title: Serum cortisol and DHEA concentrations during HIV infection.
abstract: The progression of HIV infection is accompanied by severe immunodepression and cachexia, particularly during advanced stages. The immune depression is due largely to a dramatic drop in the number of CD4 cells. The loss of body weight is mainly due to a reduced fat-free mass with no change in adipose tissue. We determined the serum concentrations of cortisol and DHEA and their correlations with absolute CD4 cell counts and changes in body weight of HIV-positive men. The results of five retrospective and prospective studies indicate that the serum concentrations of cortisol and DHEA in HIV-infected patients were different from those of HIV-negative controls. Serum cortisol was elevated at all stages of infection (+20 to +50%, p < .05 to p < .001) particularly in AIDS patients (stage IV C). In contrast, the serum DHEA concentrations were closely correlated with the stage of HIV-infection, being higher in the early stages (stages II and III or > 500 CD4) than in advanced stages (IV C or < 500 CD4)-in the latter being below those of HIV-negative men-or in controls (+40 to 100%, p < .01 to p < .001). There was a negative linear correlation between the CD4 cell counts and cortisol (r = -0.4, p < .02) and a positive linear correlation with DHEA (r = +0.36, p < .01). There was no significant correlation between delta body weight and serum cortisol. In contrast, there was a negative correlation between serum DHEA and delta body weight (%) (r = -0.69, p < .0001) and a positive correlation with the cortisol/DHEA ratio (r = +0.61, p < .0001). There is thus a link between the circulating concentrations of adrenal steroids and the progression of immunosuppression and cachexia during HIV-infection. This raises the question of whether there is a cause-and-effect relationship between clinical progression and circulating steroid concentrations. Further investigations into the relationship between the ratio cortisol/DHEA and the immune response and cachexia should indicate the contributions of these steroids to the etiology of HIV infection and lead to the development of new therapeutic strategies.
authors.affiliation: Laboratoire de Biochimie Endocrinienne/Biochimie B, Faculté de Médecine/Hôpital X. Bichat, Paris, France.
authors.forename: N
authors.initials: N
authors.lastname: Christeff
authors.forename: N
authors.initials: N
authors.lastname: Gherbi
authors.forename: O
authors.initials: O
authors.lastname: Mammes
authors.forename: M T
authors.initials: MT
authors.lastname: Dalle
authors.forename: S
authors.initials: S
authors.lastname: Gharakhanian
authors.forename: O
authors.initials: O
authors.lastname: Lortholary
authors.forename: J C
authors.initials: JC
authors.lastname: Melchior
authors.forename: E A
authors.initials: EA
authors.lastname: Nunez
mesh_terms: D000328:Adult; D015153:Blotting, Western; D016516:CD4-CD8 Ratio; D002100:Cachexia / Q000473:pathology; D003687:Dehydroepiandrosterone / Q000097:blood*; D015658:HIV Infections / Q000097:blood* / Q000503:physiopathology; D006679:HIV Seropositivity; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D008297:Male; D011446:Prospective Studies; D012189:Retrospective Studies; D015431:Weight Loss / Q000502:physiology
chemical_list: D003687:Dehydroepiandrosterone; D006854:Hydrocortisone