title: Adrenal function in HIV infected patients.
abstract: Since anatomopathological lesions of the adrenal gland have been frequently observed at autopsy in AIDS, we investigated the glucocorticoid function in 63 patients (51 men, 12 women) infected by the human immunodeficiency virus (HIV) in order to determine the incidence and the nature of any adrenocortical abnormalities at various stages of HIV infection. The patients were classified according to the Centers for Disease Control (CDC) recommendations into group II (asymptomatic; N = 13), group III (lymphadenopathy; N = 27) and group IV (clinical manifestations; N = 23). Plasma ACTH and cortisol before and after an exogenous ACTH stimulation test were measured in patients as in 30 age-matched controls. Plasma renin activity and plasma aldosterone before and after ACTH stimulation were also measured in 31 patients (group II: 12; group III: 10; group IV: 9). Compared with controls patients from group II-III had higher levels of ACTH (39.11 +/- 17.01 vs 29.73 +/- 8.53 ng/l; p = 0.003) and basal cortisol (232 +/- 91.2 vs 184.3 +/- 30.9 micrograms/l; p = 0.03). No significant differences were noted between group IV patients and controls as to ACTH and basal and stimulated cortisol levels. Among the 63 patients, only one from group IV had a blunted cortisol response after ACTH stimulation test. Plasma renin activity, and basal and stimulated aldosterone levels in the 3 groups of patients were not different from control values.
  
  
  CONCLUSIONS
  1. Adrenal insufficiency does not seem very frequent in group IV patients and is likely to be a late complication in AIDS. 2. The increased ACTH and basal cortisol levels found in group II and group III patients argue for an early dysregulation of the adrenocortical axis in HIV infection. The exact physiopathological mechanism is not yet known, but an enhanced CRH production by interleukin 1 and/or a direct role of the HIV envelope glycoprotein (gp 120) may explain the high ACTH level in HIV patients.
authors.affiliation: Department of Endocrinology, Hôpital du Bocage, University of Dijon, France.
authors.forename: B
authors.initials: B
authors.lastname: Verges
authors.forename: P
authors.initials: P
authors.lastname: Chavanet
authors.forename: J
authors.initials: J
authors.lastname: Desgres
authors.forename: G
authors.initials: G
authors.lastname: Vaillant
authors.forename: A
authors.initials: A
authors.lastname: Waldner
authors.forename: J M
authors.initials: JM
authors.lastname: Brun
authors.forename: R
authors.initials: R
authors.lastname: Putelat
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000097:blood / Q000503:physiopathology*; D000302:Adrenal Cortex / Q000503:physiopathology*; D000324:Adrenocorticotropic Hormone / Q000008:administration & dosage / Q000097:blood; D000328:Adult; D000450:Aldosterone / Q000097:blood; D005260:Female; D005938:Glucocorticoids / Q000097:blood*; D015497:HIV-1; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D012083:Renin / Q000097:blood
chemical_list: D005938:Glucocorticoids; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D012083:Renin; D006854:Hydrocortisone