MON-511 - Evaluation of the Association between Serum Cortisol and Immunological Status in HIV-Positive Patients.

Introduction: The immunodeficiency associated with the human immunodeficiency
virus (HIV/AIDS) is a major public health concern. Alterations in the hypothalamic-
pituitary-adrenal (HPA) axis have been described in HIV-positive (HIV+) patients,
suggesting the infection as a potential cause of hypercortisolism. This study evaluates
the association between basal cortisol levels and CD4+ lymphocyte counts,
considering the influence of low T3 syndrome and the CD4+/CD8+ lymphocyte ratio.
Materials and

Methods: A cross-sectional study was conducted between June 2018
and June 2019 at a medium complexity public hospital The primary
objectives were to evaluate the association between basal cortisol and CD4+
lymphocyte counts and to analyze immunological differences between
normocortisolemic and hypercortisolemic patients. Secondary objectives included
assessing the influence of low T3 syndrome and the CD4+/CD8+ ratio on these
associations. Ambulatory HIV+ patients aged ≥18 were included, excluding
those with factors that might alter the HPA axis or immunological parameters. Basal
cortisol, TSH, T4, T3, viral load, and CD4+ and CD8+ lymphocyte counts were
measured. The association between cortisol and CD4+ lymphocytes was assessed
using logistic regression, adjusting for confounding factors such as age, gender, BMI,
viral coinfections, illicit drug use, and depression.

Results: 111 patients were included. The mean basal cortisol level was 13.8 µg/dL
(SD ±4.26), with 16% of patients classified as hypercortisolemic. No significant
differences were observed between normocortisolemic and hypercortisolemic patients
in viral load suppression (50% vs. 71%, p = 0.23). The median CD4+ lymphocyte count
was 545 cells/mm³ (IQR: 28–2140) in the normocortisolemic group and 547 cells/mm³
(IQR: 247–1327) in the hypercortisolemic group (p = 0.88). The median CD8+
lymphocyte count was 957 cells/mm³ (IQR: 219–2111) in the normocortisolemic group
and 1285 cells/mm³ (IQR: 405–1963) in the hypercortisolemic group (p = 0.15). T3
levels did not differ between groups (p = 0.79). No significant linear association was
found between basal cortisol and CD4+ (r = -0.131, p = 0.189) or CD8+ lymphocyte
counts (r = 0.014, p = 0.897). However, weak but significant correlations were
observed between cortisol and T3 (r = 0.229, p = 0.034) and between T3 and CD8+
lymphocytes (r = 0.292, p = 0.017).

Conclusions:
Basal cortisol levels were not significantly associated with CD4+ lymphocyte counts in
HIV+ patients. However, the correlations between T3, cortisol, and CD8+ lymphocytes
suggest a potential interaction between thyroid function and the immune system.
Longitudinal studies, including inflammatory biomarkers and free cortisol fractions, are
needed to better understand these interactions and their clinical relevance.

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