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  • Author: Gian Michele Molinatti x
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Alberto Biglino, Paolo Limone, Brunella Forno, Annamaria Pollono, Giuseppe Cariti, Gian Michele Molinatti and Paolo Gioannini

Biglino A, Limone P, Forno B, Pollono A, Cariti G, Molinatti GM, Gioannini P. Altered adrenocorticotropin and cortisol response to corticotropin-releasing hormone in HIV-I infection. Eur J Endocrinol 1995;133:173-9. ISSN 0804-4643

Alterations of the hypothalamic-pituitary-adrenal (HPA) axis are common in HIV infection. To characterize further the site of these derangements and their possible causes, eight male drug addicts with symptomatic HIV infection (stage IV C2) underwent the following investigations: repeated baseline determinations of cortisol, adrenocorticotropin (ACTH), interleukin 1β (IL-1β), IL-6 and interferon alpha (IFN-α): and ovine corticotropin-releasing hormone (CRH) test (100 μg IV) for ACTH and cortisol determinations. Baseline cortisol levels were either normal or elevated in all patients. A significant positive linear correlation was found between baseline levels of cortisol and both IL-6 (r=0.955; p<0.001) and IL-1β (r=0.863; p<0.005), but not between cortisol and ACTH or between ACTH and circulating cytokines. Both ACTH and cortisol responses to CRH were nearly absent in six out of eight patients, and delayed in the others. The areas under the curves of both ACTH and cortisol after CRH were significantly lower in HIV patients than in a group of eight healthy control subjects (p=0.0157 for ACTH and p=0.046 for cortisol). Our data suggest the possibility of an inappropriate stimulation of the HPA axis in symptomatic HIV infection by HIV-induced release of cytokines, with a blunted pituitary and adrenal response to CRH.

Paolo Limone, Institute of Internal Medicine, University of Torino, AM Dogliotti 14, 10126 Torino, Italy

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Paolo Limone, Valerio D'Alessandro, Innocenzo Rainero, Caterina Ambrogio, Lorenzo Pinessi, Tiziana De Gennaro and Gian Michele Molinatti

In several animal species the catecholamines stimulate the release of α-MSH from the melanotrope cells of the pituitary neurointermediate lobe through β-receptors. The human hypophysis does not include a well-defined intermediate lobe and the methods for measuring α-MSH are often poorly sensitive. Neuroregulation of this hormone in man has thus received little attention. To see whether the adrenergic system is involved in the control of α-MSH secretion and whether the latter is independent of that of other peptides derived from proopiomelanocortin, such as ACTH, we studied the effects on plasma α-MSH-like immunoreactivity (α-MSH-LI). ACTH, and cortisol of some adrenergic drugs active on the β-receptors. Six normal volunteers underwent the infusion of the following drugs: isoproterenol (0.03 μg·kg−1·min−1 for 60 min), propranolol (1 mg·min−1 for 5 min followed by 0.1 mg·min−1 for 115 min), propranolol + isoproterenol (infused between 30 and 90 min of propranolol infusion), placebo (saline solution). Isoproterenol increased α-MSH-LI at 1 5 min (p<0.001). Propranolol induced a fall of α-MSH-LI between 30 and 60 min (p<0.001), followed by a return to preinfusion concentrations beginning at 75 min, and completely prevented the stimulatory effect of isoproterenol. Plasma ACTH and serum cortisol were always unaffected. These results indicate that in man the adrenergic system stimulates α-MSH-LI release through β-receptors, and that α-MSH-LI secretion is dissociated from that of ACTH and cortisol. This in turn suggests that separate neuroregulatory mechanisms exist for the melanotrope and corticotrope cells.