-9629(1993)305:5<321:HFINPW>2.0.ZU;2-7
Abstract
Patients with acquired immune deficiency syndrome (AIDS) are reported to have increased basal cortisol and reduced stimulated cortisol relea se, but the dysfunction in the hypothalamic-pituitary-adrenal (HPA) ax is is not yet understood in patients with human immunodeficiency virus (HIV) infection during the advanced stage of disease that precedes th e development of AIDS. To understand the status of the HPA axis during this phase of HIV infection, 25 non-AIDS ambulatory patients with adv anced HIV infection and without evidence of adrenal or pituitary insuf ficiency were studied. Ovine corticotropin-releasing hormone was admin istered (1 mug/kg BW) intravenously and plasma cortisol and adrenocort icotropin (ACTH) were measured over the following 120 minutes. Based o n a standard response curve, obtained from CRH testing of 10 HIV negat ive volunteers with no HPA abnormalities, 13 patients were found to ha ve normal response (group 1), 6 patients had reduced ACTH and cortisol response (group 2) and 6 patients had normal ACTH with reduced cortis ol response (group 3). Basal cortisol and basal ACTH were comparable f or control subjects and groups 1, 2, and 3. This suggests that, in adv anced non-AIDS HIV patients with no clinical evidence of pituitary or adrenal disease, about 25% (group 2) have reduced pituitary reserve wi th high basal ACTH and cortisol, and about 25% (group 3) have reduced adrenal reserve with high basal cortisol and inappropriately normal ba sal ACTH, whereas about 50% (group 1) maintain normal HPA axis activit y with increased basal cortisol secretion. The exact physiopathologic mechanism is not yet known, but an enhanced CRH production by the hypo thalamus may explain the alterations in the HPA axis in advanced HIV d isease.