Search PubMed⌕ Search

Biomedical subjects

A Liuzzi

Publications and source records attributed to A Liuzzi.

At least 91 records · Page 5Linked to original sources
PubMed1981

Size reduction of macroprolactinomas by bromocriptine or lisuride treatment.

We have administered to 29 patients with macroprolactinoma the dopamine agonists bromocriptine and lisuride for 1-50 months (mean +/- SE, 12.7 +/- 1.8) in order to assess the effects of these drugs on tumor size. Fourteen patients were treated with bromocriptine (dose range, 7.5-20 mg/day), 12 patients were treated with lisuride (0.6-2 mg/day), and 3 patients were given both drugs. Computed tomography performed before and during treatment showed the occurrence of tumor shrinkage in 18 patients (62%), but in no case was a complete disappearance of the tumor observed. In 5 of these patients, it was even possible to document tumor shrinkage within the first month of treatment with low doses of the dopamine agonists, whereas in other patients, tumors shrank only after prolonged treatment with higher doses. Visual field and acuity improved or normalized in 8 of the 13 patients with visual defects; in some cases, the improvement was reported as early as 2 days after the treatment was started. Plasma PRL levels fell in all patients who showed a reduction in tumor size; in 2 other patients, PRL levels were only poorly suppressed, and tumor size remained unchanged. In the remaining patients, PRL levels were lowered without convincing evidence of tumor shrinkage. In considering the high percentage of patients showing tumor shrinkage under medical treatment, we propose a course with dopamine agonists as the first step in the management of patients with macroprolactinomas regardless of the presence of visual impairments.

Adolescent↗
PubMed1980

Size reduction of a prolactin secreting adenoma during long-term treatment with the dopamine agonist lisuride.

A 38-year-old amenorrhoeic woman suffering from a prolactin (PRL) secreting adenoma, which had suprasellar extension as shown by caroe agonist (lisuride). PRL levels were lowered and after 1 year of treatment CAT showed a marked reduction of the tumour size. After 2 years of treatment menstruation returned and CAT demonstrated a further reduction of the adenomatous tissue. This study supports the suggestion that dopamine agonists possess an anti-proliferative effect on tumoural lactotrophic cells of humans.

Adenoma↗
PubMed1980

Homogeneity in the growth hormone-lowering effect of dopamine and somatostatin in acromegaly.

We have studied the effect of maximally inhibiting doses of dopamine (DA) or somatostatin on GH levels in 39 acromegalic patients. The GH-lowering effects of the two drugs were highly variable in different patients. A significant correlation (r = 0.45; P < 0.01) was found between the percent changes obtained during the infusions of DA (500 microgram/min) and somatostatin (3.33 microgram/min). Pretreatment with L-sulpiride markedly blunted the inhibitory effect of DA but did not affect the response to somatostatin. We conclude that the GH-secreting cells of acromegalic patients contain separate receptors for DA and somatostatin. We hypothesize that the partial or total lack of responsiveness to DA or somatostatin may be due to the loss of receptors for these agents on the GH-secreting neoplastic cells.

Acromegaly↗
PubMed1978

Effect of ergot alkaloids on growth hormone and prolactin secretion in humans.

The effects of ergot alkaloids (mainly bromocriptine) on the secretion of GH and PRL in normal subjects and in pathological conditions (i.e. acromegaly and hyperprolactinemic states) are discussed. In the normal subjects, bromocriptine releases GH whereas in about 50% of acromegalics it causes a marked and long-lasting inhibition of the hormone secretion. PRL release is reduced by the drug both in normal subjects and in hyperprolactinemic states. Physiopathological studies in the humans indicate that, according to the experimental data, bromocriptine inhibits GH release in acromegaly and PRL secretion through a dopaminergic mechanism of action playing at the pituitary level. Data are reported on the effectiveness of bromocriptine in the medical treatment of acromegaly and of hyperprolactinemic states.

Acromegaly↗
PubMed1978

Lisuride hydrogen maleate: evidence for a long lasting dopaminergic activity in humans.

In 12 acromegalics a single oral dose of 0.2 mg lisuride, an ergoline derivative, significantly reduced plasma PRL but not GH concentrations. Three-tenths milligram of the drug significantly reduced plasma levels of the two hormones. Four-tenths milligram of lisuride did not augment this inhibitory effect. Plasma PRL levels were suppressed in all patients, whereas GH levels were reduced by more than 50% of the base-line values in only seven patients who also responded to the administration of 2.5 mg bromocriptine (CB154). In the patients unresponsive to lisuride, CB154 also failed to change GH levels. The suppressive effect of lisuride started at 60 min (at 150 min for CB154) and plasma GH and PRL levels were still markedly suppressed at 300 min. Plasma GH and PRL concentrations were consistently reduced in two acromegalic patients during 2 weeks of chronic treatment with 0.3 mg lisuride four times a day. In six normal subjects, TRH-induced PRL release was significantly inhibited by pretreatment with 0.3 mg of the drug. The similarity in the effects of lisuride and CB154 suggests that the observed effects of lisuride on GH and PRL are attributable to the known dopaminergic activity of the drug. This conclusion is supported by the data showing that pimozide effectively counteracted the inhibitory action of lisuride on GH and PRL release. We suggest that lisuride may be of value in the medical treatment of acromegaly and hyperprolactinemic states.

Acromegaly↗
PubMed1977

Stimulation and maintenance by nerve growth factor of phenylethanolamine-N-methyltransferase in superior cervical ganglia of adult rats.

Treatment of newborn rats with nerve growth factor (NGF) results in a striking increase in phenylethanolamine-N-methyltransferase (PNMT) in the superior cervical ganglia. Between one and three weeks of age there is normally a 10-fold decrease in PNMT activity in ganglia of infant rats. NGF treatment maintains the PNMT in ganglia at levels 10-fold greater than in untreated controls, but the levels of enzyme in the ganglion show the same magnitude of decrease with age. Epinephrine levels are markedly increased in ganglia of NGF-treated rats younger than one week of age, but at older ages the levels of the catecholamine are only slightly greater than the controls. Dexamethasone is less effective than NGF in increasing the levels of PNMT in ganglia of infant rats and, unlike NGF, becomes ineffective by 44 days of age. These results suggest that there may be two types of PNMT-containing cells in ganglia of newborn rats.

Age Factors↗
PubMed1977

Evidence for a dopaminergic activity of methysergide in humans.

The acute administration of 2 mg of methysergide significantly reduced plasma prolactin levels in nine normal subjects and in seven hyperprolactinaemic patients. The prolactin lowering effect of this drug was abolished by sulpiride. Morever methysergide lowered plasma GH levels in four out of nine acromegalic patients, who were also responsive to a dopaminergic drug such as bromocriptine. Although methysergide did not significantly blunt the TRH-induced prolactin release, our data suggest that this drug may affect GH and prolactin release through a dopaminergic mechanism of action. This effect should be taken into account when methysergide is employed as antiserotoninergic drug in neuroendocrinological studies.

Acromegaly↗
PubMed1977

Long-term treatment with 2-Br-alpha-ergocryptine in acromegaly.

Thirty acromegalic subjects underwent chronic CB154 therapy (10-20 mg daily) for periods ranging from 3 months up to 2 years. In 18 out of 21 patients, who exhibited consistent HGH reduction following acute administration of the drug, there was also during chronic treatment, a suppression of the plasma HGH levels exceeding 50% of base line values, e.g. from mean daily values between 14-197 ng/ml (mean +/- SEM = 57.8 +/- 12.4 ng/ml pre-treatment) to 2-19 ng/ml (mean 8.3 +/- 1.2 ng/ml post-treatment). In 12 of the subjects who responsed to chronic CB154 treatment, the mean daily values of HGH were below 10 ng/ml. The suppression of plasma HGH was maintained unaltered throughout the whole course of therapy. In the 9 subjects, in whom no consistent HGH decrease was evidenced with acute CB154 administration, there was accordingly a minor or no suppression of HGH values during the chronic treatment. In 13 subjects, irrespective of the degree of their GH responses, the plasma prolactin levels were constantly inhibited by CB154; instead the drug failed to modify significantly the TRH or insulin-induced GH release. These changes in the hormonal parameters were paralleled by marked clinical amelioration and improvement of some of the metabolic alterations frequently encountered in acromegaly, e.g. reduced carbohydrate tolerance, increased insulin resistance, diminished fall of plasma phosphorus after insulin, decreased urinary excretion of phosphate, hyper-hydroxyprolinuria and hyper-calciuria. Collectively, these data demonstrate that CB154 thrapy is effective in reducing HGH hyper-secretion in many acromegalic patients during long-term treatment.

Acromegaly↗
PubMed1976

Effect of dopamine infusion on plasma levels of growth hormone in normal subjects and in agromegalic patients.

In ten normal subjects and in twenty acromegalic patients plasma levels of growth hormone were studied after administration of L-dopa and a dopamine infusion. In the ten normal subjects L-dopa, but not dopamine, increased plasma levels of GH. In the acromegalic patients both L-dopa and dopamine were followed by an inhibition of GH release. Since dopamine does not cross the blood-brain barrier, these results, although not excluding a site of action at median eminence level, support the thesis that the inhibitory effect of dopaminergic stimulation on GH release in acromegaly possibly involves receptors present on GH-secreting cells.

Acromegaly↗
PubMed1976

Stimulation of growth hormone release by thyrotropin-releasing hormone in the hypophysectomized rat bearing an ectopic pituitary.

Hypophysectomized female rats which received renal grafts of anterior pituitary (AP) or weight-matched intact controls were sampled under urethane anesthesia. Plasma growth hormone (GH) in sequential samples from each rat was measured by radioimmunoassay to determine the effect of exogenous thyrotropin-releasing hormone (TRH) on GH release from ectopic or intact AP. In a first experiment, following a baseline sample, a pre-treatment sample was taken from each rat 30 min after urethane injection, after which TRH (0.3 or 0.6 mug) or isotonic saline was injected iv, and samples were taken at 10 and 30 min post-treatment. Baseline GH levels in hypophysectomized-transplanted rats were in the range of 4.0 to 8.0 ng/ml, and were not modified significantly by urethane. TRH caused a significantly greater increase in growth hormone at 10 min than did saline. Plasma GH tended to be higher at 30 min post-treatment only in the 0.6 mug TRH-treated group. In further experiments the above described protocol was followed except that four doses of TRH were used (0.15, 0.3, 0.6, and 1.2 mug) and post-TRH blood samples were taken at 5 and 10 min. TRH caused a clear-cut increase in plasma GH both at 5 and 10 min, although no dose-effect relationship was present. In intact controls, baseline GH levels were in the range 40.0 to 80.0 ng/ml and were drastically reduced by urethane. In these animals, only the 1.2 mug TRH dose induced a GH rise at 5 and 10 min. In similar experiments, iv administration of vasopressin (100, 200, or 400 mU) induced a rise in plasma GH when given to the hypohysectomized-transplanted rats, but was ineffective in intact controls; the administration of prostaglandin E2 (5.0 and 50.0 mug) increased plasma GH in both experimental conditions. The results indicate that TRH in the hypophysectomized-transplanted rat acts directly on the AP tissue to increase GH release and that the ectopic pituitary is more susceptible than the in situ pituitary to some GH-releasing stimuli.

Animals↗
PubMed1976

Inhibitory effect of an ergoline derivative, methergoline, on growth hormone and prolactin levels in acromegalic patients.

Plasma levels of growth hormone (GH) and prolactin (PRL) were measured in twelve acromegalic patients after acute administration of an ergoline derivative (methergoline) which has been proposed as a specific serotoninergic blocking agent. The administration of methergoline (4 mg p.o.) was followed by a significant decrease in plasma GH and PRL concentrations. The administration to the same subjects of CB 154 (2.5 mg p.o.), a known stimulator of dopaminergic receptors, led to results almost superimposable to those obtained with methergoline although the suppressive effect of CB 154 on GH and PRL levels was more sustained. Also on the ground of results obtained in these patients with the use of cyproheptadine, phentolamine, or pimozide, we have concluded that methergoline inhibition of GH and PRL release is, in acromegalic patients, most probably due to a dopaminergic mechanism of action.

Acromegaly↗