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Biomedical subjects

P Rampini

Publications and source records attributed to P Rampini.

At least 55 records · Page 3Linked to original sources
PubMed1983

Thyroid function tests in chronic liver disease: evidence for multiple abnormalities despite clinical euthyroidism.

To further evaluate thyroid function in patients with liver disease, we have measured total and free T3 and T4, thyroxine binding globulin, basal and thyrotropin releasing hormone-stimulated thyrotropin and thyroglobulin antibodies in 33 patients with liver cirrhosis, in 22 with chronic hepatitis and in 30 healthy controls. All the patients but one were clinically euthyroid. T3, FT3, T3/thyroxine binding globulin and T4/thyroxine binding globulin ratios and thyrotropin after thyrotropin releasing hormone were significantly reduced, while FT4, thyroxine binding globulin and thyrotropin were significantly increased in liver cirrhosis. In chronic hepatitis group, FT3 and T3/thyroxine binding globulin ratio were significantly lower and thyroxine binding globulin and FT4 were higher than in healthy controls. The between patients comparison revealed a significantly lower T3, FT3, T3/thyroxine binding globulin and T4/thyroxine binding globulin ratios and delta thyrotropin in cirrhotics. Thyroglobulin antibodies were present at high titre only in two patients one of whom having evidence of Hashimoto's thyroiditis with subclinical hypothyroidism. The correlation coefficient between T4/thyroxine binding globulin ratio and FT4 were lower in patients than in controls. Furthermore an abnormal thyrotropin response to thyrotropin releasing hormone was shown in 10 cirrhotics and in four patients with chronic hepatitis. Serum T3 significantly correlated with serum bilirubin, albumin, and prothrombin time in both groups of patients. The present data confirm the existence of several abnormalities of thyroid function tests in patients with chronic liver disease, although showing that euthyroidism is almost always maintained, probably as a result of low-normal FT3 and high-normal FT4. Furthermore, T3 serum levels appear to parallel the severity of liver dysfunction.

Adult↗
PubMed1983

Prolactin response to the dopamine antagonists sulpiride and domperidone. Further evidence for pituitary dopamine deficiency in hyperprolactinemic disorders of different etiology.

The PRL response to the dopamine antagonists sulpiride (100 mg i.m.) or domperidone (2 or 8 mg i.v.) was evaluated in healthy controls and in 148 patients with different hyperprolactinemic disorders (50 with idiopathic hyperprolactinemia, 58 with microprolactinoma, 19 with macroprolactinoma, 2 with empty sella, 8 with acromegaly, 7 with organic lesions of the hypothalamus, and 4 with idiopathic hypopituitarism of presumed hypothalamic origin). Mean PRL response to both drugs was significantly lower in all groups of patients than in controls, and significantly higher in subjects with idiopathic hyperprolactinemia than in those with pituitary adenomas or hypothalamic disease. Absent or impaired PRL responses were found in 38% of idiopathic patients, in 91.5% of microprolactinomas and in all of the patients with either macroprolactinoma, acromegaly, or hypothalamic disorders. Since the PRL response to dopamine antagonists depends on the presence of an endogenous dopaminergic tone, it is suggested that these figures reflect the incidence of major dopamine deficiency at pituitary lactotrophs in different hyperprolactinemic states. These data suggest that the pathophysiology of hyperprolactinemia in many patients with idiopathic disease is different from that of microprolactinoma. However, the finding of a normal PRL response to sulpiride in some subjects with radiologically or surgically proven microprolactinoma indicates that this test has no diagnostic value in the individual case.

Adolescent↗
PubMed1982

Treatment of hyperprolactinemic states with different drugs: a study with bromocriptine, metergoline, and lisuride.

One hundred ninety-one hyperprolactinemic patients (78 women and 13 men; 54 with pituitary macroadenoma, 53 with microadenoma, and 84 with idiopathic disease) were treated for 2 to 48 months with one or two of the following prolactin (PRL)-lowering drugs: bromocriptine, metergoline, and lisuride. All of the three drugs used were highly effective in lowering PRL levels and restoring gonadal function both in females and in males in the majority of patients with either idiopathic or tumorous disease. In poorly responsive patients, increasing the drug doses resulted in further PRL lowering for all the three drugs. Mild side effects were frequently encountered with initiation of drug treatment but spontaneously subsided in most cases; severe side effects, necessitating stopping of the treatment, occurred in only 12 instances, but changing of the drug allowed PRL-lowering treatment to be continued in 11 of them.

Adenoma↗
PubMed1982

Functional characterization of hypothalamic hyperprolactinemia.

PRL secretory dynamics were evaluated by several stimulation and suppression tests in nine patients with hyperprolactinemia due to organic hypothalamic disease. Basal PRL levels ranged between 20-63 ng/ml. There was a normal PRL response to TRH in eight cases (i.e. doubling of basal levels), whereas none of the seven tested subjects responded to sulpiride. The same dissociation of responses was not observed in any of the patients who were still hyperprolactinemic after surgery. Concomitant dopamine infusion resulted in sulpiride-induced PRL release in the four subjects so studied. None of 50 other hyperprolactinemic patients (11 with macroprolactinoma, 18 with microprolactinoma, and 21 with idiopathic hyperprolactinemia) showed PRL response to TRH but not to sulpiride. The TRH-induced PRL increase was significantly higher than that induced by sulpiride in hypothalamic hyperprolactinemia and significantly lower in idiopathic disease as well as in healthy controls; no differences were found in prolactinoma patients. The administration of substances resulting in stimulation of pituitary dopamine receptors, such as dopamine and L-dopa, induced a normal PRL suppression in 7 patients with hypothalamic disease so tested, whereas central nervous system-acting dopaminergic drugs, such as carbidopa plus L-dopa and nomifensine, failed to lower PRL levels in most cases (even when normoprolactinemic after surgery). These data suggest that the mild to moderate hyperprolactinemia found in many patients with hypothalamic lesions is due to dopamine deficiency at the pituitary level, that TRH and dopamine receptors at the lactotropes are intact in this condition, and that paired TRH and sulpiride tests may be of some diagnostic utility in hyperprolactinemic patients. They further suggest that subjects with so-called idiopathic hyperprolactinemia do not suffer from the type of hypothalamic derangement exhibited by patients with organic lesions of the hypothalamus.

Adult↗
PubMed1981

Effects of chronic prazosin treatment on the renin-angiotensin-aldosterone system in man.

The effects of chronic prazosin treatment (3 mg/day for three weeks) on plasma renin activity (PRA) and plasma aldosterone (PA) levels were evaluated in 12 hypertensive patients, under conditions of metabolic balance. After three weeks of drug administration no significant change occurred in PRA as well as PA levels, with respect to pretreatment values, both in basal conditions and following 2 hours of ambulation. No change was observed in heart rate, while a fall in both systolic (P less than 0.02) and diastolic (P less than 0.05) blood pressure occurred in supine as well as in deambulation-stimulating condition. A mild increase in body weight (P less than 0.05) and a decrease in serum sodium (P less than 0.05) was induced by prazosin treatment. These findings are in keeping with the pharmacologic properties of prazosin, which is a selective blocker of postsynaptic alpha adrenoreceptors and therefore lowers vascular resistance without reflex sympathetic overactivity. The moderate volume expansion after prazosin does not appear to be aldosterone mediated.

Adult↗
PubMed1981

Effect of loperamide, a peripheral opiate agonist, on circulating glucose, free fatty acids, insulin, C-peptide and pituitary hormones in healthy man.

The effect of acute oral administration of loperamide (4, 8 and 16 mg), a peripheral opiate agonist used in the treatment of diarrhoea, on several metabolic and endocrine variables has been evaluated in healthy volunteers in comparison with placebo. Plasma glucose was significantly raised by all three doses, whereas serum IRI and C-peptide were decreased and serum FFA was significantly increased only after loperamide 8 and 16 mg; serum PRL, GH, LH and FSH did not change. The data suggest that opiates may be involved in the regulation of glycaemia, probably by modifying islet hormone secretion by acting at a peripheral site, since loperamide does not cross the blood-brain barrier. Although the precise mechanism of these actions is unknown, it is suggested that the effects of loperamide are mediated either by stimulation of opiate receptors per se, or by suppression of acetylcholine release from cholinergic nerve endings. The lack of change in pituitary hormone secretion by loperamide is in agreement with previous observations indicating that opiate effects on PRL, GH and gonadotropins occur at the level of the central nervous system.

Adult↗
PubMed1981

Central nervous system and pituitary mechanisms in dopaminergic stimulation of growth hormone release in women.

In an attempt to evaluate the relative importance of brain and peripheral (i.e., outside the blood-brain barrier) dopamine (DA) receptor stimulation in the regulation of GH release, DA (5 microgram/kg/min infused i.v. for 120 min), L-dopa (500 mg p.o.), L-dopa (100 mg p.o.) plus carbidopa (35 mg p.o.) after pretreatment with carbidopa (50 mg p.o. every 6 h for 1 day), and nomifensine (200 mg p.o.) have been administered to healthy women. Significant elevations in serum GH were induced by all regimens in comparison with a control placebo study, although the effect of DA was only transient in spite of continuing infusion. The between drugs analysis revealed that L-dopa alone was significantly more effective in releasing GH than carbidopa plus L-dopa as well as DA infusion and nomifensine administration. These results suggest that both central nervous system and peripheral mechanisms are involved in dopaminergic stimulation of GH release in man. Since DA does not affect somatotropes directly, increased serum GH levels by DA infusion probably reflect stimulation of median eminence dopaminergic neurons.

Adolescent↗
PubMed1981

Inhibition of luteinizing hormone release by dopamine infusion in healthy women and in various pathophysiological conditions.

To investigate the effect of dopaminergic stimulation on gonadotrophin release, serum LH and FSH concentrations were measured during dopamine infusion (5 microgram/kg/min for 120 min) in 8 healthy women in the early follicular phase, in 12 patients with hyperprolactinaemic amenorrhoea, in 5 subjects with premature ovarian failure and in 8 with polycystic ovarian disease and raised serum LH levels. Dopamine infusion produced a significant LH decrease compared with a control study using saline in all groups; there were no significant changes in FSH concentration. Between groups analysis showed a significantly greater LH fall in patients with polycystic ovarian disease than in the other groups. Dopamine inhibits LH release in healthy women and patients with anovulatory states of varying aetiology, and enhanced sensitivity to this inhibitory mechanism exists in polycystic ovarian disease. This finding suggests reduced dopamine activity at the median eminence level in this condition.

Adolescent↗
PubMed1980

Effect of two antiserotoninergic drugs, methysergide and metergoline, on gastric acid secretion and gastrin release in healthy man.

The effects of acute oral administration of the antiserotoninergic drugs methysergide (3 mg) and metergoline (4 mg) on basal, submaximal (0.6 micrograms/kg i. m.) and maximal (6 micrograms/kg) pentagastrin-stimulated gastric acid secretion, as well as on basal and food-induced gastrin release, have been evaluated in healthy volunteers. Methysergide significantly increased basal and submaximal pentagastrin-stimulated gastric acid secretion, and metergoline significantly inhibited gastric acidity in all experiments. Basal and stimulated serum gastrin concentrations were not modified by either drug. The effect of methysergide on gastric acid secretion was opposed to that of serotonin and was probably dependent on its antiserotoninergic action, but the decrease in gastric acidity caused by metergoline is not easily explained. Although the effect is similar to that of a dopamine infusion, it does not depend on dopamine infusion, it does not depend on dopamine receptor stimulation, since it was not influenced by pretreatment with metoclopramide. It is suggested that it might be due to the weak anticholinergic and/or antihistaminic properties of metergoline.

Adult↗
PubMed1980

Hyperprolactinemic primary amenorrhea: case report with successful prolactin-lowering treatment and review of the literature.

A 19-year-old girl with primary amenorrhea, galactorrhea, and hyperprolactinemia is described. Her high serum prolactin levels (95 ng/ml) did not increase after thyrotropin-releasing hormone and sulpiride, but markedly decreased after acute bromocriptine and metergoline administration. The results of other pituitary function tests were normal. Tomography of the sella turcica and CT scan of the skull were also normal. The patient was treated with metergoline, a prolactin-lowering drug which is believed to act as a serotonin antagonist, for 30 months. Serum prolactin rapidly decreased after institution of treatment, with actual normalization (less than 20 ng/ml) by the 3rd month. At this time the low serum luteinizing hormone levels began to rise and fluctuate in the normal follicular range. Galactorrhea disappeared, and menarche occurred during the 15th month of treatment. 15 further menstrual bleedings ensued over the following 15 months, albeit at irregular time intervals; ovulation was suggested by finding elevated serum progesterone levels in the presumed luteal phase by about 1 year following the menarche. The available data on 38 patients with primary amenorrhea and hyperprolactinemia reported in the literature are reviewed. 15 of them were treated with bromocriptine, and either pregnancy or cyclic menses occurred in 11. Hyperprolactinemic primary amenorrhea may be more common than previously recognized, and it may probably be successfully treated by prolactin-lowering drugs or by surgical ablation of a pituitary adenoma in a high percentage of cases.

Adult↗
PubMed1980

Failure of nomifensine administration to discriminate between tumorous and nontumorous hyperprolactinemia.

It has recently been claimed that the PRL-lowering response to nomifensine administration (200 mg, orally) reliably discriminates patients with PRL-secreting tumors from those with so-called functional hyperprolactinemia. In the present study, this test was performed in 15 healthy controls, 7 hyperprolactinemic subjects without evidence of pituitary tumor, and 16 patients with prolactinoma. A decrease of serum PRL to below 65% of basal levels, which seemed to be the cut-off point in the previous study, was obtained in 11 subjects of the first group, in 4 subjects of the second group, and in 4 subjects of the third group. The decrease of mean serum PRL concentration after nomifensine was only significant in the first and second groups. Analysis of variance showed a significant difference in the PRL inhibition by nomifensine between the tumor group and the two groups without evidence of pituitary adenoma. Nevertheless, this study shows that the nomifensine test is unable to discriminate in the individual patient the tumorous or nontumorous origin of excessive PRL secretion.

Adenoma↗
PubMed1978

Restoration of cyclic ovarian function by metergoline treatment in a patient with a prolactin-secreting pituitary microadenoma.

A patient with amenorrhea due to a prolactin-secreting pituitary microadenoma was treated with the antiserotoninergic drug metergoline for 8 months. The first menstruation occurred after 1 month of therapy, and it was followed by regular menses by the 3rd month. Presumptive evidence of ovulation was obtained in at least some instances by serum progesterone and gonadotropin determination. Serum prolactin was only slightly lowered by treatment. The patient had menses and possibly ovulation in the 2 months following drug withdrawal. Metergoline might restore ovarian function in hyperprolactinemic amenorrhea either by prolactin suppression or perhaps by direct stimulation of gonadotropin release.

Adenoma↗
PubMed1978

Inhibition of prolactin release by serotonin antagonists in hyperprolactinemic subjects.

Metergoline (4 mg) and methysergide (3 mg), two serotonin antagonists known to inhibit prolactin secretion in normal subjects, and the dopaminergic agonist, bromocriptine (2.5 mg) were orally administered in hyperprolactinemic patients. Mean serum prolactin concentration was significantly decreased between 120 and 240 min following the ingestion of all three drugs in comparison with a placebo; a consistent reduction to below 50% of basal values occurred in 10 of 14 patients after metergoline, in 5 of 10 after methysergide, and in 11 of 14 after bromocriptine administration. These data indicate that serotonin antagonists may acutely lower serum prolactin levels in hyperprolactinemic patients similarly to bromocriptine, though their mechanism of action is most likely different.

Adult↗
PubMed1978

Prolactin suppression by serotonin antagonists in man: further evidence for serotoninergic control of prolactin secretion.

To further investigate the role of serotonin in human prolactin (Prl) secretion, serotonin antagonists have been administered to healthy volunteers in basal conditions and after pretreatment with the selective blocker of dopamine receptors, pimozide (Pim). Highly significant falls (p less than 0.001) in serum Prl were observed at 120, 180, and 240 min following the oral administration of metergoline (Met) (4 mg; N = 34) and methysergide (Meth) (3 mg; N = 20) in comparison with placebo. No significant difference was found in the degree of Prl suppression induced by these two serotonin antagonists and by hte dopaminergic drug bromocriptine (Br) (2.5 mg; N = 20). After Pim pretreatment (1 mg every 6 h for 7 days) the elevated serum Prl levels were reduced to 27.1% +/- 8.1 (SEM) of basal after Met and to 54.5% +/- 8.9 after Meth administration (N = 5 for each study). It is concluded that Met and Meth inhibit Prl secretion by mechanisms which are not or only partially related to dopaminergic receptors. These data are consistent with a stimulatory role for serotonin in human Prl release.

Adolescent↗