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Published on: January 5, 2016
ACTH and cortisol secretions in children with perinatal HIV-1 infection
R Lala1, E Palomba, P Matarazzo
1Department of Pediatric Endocrinology, Regina Margherita Children's Hospital, Turin, Italy.
Insights
In children with HIV-1 infection, serum cortisol and adrenocorticotropic hormone (ACTH) levels did not differ significantly from healthy children. Adrenal failure is a potential late complication in severely ill patients with human immunodeficiency virus.
Area of Science:
- Pediatrics
- Infectious Diseases
- Endocrinology
Background:
- Perinatal HIV-1 infection can affect various endocrine functions.
- The relationship between HIV-1, adrenal hormones, and immune status (CD4 cell count) requires further elucidation.
Purpose of the Study:
- To investigate serum cortisol and adrenocorticotropic hormone (ACTH) levels in children with perinatally acquired HIV-1 infection.
- To assess the correlation between these hormone levels, CD4 cell counts, and disease severity.
- To evaluate the role of cortisol in HIV-1 pathogenesis and disease progression.
Main Methods:
- Evaluated serum cortisol, ACTH, and CD4 cell counts in 25 perinatally HIV-1-infected children.
- Classified patients into three groups based on clinical symptoms (asymptomatic, moderately symptomatic, severe).
- Compared HIV-1-infected children with 126 age- and sex-matched healthy controls.
Main Results:
- No significant differences in cortisol and ACTH levels were observed between HIV-1-infected children and controls, or among the different disease severity groups.
- CD4 cell counts declined progressively with increasing disease severity.
- No correlation was found between cortisol or ACTH levels and CD4 cell counts.
Conclusions:
- Adrenal insufficiency is not a common early complication but may occur late in severely ill HIV-1-infected patients.
- The findings do not support the hypothesis that cortisol-induced cytokine shifts mediate HIV-1 disease progression.
Abstract:
Serum cortisol and adrenocorticotropic hormone (ACTH) values and CD4 cell count were evaluated in 25 perinatally HIV-1-infected children. The children were divided into three groups: group 1 included eight asymptomatic or paucisymptomatic children, group 2 nine moderately symptomatic children, and group 3 eight children with severe clinical manifestations. Group 1 children were without antiretroviral therapy; the remaining children received zidovudine (AZT) treatment. Only one group 3 patient had primary adrenal insufficiency. No significant differences in cortisol and ACTH secretion were found either between all HIV-1-infected and 126 age- and sex-matched normal children or among the three groups of patients. Mean CD4 cell count of each group declined in parallel to disease progression. No correlations were found between cortisol or ACTH values and CD4 cell count. Adrenal failure may be a late complication of HIV-1 infection and should be searched for in severely ill patients. Our data argue against the hypothesis of a cortisol-induced shift from T-helper-1 (Th1) to Th2 cytokine production profile as the pathogenetic mechanism of progression to AIDS.
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