SERUM CORTISOL AND DHEA CONCENTRATIONS DURING HIV-INFECTION

Citation
N. Christeff et al., SERUM CORTISOL AND DHEA CONCENTRATIONS DURING HIV-INFECTION, Psychoneuroendocrinology, 22, 1997, pp. 11-18
Citations number
30
Categorie Soggetti
Neurosciences,"Endocrynology & Metabolism
Journal title
ISSN journal
03064530
Volume
22
Year of publication
1997
Supplement
1
Pages
11 - 18
Database
ISI
SICI code
0306-4530(1997)22:<11:SCADCD>2.0.ZU;2-Z
Abstract
The progression of HIV infection is accompanied by severe immunodepres sion and cachexia, particularly during advanced stages. The immune dep ression 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 count s and changes in body weight of HIV-positive men. The results of five retrospective and prospective studies indicate that the serum concentr ations of cortisol and DHEA in HIV-infected patients were different fr om those of HIV-negative controls. Serum cortisol was elevated at all stages of infection (+20 to +50%, p<.05 to p<.001) particularly in AID S patients (stage IV C). In contrast, the serum DHEA concentrations we re closely correlated with the stage of HIV-infection, being higher in the early stages (stages II and III or >500 CD4) than in advanced sta ges (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 negati ve 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 se rum cortisol. In contrast, there was a negative correlation between se rum DHEA and Delta body weight (%) (r=-0.69, p<.0001) and a positive c orrelation with the cortisol/DHEA ratio (r=+0.61, p<.0001). There is t hus a link between the circulating concentrations of adrenal steroids and the progression of immunosuppression and cachexia during HIV-infec tion. This mises the question of whether there is a cause-and-effect r elationship between clinical progression and circulating steroid conce ntrations. Further investigations into the relationship between the ra tio 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. (C) 1997 El sevier Science Ltd.