The relationship of serum DHEA-S and cortisol levels to measures of immune function in human immunodeficiency virus-related illness.

Human immunodeficiency virus (HIV) is a major cause of immunoincompetence. Whether the virus, itself, accounts for all the deficiency remains in question. Steroids can also influence immune function; glucocorticoids cause immunoincompetence while dehydroepiandrosterone (DHEA) enhances immune function. Changes in the levels of such hormones during the course of HIV illness might result in significant changes in immune competence. The purpose of this study is to investigate whether dehydroepiandrosterone-sulphate (DHEA-S) or cortisol levels correlate with absolute CD4 lymphocyte levels. Plasma for cortisol and DHEA-S was drawn from 98 adults with HIV. Of these, 67 had simultaneous CD4 levels. Cortisol levels were 12.4 +/- 4.6 micrograms/dl, DHEA-S 262 +/- 142 micrograms/dl, and CD4 levels were 308 +/- 217/mm3 (mean +/- SD). Correlational analysis revealed a significant relationship between DHEA-S and CD4 levels (r = 0.30; p = 0.01) but not between CD4 levels and cortisol (r = 0.11; p = 0.36) or cortisol/DHEA-S ratios (r = 0.17; p = 0.16). When analyzed by clinical subgroups, significant differences were also found with a decrease in DHEA-S levels seen in persons with more advanced illness. The data exhibit a positive relationship between the immune status of patients with HIV-related illness and DHEA, leading to the hypothesis that DHEA deficiency may worsen immune status.

Relationship between serum cyclo(His-Pro) concentrations and the nutritional status of HIV-infected patients.

Cyclo(His-Pro) (CHP) is a gut-neuropeptide that influences both appetite and carbohydrate metabolism. This study was undertaken to determine whether concentrations of CHP correlated with various clinical markers of nutritional status and progression of HIV infection. Serum concentrations of CHP were analyzed in a clinical sample of 100 HIV-positive patients whose HIV clinical status ranged from asymptomatic to advanced disease with weight loss. We found a relationship between CHP concentrations and serum albumin and hemoglobin levels, markers of chronic nutrition and disease. However, no correlation was seen between CHP and cortisol concentrations, a marker of acute stress. To analyze the relationship of HIV clinical stage and CHP, patients were divided into three subgroups: asymptomatic, mildly symptomatic, and clear-cut AIDS. CHP concentrations were significantly correlated with HIV clinical stage. These data lead to the hypothesis that CHP is a marker of disease progression and that it potentially plays a role in modulating the nutrition of HIV-infected patients.

Hematogenous dissemination of Mycobacterium tuberculosis in patients with AIDS.

Proof of hematogenous dissemination of Mycobacterium tuberculosis was initially reported in the early 1900s and was noted to be most frequent in patients with miliary tuberculosis. More recently, M. tuberculosis bacteremia has been reported in human immunodeficiency virus (HIV)-infected patients. We describe 13 adult HIV-infected patients in whom hematogenous M. tuberculosis dissemination was evident. Although for most patients whose bone marrow aspirate cultures yielded M. tuberculosis a chest roentgenogram revealed a miliary pattern, roentgenograms for those with M. tuberculosis bacteremia usually revealed evidence of lobar or diffuse infiltrates. Most patients with M. tuberculosis bacteremia had other risk factors for M. tuberculosis, and many had a rapid death, suggesting acute fulminant infection. Our own experience suggests that there are various syndromes associated with hematogenous dissemination in patients infected with M. tuberculosis.