Search PubMed⌕ Search

Biomedical subjects

M Giusti

Publications and source records attributed to M Giusti.

At least 127 records · Page 7Linked to original sources

Alterations of granulopoiesis in chronic uremic patients treated with intermittent hemodialysis.

Granulocyte-macrophage progenitor cells (CFU-GM), leukocyte colony-stimulating activity (CSA), granuloblast differentiation and proliferation and the effect of uremic serum on the in vitro growth of normal CFU-GM have been studied in 8 chronic uremic patients treated with intermittent hemodialysis three times a week. The studies were performed in the postabsorptive state twice in each patient, that is at the longest and shortest dialytic interval. CFU-GM growth in agar and leukocyte CSA did not differ significantly from the normal level in uremic subjects. The granulocytic and macrophagic differentiation in a liquid culture system was significantly reduced in uremic patients, notwithstanding the appearance of high numbers of undifferentiated blastic cells. The serum of uremic patients had no effect on normal CFU-GM and leukocyte CSA.

Adult↗

Growth hormone response to growth hormone-releasing hormone in normal and uraemic children. Comparison with hypoglycaemia following insulin administration.

The uraemic syndrome is characterized by several endocrinological disturbances. This study was undertaken in order to evaluate the GH response to growth hormone-releasing hormone (GRH) in children with chronic renal failure (CRF) and to compare the results with those observed after insulin hypoglycaemia. Twenty-two children with CRF, 10 undergoing continuous ambulatory peritoneal dialysis (CAPD) and 12 on conservative treatment (CT), age ranges 2-15 years, were studied and the data were compared with those from 14 children with normal renal function and normal hormonal behaviour, affected by short stature (NC), and those form 13 healthy adult volunteers (NA). The GRH test (l micrograms/kg body weight, iv) was carried out in 8 CAPD, 8 CT, 9 NC and 10 NA subjects. The blood samples were taken every 30 min for 3 h in CAPD and CT and for 2 h in NC and NA starting at 09.00 h. The following hormones were measured: GH, LH, FSH, Prl, TSH and cortisol (F). The insulin test (0.1 U/kg body weight, iv) was carried out in 5 CAPD, 5 CT, 10 NC and 9 NA on blood samples taken every 30 min for 2 h, measuring GH and glycaemia. No adverse effects were observed after the infusion of GRH. GRH administration induced a prompt response in all subjects, but GH plasma levels were significantly higher in uraemic children than in adults (peak value of 43.5 +/- 8.2, 45.0 +/- 8.4, 27.8 +/- 6.0; 13.5 +/- 2.6 micrograms/ml in CAPD, CT, NC and NA, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Effect of simultaneous administration of GHRH (1-40) and TRH on GH, PRL and TSH secretion in normal man.

The GHRH test represents a new tool in the study of secretion in man. Nine normal fasting males received on separate occasions in random order 1) GHRH 1-40 (1 microgram/Kg bw) iv at time 0; 2) TRH (6 micrograms/min) infusion between -30 and +120 min; 3) GHRH 1-40 (1 microgram/Kg bw) iv at time 0 plus TRH (6 micrograms/min) infusion between -30 and +120 min. Blood samples were drawn for GH, PRL and TSH at -90, -60, -30, 0 min and then every 15 min for 2 h. GHRH significantly increased GH in all subjects. The same GH response was found during GHRH plus TRH test. No effect was found either on PRL and TSH secretion after GHRH administration, or on GH pattern after TRH administration. A significant decrease of TSH, but not of PRL response was observed after GHRH plus TRH administration in comparison to TRH alone. These results underline that the inhibitory effect exerted by TRH on GH secretion during some experimental conditions is not linked to a pituitary interference between GHRH and TRH. The difference in TSH secretion, following GHRH plus TRH in comparison with TRH alone, could be due to a GHRH-induced central inhibitory mechanism, probably GHRH-related.

Adolescent↗

Sex hormone status in women suffering from rheumatoid arthritis.

We studied the sex hormone status of 21 seropositive (IgM-RF) women with rheumatoid arthritis (RA), who were subdivided according to their premenopausal and postmenopausal status. Age matched women with secondary osteoarthritis were used as controls. The hormones evaluated were luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin (PRL), 17-beta-estradiol (E2), progesterone (Pg), testosterone (T), delta 4-androstenedione (A), dehydrotestosterone (DHT), dehydroepiandrosterone sulphate (DHEAS) and cortisol (C). Normal concentrations of all the hormones considered were found in premenopausal women with RA. Statistically higher concentrations of T (p less than 0.05), A (p less than 0.05) and DHEAS (p less than 0.01) were observed in postmenopausal women with RA when compared to controls, whereas no differences were found for all other hormones studied. Although the significance of observed relative hyperandrogenism in postmenopausal women with RA is not clear, our data seem to indicate that sex hormone levels are altered in patients with RA.

Adolescent↗

The effects of growth hormone-releasing factor (GRF) and dopamine on growth hormone (GH) secretion in acromegaly.

GRF (1-40), dopamine (DA), DA plus GRF and placebo were administered to 6 acromegalic patients. The GRF administration induced a highly variable GH release (GH delta % 167.3 +/- 21.4; mean +/- SE). GRF did not provoke any change in PRL serum levels. During simultaneous GRF and DA administration GH release was found to be reduced (GH delta % 80.2 +/- 17.8) compared to that observed for a corresponding period of time after GRF alone (p less than 0.05). Our data underscore that in acromegaly the DA tonus inhibits GH secretion after GRF by acting directly at the pituitary level.

Acromegaly↗

Morphine-induced TSH release in normal and hypothyroid subjects.

The effects of morphine (10 mg i.v.), an opioid agonist, and of naloxone (10 mg i.v.), an opioid antagonist, on serum levels of TSH and PRL were studied in 7 hypothyroid patients and in 5 normal volunteers. Morphine administration induced a prompt, significant increase in serum TSH and PRL in all subjects. The degree of PRL release after morphine was similar in the two groups, while, as regards TSH, the increase was more evident in hypothyroid subjects. Pretreatment with naloxone (4 mg i.v. 5 min before morphine administration) blocked these effects in all subjects. In contrast, naloxone alone was not able to affect significantly TSH and PRL secretion. Moreover, in 5 other euthyroid volunteers, morphine significantly enhanced the response of TSH and PRL to TRH stimulation (200 micrograms i.v.). These data demonstrate that morphine exerts a stimulatory action on TSH and PRL secretion: the possible mode of action of this drug and the physiologic significance of these findings are discussed.

Adult↗

Variations of thyroid hormones during total fasting in obese and in obese diabetic subjects.

Fasting and hypocaloric diets are known to induce a reduction of triiodothyronine (T3) and to increase reverse triiodothyronine (rT3) in normal and obese subjects. The effect of 8-day fasting was evaluated on T3, thyroxine (T4), free T4, rT3, TSH, immunoreactive insulin (IRI), thyroxine binding globulin (TBG) and glycemia in 21 obese subjects (5 males, 16 females) grouped according to the average starting blood glucose concentration in: group I, diabetic obese subjects (9 patients); group II, non diabetic obese subjects (12 patients). All patients had no history of recent weight loss due to dietetic therapy or drugs. Blood samples were drawn in the morning at 0, 2, 4, 6, 8 days after total caloric deprivation and 2 days after refeeding. A superimposable variation of weight and glucose concentration were seen in both groups. In addition, no difference was observed in ketone body excretion, SH, TBG, T4, free T4. In group II a significant decrease of IRI was observed during diet (p less than 0.05); T3 decreased (p less than 0.01) and rT3 increased (p less than 0.01) significantly. No variations in T3 and rT3 values were observed in group I. These results are consistent with a possible role of glucose metabolism in the genesis of the low T3 syndrome.

Adult↗

Effects of GRF(1-40) and domperidone on GH secretion in normal man.

In eight normal adult men pituitary secretion following GRF(1-40) was studied. GRF administration (50 micrograms i.v.) was followed by an increase in GH release with a peak value between the 15 and 60 min. No effects were noticed on LH, FSH, PRL, TSH and ACTH secretion. GH and PRL release was also studied after domperidone (DOM) (5 mg i.v./h), and GRF plus DOM. PRL increased significantly after DOM and GRF plus DOM. During GRF plus DOM a more marked GH release was observed in comparison with the hormone response to GRF alone at 15-45 and 120 min (P less than 0.05). This phenomenon was found in in six out of eight subjects studied. Mean peak and secretory area was greater (P less than 0.05) after GRF plus DOM than after GRF alone. These data suggest that GRF(1-40) at the dose used is a useful tool in the study of GH secretion. The GH pattern during GRF plus DOM seems to indicate that dopaminergic tone may play a direct inhibitory role on GH secretion in man.

Adolescent↗

Nomifensine decreases the thyroid-stimulating-hormone response to thyrotropin-releasing-hormone in normal subjects.

The Thyroid-stimulating-hormone (TSH) secretion has been studied in 12 normal euthyroid subjects (4 males, 8 females) after nomifensine (NOM) administration (200 mg po). NOM is a drug which activates dopaminergic neurotransmission at the Central Nervous System level. Blood samples were drawn every h for 4 h after NOM or placebo, respectively. At the 4th hour thyrotropin-releasing-hormone (TRH) was administered in bolus (200 micrograms iv), in both studies, and additional samples were collected for 90 min. The results show a moderate suppression (NS) of TSH and a clear-cut reduction in the secretory response to TRH after NOM administration (secretory area: TRH after placebo 723 +/- 132, TRH after NOM 400 +/- 83; p less than 0.01). The data appear to confirm that dopaminergic neurotransmission exerts an inhibitory role upon TSH secretion. The mechanism by which NOM induced dopaminergic activation leads to the suppression of TSH release after TRH has not yet been elucidated. An interference in TSH storage and/or in the post receptor mechanisms involved in TRH action might be hypothesized.

Adult↗

The effect of nomifensine on thyroid-stimulating hormone (TSH) in normal and hyperprolactinemic subjects.

Thyroid-stimulating-hormone (TSH) secretion was studied in 28 normal subjects (12 males; 16 females) and in 8 subjects with prolactin (PRL) secreting tumors (1 male; 7 females) after nomifensine (NOM) administration (200 mg orally). NOM is a drug which activates dopaminergic (DA) neurotransmission at the central nervous system level. Blood samples were drawn every hour for 4 h after NOM or placebo administration. On the 4th h thyrotrophin-releasing-hormone (TRH) was administered in bolus (200 micrograms i.v.), to both groups, and additional samples were collected at 10-, 20-, 30-, 60- and 90-min intervals. The results indicate that in normal subjects, but not in prolactinomas, NOM induces a moderate but significant reduction in TDH secretion. Furthermore, the TSH response to TRH was found to be significantly reduced. No variation was discerned, however, in PRL secretion after NOM. The hormone response to TRH remained unaffected. The data confirm that in normal subjects the DA neurotransmission exerts an inhibitory role upon TSH secretion. In subjects affected by prolactinomas, an alteration in central DA availability may be hypothesized.

Adult↗

Participation of endogenous opiates in regulation of the hypothalamic-pituitary-testicular axis in normal men.

To assess the influence of endogenous opioids on human gonadotropin secretion, integrated concentrations of gonadotropins during 24-h naloxone infusion (2.08 mg/h) were examined in a group of six normal men. Naloxone significantly stimulated LH secretion in all subjects, whereas serum FSH levels were similar during both saline and naloxone infusion. Serum testosterone, dihydrotestosterone, and 17 alpha-hydroxyprogesterone levels increased during the infusion of naloxone, but the delta 4-androstenedione concentration was not modified. The frequency and amplitude of LH secretory episodes were clearly increased when an equal amount of the drug was given and LH concentrations were measured every 15 min for 6 h. The results suggest the endogenous opioids inhibit the hypothalamic-pituitary-gonadal axis in normal men.

17-alpha-Hydroxyprogesterone↗

[Effect of the oral administration of ranitidine on pituitary secretion].

The acute oral administration of Ranitidine (200 mg.) does not determine significant variations in the plasma levels of PRL, LH, FSH, HGH, ACTH and Cortisol. This fact seems to exclude a vigorous action of the drug, in therapeutic doses, on the hypothalamo-pituitary axis. Furthermore, it cannot be excluded that the chronic administration of Ranitidine cam determine significant variations in the hormones themselves.

Administration, Oral↗

PTH radioimmunoassay and loading tests in the diagnosis of patients with primary hyperparathyroidism.

PTH radioimmunoassay today represents an unreplaceable tool in the diagnosis of primary hyperparathyroidism. However, the diagnostic importance of its dosage on selective venous samples is still discussed. Herein, we report our experience of 47 patients operated on for primary hyperparathyroidism. The catheterization of neck veins was performed according to Doppman and co-workers. The PTH assay was carried out with COOH- and NH2-specific antisera. (In 5 cases an inhibition test with CaCl2 infusion was practiced during selective catheterization to preoperatively discriminate between adenoma and hyperplasia.) In 8 cases loading tests with EDTA and in 6 cases with CaCl2 were also performed in association with peripheral venous sampling, in an attempt to improve its sensibility. The 47 cases operated upon showed the following results: the peripheral PTH values were significantly raised in 60% of the cases; the selective PTH dosage with COOH-specific antiserum showed a parathyroid hyperfunction in 100% of the surgically confirmed cases, whereas with the NH2-specific antiserum an increased PTH rate was found only in 84%. A right preoperative localization was obtained in 73%. The value of loading tests is more difficult to evaluate and is discussed in detail.

Adult↗