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Biomedical subjects

A Polleri

Publications and source records attributed to A Polleri.

At least 19 recordsLinked to original sources
PubMed1991

Urine melatonin in alcoholic patients: a marker of alcohol abuse?

Ethanol is known to alter central neurotransmission and endocrine functions. Urine melatonin was studied in 10 male chronic alcoholic patients, before and after two weeks of controlled alcohol abstinence, and in sex and age matched healthy controls. In both groups, 24-hour urines were collected in two fractions corresponding to day- (D) (08:00-20:00) and night- (N) (20:00-08:00) time. Urine melatonin was assayed by RIA after methylene chloride extraction. Twenty-four hour urine melatonin levels were calculated adding up D and N values. In patients during alcohol intake, the 24-hour urine melatonin levels were significantly higher than in controls (p = 0.004, Student's t test). A disruption of the physiological ratio between N and D values was also observed, since the higher melatonin levels occurred in the D fraction. In drinking alcoholics, melatonin D values were significantly higher than the D values found in controls (p less than 0.01, Student's t test) and in the same patients after alcohol withdrawal (p less than 0.05). The N/D ratio approximated 1 during alcohol intake and became larger than 1 after alcohol withdrawal, as in the controls. The melatonin data were correlated with the suppressive effects of dexamethasone (DXT) on cortisol secretion evaluated both during alcohol intake and during abstinence. After alcohol withdrawal, the two (out of 10) patients, who remained unresponsive to the DXT suppression test, showed high D melatonin values and a low N/D ratio. These preliminary data indicate that in chronic alcoholism the pattern of urinary "melatonin- like immunoreactivity" is altered.

Adult↗
PubMed1990

Sex steroids and cluster headache: hypotheses.

The pathophysiological significance of the changes in gonadal function observed in cluster headache is far from clear. Some features of the disease, such as the sex predominance, the lateralization of symptoms and the character of pain itself may be connected to some biological effects of gonadal steroids.

Animals↗
PubMed1989

Cluster headache in the male: sex steroid pattern and gonadotropic response to luteinizing hormone releasing hormone.

Serum testosterone, dihydrotestosterone, delta 4-androstendione and 17 beta-estradiol, sex hormone binding globulin (SHBG) and gonadotropic response to luteinizing hormone releasing hormone (LHRH) were studied in 34 male subjects with episodic or chronic cluster headache (CH). The sex steroid free fractions and those bound to SHBG and albumin were determined by a simulatory computerized method based on the mass action law. Individual steroid values were dispersed over a wide range in CH patients. Total, free and carrier protein-bound testosterone levels were significantly diminished only in chronic CH, where luteinizing hormone (LH) peak values after intravenous administration of LHRH were also decreased. Basal and peak follicle stimulating hormone (FSH) levels were significantly increased in episodic and in chronic CH groups, in comparison to healthy controls.

Adult↗
PubMed1987

Luteinizing hormone pulsatile secretion and pituitary response to gonadotropin releasing hormone and to thyrotropin releasing hormone in male epileptic subjects on chronic phenobarbital treatment.

Endocrine changes have been reported in treated epileptic subjects, who often exhibit sexual dysfunctions, but the endocrine effects of single antiepileptic drugs have not been completely elucidated. In this study we have investigated the influence of phenobarbital (PB) on adenopituitary function and on peripheral sexual steroid pattern in 8 epileptic males. Chronic PB treatment does not modify luteinizing hormone (LH) pulsatile secretion. In the same subjects, LH and follicle stimulating hormone (FSH) response to Gonadotropin Releasing Hormone was blunted with respect to healthy controls both in terms of absolute values and of secretion areas. No difference was found in prolactin (PRL) response to Thyrotropin Releasing Hormone. In the epileptic group a significant increase in the levels of sex hormone binding globulin and a consequent decrease of the percent free testosterone have been observed. PB treatment also significantly lowers 17-beta-estradiol mean levels. These data suggest that PB independently affects both gonadotropin secretion and peripheral steroid pattern.

Adult↗
PubMed1987

Thyroid-stimulating hormone and prolactin responses to thyrotropin-releasing hormone in common migraine.

Intravenous administration of 50 micrograms or 200 micrograms thyrotropin-releasing hormone (TRH) to men with common migraine elicited blunted prolactin (PRL) responses, when compared with healthy controls. The thyroid-stimulating hormone (TSH) response was enhanced after 50 micrograms TRH in the migraineurs, but not after 200 micrograms. The physiologic TSH dose-response relationship was abolished in migraine sufferers. The data may be interpreted in the light of dopaminergic and noradrenergic supersensitivity, for PRL and TSH, respectively. The TSH response in migraine differs from the one that occurs in depression.

Adult↗
PubMed1986

Changes in the dopaminergic control of prolactin secretion and in ovarian steroids in migraine.

Prolactin (PRL) responses to dopamine (DA) blockers and to direct and indirect DA agonists have been studied in 23 healthy women, 17 women with catamenial migraine and 17 with non-catamenial migraine in both their follicular and luteal phases. PRL responses to the DA blockers were greater in the follicular phase of both migraine groups than in controls. The inhibitory effect of nomifensine on PRL secretion was dampened in the follicular phase of both migraine groups. These findings demonstrate an increased PRL reserve in migraine and suggest the existence of a dopaminergic supersensitivity of the lactotrophic postsynaptic DA receptors. The impaired inhibitory effect of nomifensine on PRL secretion hints at a decrease of the presynaptic DA content in tuberoinfundibular DA neurons. In migrainous women 17-beta-oestradiol levels are higher in both ovarian phases, whereas progesterone concentrations and the progesterone to oestradiol ratio are lower than in healthy subjects in the luteal phase. These data suggest the existence of a change in the oestrogen-dependent modulation of pituitary DA receptors.

Adult↗
PubMed1985

Benserazide effects on growth hormone, prolactin, and thyrotropin in normal and acromegalic man.

The effect of benserazide administration on the secretion of GH, PRL, and TSH has been considered as an index of dopamine regulatory actions. Nine acromegalic patients and nine normal subjects were given a single 125 mg oral dose of benserazide, and serum GH, PRL, and TSH were determined by RIA methods every 30 min for 4 h. Benserazide did not alter GH values either in normal subjects or in acromegalic patients. A significant increase of serum PRL was found in both groups, and the increase was similar in normoprolactinemic and in hyperprolactinemic acromegalic patients. A significant increase in TSH levels was found only in acromegalic patients. Thus, a decrease in dopamine outside the blood-brain barrier did not affect GH secretion, whereas PRL secretion was changed in the acromegalic as well as in the control group.

Acromegaly↗
PubMed1983

Neuroendocrinological signs of central neurotransmission disorders.

Modulation mechanisms of nociception have several neurotransmission interactions that are impaired in the disorder of painful perceptions. Neurotransmission changes may show up in several ways on the clinical level. They also have endocrinological correlations, since the neurotransmission systems implicated in the nociception disorders share transmitters with the regulation system operating at the pituitary level. In this sense, nocipathies exhibit analogies and may be compared to disorders of motricity and behaviour that also show endocrine changes that may be likewise explained. Though specifically different in each instance, the neurotransmission alteration that is a common denominator of these disorders allows comparisons, especially in those situations, such as the nocipathic and behavioural ones, where correlations are relevant on clinical and interpretative grounds.

Aging↗
PubMed1980

Spontaneous nocturnal plasma prolactin and growth hormone secretion in patients with Parkinson's disease and Huntington's chorea.

Plasma prolactin (PRL) and growth hormone (GH) levels were measured in 8 patients with Parkinson's disease (PD) and in 6 patients with Huntington's chorea (HC) during the night. The sleep was evaluated with all-night poligraphic recordings. Plasma PRL levels were significantly lower in parkinsonian patients than in age-matched controls. Plasma GH values did not differ between the two groups. In HC patients no statistically significant differences were found in the PRL and GH secretory patterns when compared to the age-matched control subjects. These data indicate that changes of nocturnal PRL and GH profile in PD and HC patients in respect to age-matched healthy subjects, may be present, but a straight forward differentiation among groups is not possible because of the wide individual variations.

Aged↗
PubMed1979

Effects of the inhibition of aromatic aminoacids decarboxylase on prolactin secretion in humans.

Carbidopa, at the dose of 250 mg. and benserazide at the dose of 125 mg, given orally in a single dose to healthy women aged between 23 - 26 years enhance significantly serum prolactin. The effect is not shared by two other inhibitors of AADC, namely alpha-methyl DOPA (500 mg) and fentiazac (400 mg). The effect of benserazide is suppressed by bromocriptine (2.5 mg) and blunted by 1-DOPA (400 mg) given orally simultaneusly.

Adult↗
PubMed1979

Dose and sex related effects of benserazide on prolactin secretion.

Benserazide, given orally at various doses ranging from 10 to 125 mg. to healthy women aged 21 to 33 years induces a dose related increase of prolactin titres in serum. When 125 mg are administered the percent increase of the hormone is larger in women than in men.

Adult↗
PubMed1979

Lack of counteracting effect of liposomes on benserazide-induced hyperprolactinemia.

Benserazide induces an increase of serum prolactin in man, possibly as the result of an impairment of the dopamine effect on the pituitary and/or on the outer median eminence caused by the inhibition on L-dopa decarboxylase. On the other hand, liposomes obtained from bovine brain cortex phospholipids reduced serum prolactin possibly through an effect of phosphatidylserine on dopamine biosynthesis at the level of tyrosine hydroxylase. Benserazide, given orally (125 mg) to 5 normal subjects, induced an increase of serum prolactin that did not change when 300 mg of phospholipid liposomes were given intravenously 60 min later. An increase of L-dopa synthesis does not seen to be capable to overcome the effects of the decarboxylase inhibition.

Adult↗