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
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.