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Biomedical subjects

R Volpi

Publications and source records attributed to R Volpi.

At least 19 recordsLinked to original sources
PubMed2005

Extraprostatic complications of testosterone replacement therapy.

Testosterone therapy has been reported to be useful in the treatment of hypogonadism and partial androgen deficiency of the aging male (PADAM) syndrome. Testosterone administration is needed in order to maintain secondary sexual characteristics, muscle mass, bone mineral density, cognitive function and sexual drive. Newer testosterone-containing compounds, particularly gel preparations, are known to produce more stable circulating testosterone levels than im-administered drugs, with scarce side-effects and good patient compliance. All patients treated with testosterone must undergo a careful follow-up to prevent the development of the major side effects, such as sleep-apnea, erythrocytosis, cardiovascular diseases and the alterations of hepatic function and plasma lipid concentrations.

Acne Vulgaris↗
PubMed2004

Difference between diabetic and nondiabetic smokers in the pituitary response to physical exercise.

The growth hormone (GH), cortisol, and arginine vasopressin (AVP) responses to bicycle ergometry (with increasing workload until exhaustion) were measured in 20 patients affected by insulin-dependent diabetes mellitus (IDDM) (10 habitual smokers and 10 nonsmokers) and 20 nondiabetic subjects (normal controls) (10 habitual smokers and 10 nonsmokers). Cardiorespiratory parameters such as heart rate, blood pressure, ventilation, frequency of breathing, tidal volume, oxygen consumption (Vo(2)), carbondioxide production (Vco(2)), and respiratory exchange ratio (R) were monitored before and during exercise tests. No significant differences between groups were observed; furthermore, there were no differences in circulating somatomedin-C (SM-C) and free fatty acids (FFA) levels between groups. Blood glucose levels were similar before exercise and followed a similar pattern during tests in diabetic smokers and nonsmokers. Basal GH, cortisol, and AVP levels were similar in diabetic smokers, diabetic nonsmokers, normal smokers, and normal nonsmokers. In all groups, exercise induced a significant increase in the serum concentrations of all examined hormones. Increments were significantly higher in diabetic than in nondiabetic groups. No significant differences were observed between diabetic smokers and nonsmokers for all examined hormones. AVP responses during tests were similar in normal smokers and nonsmokers. In contrast, exercise-induced GH and cortisol increments were significantly lower in normal smokers than in normal nonsmokers. These data support the hypothesis that in normal subjects habitual nicotine consumption may attenuate both GH and cortisol responses to a releasing stimulation, such as physical exercise. This phenomenon may represent an expression of adaptation of nicotinic neurotransmission to chronic stimulation. Furthermore, the data show that the effect induced by habitual smoking is absent in diabetics, probably because of diabetes-induced neuroendocrine alterations in the central nervous system.

Arginine Vasopressin↗
PubMed2004

[Knee arthrodesis using a customized intramedullary nail: 14 cases].

We report our experience with knee arthrodesis using a customized intramedullary nail implanted in 14 patients. Indications for knee arthrodesis were: recurrent prosthesis infection (n=11), post-traumatic septic arthritis (n=1), aseptic loosening of a hinge prosthesis (n=1), and nonunion (n=1). A two-stage procedure was used for the 12 patients with infected joints. Mean follow-up was 19 months. Weight bearing began during the first week after arthrodesis in 13 patients. First intention bone healing was achieved in 13 patients. Mean time to healing was three months. All patients rapidly recovered full independence. Complications were: one misinsertion of the tibial stem, one nonunion which fused after repeated grafting, and two recurrent infections (controlled chronic fistulae) which required skin flaps for cover. We have found that this customized nail is a useful method for achieving bone fusion in patients with difficult indications for arthrodesis, particularly recurrent prosthesis infection.

Aged↗
PubMed2003

Serum total prostate-specific antigen assay in women with Cushing's disease or alcohol-dependent pseudo-Cushing's State.

BACKGROUND: The distinction between Cushing's disease (Cushing's syndrome dependent on adrenocorticotropic hormone (ACTH)-secreting tumors of pituitary origin) and pseudo-Cushing's states (Cushingoid features and hypercortisolism sometimes present in alcoholic, depressed or obese subjects) can present a diagnostic challenge in clinical endocrinology. Recently, the availability of a highly sensitive immunofluorometric assay for the measurement of total prostate-specific antigen (PSA) provided the possibility to measure serum PSA levels in women. Interestingly, PSA gene expression and protein production has been found to be upregulated by steroid hormones, such as androgens, glucocorticoids, mineral corticoids and progestins. In fact, serum total PSA concentrations appear to be higher in female patients with Cushing's disease than in normal women. We wondered whether a similar phenomenon also occurs in pseudo-Cushing's state. METHODS: In order to answer this question, we compared the serum total PSA levels measured in 10 female subjects with alcohol-dependent pseudo-Cushing's state with those observed in 8 female patients with Cushing's disease and in 15 age-matched healthy women. Serum testosterone, ACTH and cortisol, and 24-hour urinary cortisol levels were measured; cortisol suppression after dexamethasone was also tested in all subjects. RESULTS: The basal serum levels of ACTH and cortisol were significantly lower in normal subjects than in patients with Cushing's disease or pseudo-Cushing's state; these latter groups showed similar basal hormonal values. Dexamethasone administration was unable to suppress serum cortisol levels in 5 subjects with Cushing's disease and 6 subjects with pseudo-Cushing's state. Serum testosterone values in the group with Cushing's disease were higher than in the other groups. No differences were observed between pseudo-Cushing's and normal subjects. Serum total PSA levels were significantly higher in women with Cushing's disease than in subjects with pseudo-Cushing's state and normal controls; these latter groups showed similar PSA values. When serum total PSA and testosterone levels were considered together, a significant positive correlation was observed in the group with Cushing's disease, but not in the other groups. CONCLUSIONS: These data indicate that the steroid milieu responsible for the elevation in serum PSA in women with Cushing's disease is not present in subjects with alcohol-dependent pseudo-Cushing's state, suggesting the possible use of PSA as a marker of differentiation between these pathological conditions in women.

Adult↗
PubMed2003

Effect of oxytocin on nitric oxide activity controlling gonadotropin secretion in humans.

BACKGROUND: Previously described inhibitory effects of the nitric oxide synthase (NOS) inhibitor L-NAME on luteinizing hormone-releasing hormone (LH-RH)-induced LH and follicle stimulating hormone (FSH) secretion in humans suggested modulation by nitric oxide (NO) of the gonadotropin-releasing action of LH-RH. DESIGN: In order to establish whether oxytocin (OT) participates in this regulatory mechanism, 10 normal men were treated with LH-RH (100 micro g as an i.v. bolus) given alone or in the presence of L-NAME (40 micro g kg-1 injected plus 50 micro g kg-1 infused i.v. for 60 min), OT (2 IU injected plus 4 IU infused i.v. for 60 min) or a combination of both drugs. RESULTS: The administration of OT was unable to change the gonadotropin responses to LH-RH. In contrast, L-NAME significantly reduced both FSH and LH increments induced by LH-RH. When L-NAME was given in the presence of OT, the LH and FSH responses to LH-RH were similar to those observed after the administration of LH-RH alone. CONCLUSION: These data suggest antagonistic actions of OT and L-NAME in the control of NOS activity in regulation of gonadotropin secretion induced by LH-RH.

Adult↗
PubMed2001

Effect of dexamethasone on TSH secretion induced by TRH in human obesity.

BACKGROUND: The presence of an abnormally high thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH) makes it difficult to distinguish some euthyroid obese subjects from subelinically hypothyroid obese patients. Here, we examine whether such distinction may be achieved after treatment with glucocorticoids, which inhibit TSH secretion at the hypothalamic-pituitary level. METHODS: TRH tests (200 microg as an intravenous bolus injection) were performed in 30 age- and weight-matched, obese, but otherwise healthy, men. All subjects were tested again with TRH after treatment with dexamethasone (dex) (2 mg/d in four divided doses orally for 3 days). RESULTS: In all subjects, total thyroxine and triiodothyronine concentrations were in the normal range. According to basal and TRH-stimulated serum thyrotropin (TSH) levels, subjects were divided into the following three groups: group I (n=10), euthyroid subjects; group II (n=10), euthyroid subjects with normal basal but abnormally elevated TSH responses to TRH; group III (n=10), subjects with elevated basal and TRH-induced TSH levels (subclinical hypothyroidism). Basal TSH levels were 1.8+/-0.4 mU/L in group I, 1.7+/-0.3 in group II, and 6.0+/-0.7 in group III. In both groups II and III, TRH-induced TSH increments were above the normal range (maximal increment> 15 mU/L) and were significantly higher than in group I. After the second treatment with TRH, pretreatment with dex significantly decreased both basal TSH levels and peak TSH responses to TRH in all groups. However, a striking percentage decrease (>50%) in TRH-induced peak TSH responses was observed in euthyroid obese subjects of groups I and II, whereas hypothyroid subjects of group III showed only a slight decrement (<25%). CONCLUSIONS: The sensitivity of the TSH secretory system to glucocorticoid inhibitory action is preserved in obese subjects with abnormally elevated TSH response to TRH, but not in subclinically hypothyroid obese patients. The TRH plus dex test might be useful in future studies to understand the mechanisms underlying alterations in TSH secretion in obesity.

Dexamethasone↗
PubMed2000

Muscarinic cholinergic mediation of the GH response to gamma-hydroxybutyric acid: neuroendocrine evidence in normal and parkinsonian subjects.

We have recently reported that parkinsonian patients show a significant GH response to gamma-hydroxybutyric acid (GHB), but not to gamma-aminobutyric acid (GABA)-ergic drug administration. In order to establish whether muscarinic cholinergic receptors mediate the GH secretion induced by GHB, normal men and parkinsonian patients were tested with GHB both in the absence and in the presence of the anticholinergic agent, pirenzepine. Both normal controls and parkinsonian patients showed a significant serum GH rise in response to GHB (25 mg/kg body weight p.o.) even though a slightly, but significantly lower response was observed in parkinsonian patients. Pretreatment with pirenzepine (100 mg p.o. 2 h before GHB) completely suppressed the GHB-induced GH release in both normal controls and parkinsonian patients. These data indicate that a cholinergic mechanism mediates the GH response to GHB in normal men. In addition the data indicate that this pathway is preserved in the parkinsonian brain.

Aged↗
PubMed2000

Desmopressin and hexarelin tests in alcohol-induced pseudo-Cushing's syndrome.

BACKGROUND: A challenge in clinical endocrinology is the distinction between Cushing's disease (Cushing's syndrome dependent by adrenocorticotrophic hormone (ACTH)-secreting tumours of pituitary origin) and alcohol-dependent pseudo-Cushing's syndrome. Patients with Cushing's disease are known to have high ACTH/cortisol responses to desmopressin (DDAVP, a vasopressin analogue) and to hexarelin (HEX, a synthetic GH-releasing peptide). OBJECTIVE: To compare the ACTH/cortisol responses to desmopressin and to hexarelin of subjects with alcohol pseudo-Cushing's syndrome with those obtained in patients with Cushing's disease and in normal controls. DESIGN: Randomized, single-blind study. SETTING: University medical centre. SUBJECTS: Eight alcoholics with pseudo-Cushing's syndrome, six patients with Cushing's disease and nine age-matched normal controls. INTERVENTION: Three tests at weekly intervals. The dexamethasone (1 mg) suppression test (DST) was carried out first. The desmopressin (10 microg intravenously at 09:00 h) test and hexarelin (2 microgram kg-1 intravenously at 09:00 h) test were carried out in random order. MEASUREMENTS: Plasma ACTH and cortisol levels. RESULTS: The basal plasma levels of ACTH and cortisol were significantly lower in normal subjects than in patients with Cushing's disease and in alcoholic subjects; these latter groups showed similar basal hormonal values. All normal controls, two patients with Cushing's disease and two alcoholics showed suppression of plasma cortisol levels (<5 microgram dL-1) after dexamethasone administration. Both desmopressin and hexarelin induced striking ACTH/cortisol responses in patients with Cushing's disease, whereas hexarelin, but not desmopressin, slightly increased ACTH/cortisol secretion in the normal controls. Neither desmopressin nor hexarelin administration induced any significant change in ACTH/cortisol secretion in alcoholics. CONCLUSIONS: These data suggest that either the hexarelin or desmopressin test can be used to differentiate patients with Cushing's disease from subjects with alcohol-dependent pseudo-Cushing's syndrome.

Adrenocorticotropic Hormone↗
PubMed2000

Effect of systemic oxytocin administration on dexamethasone-induced leptin secretion in normal and obese men.

To establish whether the regulatory mechanism of leptin secretion is sensitive to oxytocin (OT), seven healthy nonobese men were tested with dexamethasone (dex; 4 mg, iv, at 0730 h) in feeding (2000 Cal given at 3 meals over 7 h) conditions either in the absence (iv normal saline infusion) or in the presence of a constant iv infusion of OT (1, 2, or 4 mIU/min from 0730 h for 10 h). In six additional subjects under similar experimental conditions, normal saline or OT (1, 2, or 4 mIU/min from 0730 h for 10 h) were infused iv without the previous treatment with dexamethasone. Serum leptin concentrations were measured in samples taken at 60-min intervals during infusion. Leptin levels remained constant during the infusion of normal saline or OT (1, 2, or 4 mIU/min) alone. In contrast, serum leptin concentrations rose significantly from the baseline after dex administration. The leptin response to dex was not modified by the concomitant infusion of 1 mIU/min OT, whereas it was completely abolished by the administration of 2 or 4 mIU/min OT. These findings led us to evaluate the secretory pattern of leptin in 12 obese patients in similar experimental conditions. In all patients basal leptin levels were significantly higher than those in normal weight subjects. In 6 obese subjects, the infusion of OT alone (1, 2, or 4 mIU/min) was unable to change serum leptin levels. In the remaining 6 obese subjects, dex administration significantly increased serum leptin levels; however, the leptin response to dex was not modified by the concomitant infusion of 1, 2, or 4 mIU/min OT. These data show inhibition by elevated circulating OT levels of glucocorticoid-induced, but not basal, leptin secretion in normal weight subjects, suggesting a possible role for OT in the regulatory control of leptin. Furthermore, the results obtained in obese subjects indicate that this regulation is disrupted in obesity.

Adult↗
PubMed2000

Dopaminergic and cholinergic involvement in the inhibitory effect of dexamethasone on the TSH response to TRH.

BACKGROUND: Glucocorticoid administration is associated with reduced basal thyroid-stimulating hormone (TSH) levels and a blunted TSH response to thyrotropin-releasing hormone (TRH), despite thyroid hormone levels within the normal range. In light of the inhibitory effect of somatostatin and dopamine on TSH secretion, we examined whether this condition is caused by glucocorticoids through an increased hypothalamic somatostatinergic and/or dopaminergic inhibitory control of TSH. We measured the TSH response to TRH and serum-free T4 and T3 levels. The study group comprised 18 normal men (age 24-35) within 10% of the ideal body weight, randomly divided into 3 groups of six. METHODS: We used the antidopaminergic agent metoclopramide (MCP) and the acetylcholinesterase inhibitor pyridostigmine, which enhances acetylcholine and thus inhibits hypothalamic somatostatin release. Subjects from group 1 were tested with TRH (20 micrograms in an intravenous bolus) after placebo, dexamethasone (dex) (2 mg/day in 4 divided doses for 3 days before the experimental day), or dex plus pyridostigmine (120 mg p.o.). Subjects from group 2 were tested with TRH after placebo, dex, or dex plus MCP (2.5 mg in an i.v. bolus injection). Subjects from group 3 were tested with TRH after placebo, dex, or dex plus pyridostigmine plus MCP. RESULTS: In all subjects from groups 1, 2, and 3, TRH-induced TSH rise was significantly lower after dex than after placebo treatment. Neither pyridostigmine nor MCP, given alone, changed the TSH response to TRH after dex treatment. In contrast, the concomitant administration of MCP and pyridostigmine significantly enhanced the TRH-induced TSH rise in dex-treated subjects and made the TSH response to TRH similar to that observed in the TRH plus placebo test. CONCLUSIONS: These data indicate that enhanced-hypothalamic somatostatinergic and dopaminergic inhibitory activities are involved in the mechanism underlying the reduced TSH response to TRH induced by glucocorticoid treatment.

Adult↗
PubMed2000

Effect of aging on the arginine-vasopressin response to physostigmine and angiotensin II in normal men.

The effect of age on the stimulatory control exerted by cholinergic- and angiotensin II (ANG II)-mediated neurotransmission on arginine vasopressin (AVP) secretion was evaluated by measuring and comparing the AVP responses to the administration of either the cholinesterase inhibitor physostigmine (13.5 micrograms/kg in 50 mL normal saline infused in 10 minutes) or ANG II (increasing doses of 4, 8, and 16 micrograms/kg/min, each dose for 20 min) in 8 younger (23-37 years), 8 middle age (42-60 years), and 8 older (63-79 years) healthy male subjects. Both drugs induced significant increments in plasma AVP levels in the youngest group, with mean peak levels 4.8 times higher than baseline at 20 minutes after the beginning of physostigmine infusion and 1.5 times higher than baseline at 60 minutes after the beginning of ANG II infusion. Similar responses were observed in the middle age group. Basal AVP levels in older subjects were similar to those observed in the other groups. However, the AVP increases induced by physostigmine (mean peak was 9 times higher than baseline) and ANG II (mean peak was 2.2 times higher than baseline) were significantly higher in the oldest group than in the other groups. These data suggest age-related enhancement of the stimulatory regulation exerted by cholinergic- and ANG II-mediated neurotransmission on AVP secretion.

Adult↗
PubMed1999

Enhancement of the GH responsiveness to GH releasing stimuli by lysine vasopressin in type 1 diabetic subjects.

OBJECTIVE: We tested the possibility that lysine vasopressin (LVP) changes the GH responsiveness to exogenously administered GH-RH (at its minimal and maximal doses), clonidine (which is thought to stimulate endogenous GH-RH release) and arginine (which is thought to inhibit somatostatin) in patients with type 1 diabetes mellitus and normal subjects. DESIGN AND PATIENTS: Normal male subjects (NC) and age- and weight-matched insulin-dependent diabetic men (DM) with good metabolic control were studied. An iv bolus of LVP at a dose (15 microg/kg body weight (BW)) lower than the minimal GH releasing effective dose was injected just before the I.V. injection of the minimal effective dose of GH-RH (0.035 microg/kg BW) in 10 NC and 10 DM, the I.V. injection of the maximal effective dose of GH-RH (100 microg) in 7 NC and 7 DM, the I.V. infusion of arginine (30 g over 30 min) in 7 NC and 8 DM or the oral administration of clonidine (150 microg) in 7 NC and 8 DM. On different occasions, GH stimuli, LVP or normal saline were given alone to the same normal and diabetic subjects. MEASUREMENTS: GH responses in the presence and absence of LVP were measured and compared within each group and between normal and diabetic groups. RESULTS: LVP or normal saline administration did not modify the basal concentrations of GH in any subject. The administration of GH-RH (at the minimal dose), arginine or clonidine alone induced significantly higher GH responses in the diabetic subjects than in the normal controls. At the maximal dose GH-RH induced similar GH responses in normal and diabetic subjects. The simultaneous administration of LVP did not change the GH response to any challenging stimulation in the normal controls; in contrast, GH-RH- (at both minimal and maximal dose), arginine- and clonidine-induced GH increments were significantly enhanced by LVP in the diabetic subjects. CONCLUSIONS: These data show that in diabetic, but not in normal subjects LVP enhances the GH responsiveness to secretagogues, such as GH-RH, clonidine and arginine, which act through three different mechanisms. These findings suggest that in diabetes mellitus, vasopressin functions as a primer for various GH responses.

Adult↗
PubMed1999

Effects of pyridostigmine and naloxone on the abnormal TSH response to TRH during starvation in humans.

BACKGROUND: Starvation is associated with a blunted TSH response to thyrotropin-releasing hormone (TRH) (peak minus baseline < 5 mIU/L), despite basal TSH and thyroid hormone levels within the normal range. In light of the inhibitory effect of somatostatin on TSH secretion, we examined whether this condition is caused by an increased hypothalamic somatostatinergic tone in starving subjects. The possible involvement of endogenous opioids in the mechanism underlying the abnormal TSH response to TRH was also evaluated. METHODS: The TSH response to TRH (25 micrograms in an intravenous bolus), serum total and free T4 and T3 levels, and 24-hour urinary-free cortisol levels were measured in 28 normal men (age 27-35 years) within 10% of their ideal body weight. They were randomly divided into 4 groups of 7. In 21 subjects (groups 1, 2, and 3), TRH tests were performed after an overnight (8 hours) fast, placebo administrations (control test), and after prolonged (56 hours) starvation. TRH tests after prolonged starvation were performed either after placebos (in all subjects) or the administration of pyridostigmine (180 mg orally) (in 7 subjects, group 1); naloxone (0.8 mg in an i.v. bolus injection) (in 7 subjects, group 2); or the combination of pyridostigmine and naloxone (in 7 subjects, group 3). The remaining 7 subjects (group 4) were tested at weekly intervals with TRH plus placebo, TRH plus naloxone, TRH plus pyridostigmine, and TRH plus naloxone plus pyridostigmine after a fasting period of 8 hours. RESULTS: In all subjects of groups 1, 2, and 3, TRH-induced TSH rise was significantly lower after prolonged starvation than after overnight fast. Neither pyridostigmine nor naloxone, given alone, changed the basal levels of TSH and the TSH response to TRH after prolonged starvation. In contrast, the concomitant administration of naloxone and pyridostigmine significantly enhanced the TRH-induced TSH rise. After overnight fasting, naloxone administration in group 4 subjects did not change the TSH response to TRH, whereas pyridostigmine significantly enhanced the TSH response to TRH. When naloxone was given together with pyridostigmine and TRH the TSH response was similar to that observed in the TRH plus pyridostigmine test. CONCLUSIONS: These data indicate that naloxone-sensitive endogenous opioids exert an inhibitory effect on the cholinergic stimulatory control of TSH secretion during prolonged starvation. This suggests that an enhanced hypothalamic somatostatinergic activity is involved in the mechanism underlying the reduced TSH response to TRH.

Adult↗
PubMed1998

Stimulation of ACTH and GH release by angiotensin II in normal men is mediated by the AT1 receptor subtype.

This study was performed in order to determine whether the stimulatory effect of plasma angiotensin II (ANG II) on Adrenocorticotropic hormone (ACTH) and growth hormone (GH) secretion in humans is mediated by AT1 subtype receptors. For this purpose, the effects of the administration of the AT1 receptor antagonist, losartan (50 mg p.o.) or a placebo on the ACTH and GH responses to ANG II (i.v. infusion for 60 min of successively increasing doses (4, 8 and 16 ng/kg/min); each dose for 20 min) were evaluated in eight normal men. ANG II infusion induced significant increases in both serum ACTH and GH levels (mean peaks were 1.6- and four-times higher than baseline, respectively). The ACTH response to ANG II was completely abolished by pretreatment with losartan. Also, the ANG II-induced GH rise was reduced by administration of losartan, but the GH response was still significantly higher than the basal value (mean peak was twice as high as the baseline). These data provide evidence of AT1 receptor involvement in mediation of the ANG-II stimulating effect on ACTH and GH secretion.

Adrenocorticotropic Hormone↗