Abstract
Although endocrine abnormalities have been reported in HIV-1 infection, the role of risk factors is not understood. Injecting drug use (IDU) is an important risk factor for contracting HIV-infection and studies suggest that substance use may also be associated with endocrine dysfunction. In order to investigate hypothalamic pituitary adrenal (HPA) axis activity in this population, this study investigated cortisol response to the cold pressor challenge in IDUs with and without HIV infection. After controlling for the effects of gender, duration of marijuana use and time since the last use of heroin, the findings show that the pattern of cortisol response depended upon HIV serostatus. Cortisol levels peaked later in HIV+ IDUs and recovered at a slower rate than HIV negative IDUs. These findings support our hypothesis that dysregulation in HPA axis activity occurs in HIV infected IDUs.
Highlights
A number of endocrine and metabolic abnormalities have been described among individuals infected with HIV-1 and these abnormalities may contribute to increased morbidity and mortality[1,2,3,4]
It has been proposed that HIV-1 infection may directly or in association with other factors bring about adverse effects on the neuroendocrine systems[5,6] and in particular, on the hypothalamic pituitary adrenal (HPA) axis
Cortisol response, rather than its level alone, reflects HPA activity, which consists of two distinct processes: (I) response of the hippocampushypothalamus-pituitary-adrenal axis to stressors resulting in increased secretion of cortisol and (2) the negative feedback inhibition of HPA activity by cortisol resulting in inhibition of continued secretion of cortisol
Summary
A number of endocrine and metabolic abnormalities have been described among individuals infected with HIV-1 and these abnormalities may contribute to increased morbidity and mortality[1,2,3,4]. It has been proposed that HIV-1 infection may directly or in association with other factors bring about adverse effects on the neuroendocrine systems[5,6] and in particular, on the hypothalamic pituitary adrenal (HPA) axis. Findings on the effects of HIV infection on cortisol, the most important regulator of HPA axis activity, have so far been inconsistent and have shown levels of cortisol to be increased[8,9], normal[10] or decreased[11]. Cortisol response, rather than its level alone, reflects HPA activity, which consists of two distinct processes: (I) response of the hippocampushypothalamus-pituitary-adrenal axis to stressors resulting in increased secretion of cortisol and (2) the negative feedback inhibition of HPA activity by cortisol resulting in inhibition of continued secretion of cortisol. Other viral auxiliary proteins, viral protein R, vpr and viral infectivity factor, vif, can interact with the glucocorticoid receptors[16,17]
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