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Enrico Mazza, Stefania Goffi, Paolo Barchi, Emanuela Arvat, Jaele Bellone, Paolo Limone, Ezio Ghigo and Franco Camanni

Mazza E, Goffi S, Barchi P, Arvat E, Bellone J, Limone P, Ghigo E, Camanni F. Enhanced adrenocorticotrophic hormone and cortisol responses to corticotrophin-releasing hormone in central idiopathic diabetes insipidus. Eur J Endocrinol 1994;130:121–4. ISSN 0804–4643

It is well known that arginine vasopressin (AVP) exerts a stimulatory effect on adrenocorticotrophic hormone (ACTH) secretion. Moreover, there is consistent evidence that the hypothalamic AVP-secreting neurons are involved in the neuroregulation of ACTH secretion. With the aim to throw further light on the interaction between AVP and corticotrophin-releasing hormone (CRH) in the neuroregulation of ACTH secretion, in this study we compared the ACTH and cortisol responses to human CRH (100 μg iv as a bolus) in 18 normal subjects (15 females and three males, age 22–35 years) and seven patients with central isolated diabetes insipidus (six females and one male, age 16–40 years). Two patients were newly diagnosed and five had discontinued substitution therapy with desamino-D-AVP 24 h before testing. All had free access to water before and during the test period. The ACTH and cortisol responses to CRH were higher in subjects with diabetes insipidus than in controls, either when evaluated as peak values (ACTH, mean±sem: 17.0±1.2 vs 7.7±0.7 pmol/l, p=0.0003; cortisol: 611.3±59.4 vs 450.7±21.2 nmol/l, p=0.01) or area under curve values (ACTH: 672.5±75.7 vs 364.0±33.6 pmol·1−1·h−1. p=0.002; cortisol: 29158.0±2937.0 vs 23236.7±1052.1 nmol·l−1 · h−1, p=0.03). These results show that patients with diabetes insipidus have an exaggerated pituitary-adrenal response to CRH. This may be due to the fact that in diabetes insipidus AVP secretion from parvocellular neurons of the paraventricular nucleus in the hypophysial portal system is not impaired. Alternatively, AVP secretion may be defective in both magnocellular and parvocellular hypothalamic AVP-secreting neurons. In this case, it could be hypothesized that adjustment is made to the feedback regulatory mechanisms of the hypothalamic–pituitary–adrenal axis, so that the CRH–ACTH axis assumes a main role with respect to the AVP–ACTH axis.

Franco Camanni, Divisione di Endocrinologia, Ospedale Molinette, corso Dogliotti 14, 10126 Torino. Italy

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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.

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Maurilio Deandrea, Francesca Garino, Mormile Alberto, Roberto Garberoglio, Ruth Rossetto, Nadia Bonelli, Stefano Spiezia, Massimo De Santis, Salvatore Monti, Maria Grazia Deiana, Toscano Vincenzo, Christian Cugini, Ghassan El Dalati and Paolo Piero Limone


The purpose of this study was to confirm the generalisation of radiofrequency ablation (RFA) in the treatment of benign thyroid nodules (BTN) and to look for a correlation between final shrinkage and some ultrasound (US) findings in a large Italian population data set.


This prospective study included 337 patients with solid cold BTN from six Italian institutions. Nodule volume, US pattern, thyroid function, symptom/cosmetic scores and complications were evaluated before treatment and at 6 and 12 months. The primary outcome was to find a correlation between basal volume and US pattern of the nodules and final shrinkage. The secondary outcome was to confirm the efficacy and safety of RFA in a large data set.


The median basal volume was 20.7 mL, and this significantly decreased after RFA at 6 months (7.3 mL (−63.5%), P < 0.001) and at 12 months (6 mL (−70%), P vs 6 months = 0.009). A significant correlation was found for US structure (a spongiform pattern showing a 76% reduction vs 67 and 66% of mix and solid patterns respectively, P < 0.01) as well as for vascularity (intense peripheral and intranodal patterns showing 71 vs 68 and 67% of weak peripheral and intranodal and peripheral patterns respectively, P < 0.03), but not for macrocalcifications. A slight inverse correlation was found between nodule basal volume and shrinkage (Spearman: −0.23). Mean symptoms/cosmetic scores were significantly reduced. No major complications were encountered.


This multicentre study validated the efficacy and safety of RFA for treating BTN and showed a clear correlation between final shrinkage and some common US findings.

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Marco Bonomi, Valeria Vezzoli, Csilla Krausz, Fabiana Guizzardi, Silvia Vezzani, Manuela Simoni, Ivan Bassi, Paolo Duminuco, Natascia Di Iorgi, Claudia Giavoli, Alessandro Pizzocaro, Gianni Russo, Mirella Moro, Letizia Fatti, Alberto Ferlin, Laura Mazzanti, Maria Chiara Zatelli, Salvo Cannavò, Andrea M Isidori, Angela Ida Pincelli, Flavia Prodam, Antonio Mancini, Paolo Limone, Maria Laura Tanda, Rossella Gaudino, Mariacarolina Salerno, Pregnolato Francesca, Mohamad Maghnie, Mario Maggi, Luca Persani and Italian Network on Central Hypogonadism


Isolated hypogonadotropic hypogonadism (IHH) is a rare disorder with pubertal delay, normal (normoosmic-IHH, nIHH) or defective sense of smell (Kallmann syndrome, KS). Other reproductive and non-reproductive anomalies might be present although information on their frequency are scanty, particularly according to the age of presentation.


Observational cohort study carried out between January 2008 and June 2016 within a national network of academic or general hospitals.


We performed a detailed phenotyping of 503 IHH patients with: (1) manifestations of hypogonadism with low sex steroid hormone and low/normal gonadotropins; (2) absence of expansive hypothalamic/pituitary lesions or multiple pituitary hormone defects. Cohort was divided on IHH onset (PPO, pre-pubertal onset or AO, adult onset) and olfactory function: PPO-nIHH (n = 275), KS (n = 184), AO-nIHH (n = 36) and AO-doIHH (AO-IHH with defective olfaction, n = 8).


90% of patients were classified as PPO and 10% as AO. Typical midline and olfactory defects, bimanual synkinesis and familiarity for pubertal delay were also found among the AO-IHH. Mean age at diagnosis was significantly earlier and more frequently associated with congenital hypogonadism stigmata in patients with Kallmann’s syndrome (KS). Synkinesis, renal and male genital tract anomalies were enriched in KS. Overweight/obesity are significantly associated with AO-IHH rather than PPO-IHH.


Patients with KS are more prone to develop a severe and complex phenotype than nIHH. The presence of typical extra-gonadal defects and familiarity for PPO-IHH among the AO-IHH patients indicates a common predisposition with variable clinical expression. Overall, these findings improve the understanding of IHH and may have a positive impact on the management of patients and their families.