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PubMed1977

Study of the effects of bromocriptine on sexual impotence.

Serum testosterone, prolactin, LH, FSH and plasma 17 beta-oestradiol levels were determined in forty-seven male patients with sexual impotence. Low testosterone values and slightly elevated prolactin levels were observed in 19% and in 17% of cases, respectively. Since sexual function in the male seems to be controlled by both dopaminergic stimulatory and serotoninergic inhibitory mechanisms, bromocriptine was given orally to seventeen patients. As the preliminary results appeared encouraging, a double blind study was undertaken in the other thirty patients. No appreciable difference in hormonal pattern was noticed between bromocriptine and placebo treatment. As far as sexual function was concerned, good results were obtained in 52% of cases treated with bromocriptine and in 44% of patients given placebo.

Adult↗
PubMed1978

Bromocriptine treatment of males with pituitary tumours, hyperprolactinaemia, and hypogonadism.

Plasma prolactin concentrations were measured in thirty-four males with pituitary tumours and twenty-two patients (65%) were found to have hyperprolactinaemia. Plasma testosterone concentrations were subnormal in twenty-nine patients. Ten patients with hyperprolactinaemia were treated with bromocriptine; prolactin was restored to normal values in eight patients but testosterone secretion remained deficient. Two patients were resistant to bromocriptine. Some improvement in libido and potency was obtained after restoration of normal prolactin concentrations in four cases in spite of persistently low testosterone secretion. For maximal improvement in sexual function treatment with both bromocriptine and testosterone was required.

Bromocriptine↗
PubMed1979

Bromocriptine treatment of seven women with primary amenorrhoea and prolactin-secreting pituitary tumours.

Seven women with primary amenorrhoea and hyperprolactinaemia were treated with bromocriptine. All the women had started to develop secondary sex characteristics at normal age but pubertal development stopped and menarche did not occur. Radiological signs of a pituitary tumour were found in all the women. Before the pituitary tumour was diagnosed, four women had been given longterm cyclical oestrogen replacement therapy. Three women had received primary tumour therapy with surgery and/or irradiation but had persistent hyperprolactinaemia. The basal luteinizing hormone (LH) levels were low in four of the women while all the women had normal basal levels of follicle-stimulating hormone (FSH) and normal or exaggerated gonadotrophin responses to luteinizing hormone-releasing hormone (LHRH). None of the women had evidence of endogenous oestrogen production before treatment. Bromocriptine treatment normalized the raised serum prolactin levels (46-2900 microgram/l) in all but one woman, in whom the prolactin level decreased from 160 to 38 microgram/l. Regular ovulatory menstrual cycles appeared in four women, one of whom had previously been treated by transsphenoidal adenomectomy followed by external irradiation. Two other women with persistent hyperprolactinaemia after previous surgical and/or irradiation treatment of large pituitary tumours did not menstruate after more than one year of treatment with bromocriptine. One infertile patient with a microadenoma conceived at the first ovulation on therapy and developed symptoms and signs of tumour growth during pregnancy.

Adenoma, Chromophobe↗
PubMed1979

The influence of bromocriptine on serum levels of growth hormone and other pituitary hormones and its metabolic effects in active acromegaly.

The effect of treatment with bromocriptine for 12--18 months on serum GH and metabolic responses was studied in sixteen patients with active acromegaly. Of this group ten patients showing a sustained GH reduction of more than 50% during an 8 h bromocriptine test, proved to be responsive to long-term therapy. In the responding patients GH levels decreased to 38% of the pretreatment level after 12 months of therapy. A dose higher than 10 mg did not produce a significantly greater effect. Prolactin and LH levels decreased in all patients, FSH levels showed a significant rise. Testosterone levels in the male patients increased significantly, indicating that the state of hypogonadism can at least be partially reversed. The GH levels became normal in only one patient. We conclude that the role of bromocriptine in acromagaly is limited and selective pituitary operation and/or irradiation is preferred as definitive treatment in most patients.

Acromegaly↗
PubMed1979

Chronic dopamine receptor stimulation using bromocriptine: failure to modify thyroid function.

Administration of 2.5 mg bromocriptine (Parlodel), a dopamine agonist, on two occasions to six normal volunteers did not alter the plasma TSH response to an i.v. injection of 100 micrograms TRH, but significantly (P less than 0.01) blunted it after 200 micrograms. Chronic bromocriptine treatment (7.5--50 mg/day) of fifteen acromegalic subjects failed to influence basal plasma TSH or the response pattern to 200 micrograms TRH. The thyroxine Binding Index (TBI) and the levels of T3 and T4 were not modified by treatment. These results indicate that chronic dopaminergic therapy with bromocriptine does not alter thyroid function.

Acromegaly↗
PubMed1981

Pituitary function in prolactinoma. Effect of surgery and postoperative bromocriptine therapy.

Forty-five women and fifteen men with prolactinomas have been treated surgically. Patients with large tumours received pituitary irradiation and postoperative hyperprolactinaemia was treated with bromocriptine. The patients have been followed-up for 6-36 months following the operation. The tumours were larger and the levels of production higher in men as compared with women. All women had amenorrhoea. Galactorrhoea was present in forty-three women but not in the men. After surgery serum prolactin levels fell significantly in all women but remained above normal in thirty-six; prolactin remained high in twelve men. Bromocriptine effectively decreased the postoperative hyperprolactinaemia. The surgical complications were oculomotor nerve paresis in one woman and one man. After surgery six (23%) women developed impaired GH secretion, six (15%) impaired thyroid function, eight (18%) impaired cortisol secretion and five (17%) impaired LH secretion in isolation or combination which had not been present preoperatively. Three patients relapsed. Fifteen women menstruated after surgery and ten began to do so during the subsequent bromocriptine treatment. Thus, menstruation was restored in all six women with microadenomas in sixteen of twenty patients with intrasellar macroadenomas and three of nineteen patients with suprasellar adenomas. The preoperative LH-reserve proved to be an important prognostic indicator. Nine patients, i.e. 50% of patients desiring fertility became pregnant. In the men gonadal function deteriorated in four patients and did not improve in any without testosterone treatment.

Adenoma↗
PubMed1981

The effect of bromocriptine on insulin secretion and glucose tolerance in patients with acromegaly.

The oral administration of bromocriptine 5 mg 6-hourly to twelve patients with acromegaly for a mean period of 12 (range 3-27) months significantly reduced whole blood glucose, plasma insulin and plasma growth hormone (GH) concentrations during a 50 g oral glucose tolerance test (OGTT). After this period of treatment, bromocriptine was withdrawn for 48 h resulting in a significant rise in whole blood glucose, plasma insulin and plasma GH concentrations during a repeat OGTT. It is concluded that bromocriptine therapy improves glucose tolerance in acromegaly by suppressing GH secretion and consequently GH-mediated antagonism of insulin.

Acromegaly↗
PubMed1981

Bromocriptine suppresses ACTH secretion from human pituitary tumour cells in culture by a dopaminergic mechanism.

Bromocriptine (0.13-13 microM) significantly inhibited ACTH secretion in a dose-dependent manner when added to cell cultures of a human corticotrophic adenoma for 24 h. Haloperidol (13 microM), but not serotonin (13 microM), blocked this inhibition but had no significant effect when added alone. In addition, dopamine (10 microM) reduced ACTH secretion during a 4-h incubation, whereas serotonin (0.01-10 microM) was ineffective. An ectopic ACTH secreting lung carcinoid was non-responsive to doses of bromocriptine up to 13 microM. These results demonstrate a direct suppressive action of bromocriptine on a human pituitary corticotrophic adenoma through dopaminergic rather than serotoninergic mechanisms.

Adenoma↗
PubMed1982

Treatment of acromegaly by trans-sphenoidal operation, 90-yttrium implantation and bromocriptine: results in 230 patients.

Two hundred and thirty patients with acromegaly were diagnosed and treated in a prospective cooperative study in twelve university clinics. Primary treatment was: trans-sphenoidal surgery (152 patients), trans-sphenoidal surgery with additional cryotherapy (eighteen patients), Yttrium-90-implantation (thirty patients), bromocriptine (thirty patients). The results of endocrine assessment before treatment and 6 months after operation, 90-Y implantation or commencement of bromocriptine therapy are reported. The best results (low GH, no or little deterioration of pituitary function, low complication rate) were achieved by trans-sphenoidal surgery, especially in patients with intrasellar tumours (basal GH less than 5 ng/ml in 59.7%). Results were less good with increasing tumour size. Additional cryosurgery was accompanied by a high rate of anterior pituitary insufficiency and is no longer employed. Yttrium-90-implantation resulted in less improvement in GH levels (basal GH less than 5 ng/ml in 51.7% of patients with intrasellar tumours), a high rate of pituitary insufficiency and more complications. Bromocriptine treatment was least effective in lowering GH concentrations (basal GH less than 5 ng/ml in 33% of patients with intrasellar tumours). Different criteria for treatment success were compared. In the entire group, basal GH concentrations below 5 ng/ml were attained in 51.7% of all patients whose values were higher than this prior to treatment. Suppressibility of GH below 2 ng/ml during glucose loading occurred in only 34.9%. An abnormal GH response to TRH/LHRH was present in 47.2% before and in 43.4% after/during treatment. The prognostic significance of this latter finding must be evaluated by further study.

Acromegaly↗
PubMed1982

Pulsatile gonadotrophin secretion in hyperprolactinaemic amenorrhoea an the response to bromocriptine therapy.

Serum gonadotrophin concentrations were measured every 15 min for 8 h in six patients before and at weekly intervals during initiation of bromocriptine treatment of hyperprolactinaemic amenorrhoea. Before treatment mean gonadotrophin levels were similar to those found in the normal follicular phase, but LH secretion was characterized by infrequent pulses of large amplitude. In three subjects the patterns of LH pulsatility and serum oestradiol levels returned to normal within 7 days of starting bromocriptine. The other three subjects responded with an increase in the frequency of LH pulses and mean LH levels, but little rise in oestradiol. Thus some hyperprolactinaemic subjects have a defect in the ovarian response to endogenous gonadotrophin stimulation, which may persist for a few weeks after return of prolactin levels to normal. The restoration of a normal rate of LH pulsatility with bromocriptine can occur without any change in serum oestradiol concentration.

Adult↗
PubMed1984

The effect of bromocriptine in the polycystic ovary syndrome.

The effect of chronic administration of bromocriptine to 20 patients with the polycystic ovary syndrome (PCOS) was studied. All patients had normal serum prolactin levels. Bromocriptine 7.5 mg daily was administered for up to 1 year and the biochemical and clinical responses assessed at 3-monthly intervals. Over a period of 3 to 12 months significant reductions in serum LH levels, LH/FSH ratios and in plasma testosterone were observed. In 14 patients, blunting of the previously enhanced LH response to LHRH was observed. Clinical improvement also occurred, most notably in menstrual function. In 12 out of 20 patients a monthly cycle was established and in a further three there was an increase in the frequency of menstruation towards normal. Eleven out of 20 patients ultimately noted a subjective improvement in hirsutism. We conclude that bromocriptine, given to patients with polycystic ovarian disease, inhibits LH hypersecretion, leading to restoration of cyclic ovarian function and reduced androgen synthesis.

Adult↗
PubMed1985

Bioactive forms of serum lactogens: effects of treatment of prolactinoma patients with bromocriptine.

An in vitro bioassay for lactogenic hormones, based on the specific mitogenic effects of lactogens on cultured Nb2 node rat lymphoma cells, was used to measure the levels of lactogens in whole serum and in fractionated serum samples from three patients with prolactin (PRL) secreting pituitary adenomas. Under basal conditions, after pituitary stimulation, and following treatment with bromocriptine which greatly decreased the serum PRL levels, the bioassay (BA) results closely paralleled fluctuations in the sum of radioimmunoassay (RIA) estimates of serum PRL and growth hormone concentrations. The extreme sensitivity (10 pg/ml) of the BA facilitated measurement of PRL in fractions obtained after Sephadex G-100 chromatography of only 0.1 to 0.3 ml of sera from both untreated and bromocriptine-treated prolactinoma patients. In both types of samples, similar heterogenous patterns of bioactive PRL were observed, although most of the recovered activity appeared to be due to monomeric PRL. BA and RIA of fractions obtained after DEAE cellulose chromatography of sera from untreated prolactinoma patients revealed two PRL peaks, the first one containing 75% of the activity. Therapy with bromocriptine led to a reduction in the total serum PRL activity and, in particular, in the activity of the second peak.

Adenoma↗
PubMed1986

The effect of ovine corticotrophin releasing factor (oCRF), bromocriptine and TRH on the secretion of ACTH and alpha-MSH in Nelson's syndrome and Cushing's disease.

The circulating levels of ACTH and alpha-melanocyte stimulating hormone (alpha-MSH) were measured in 9 patients with Nelson's syndrome after the administration of saline, ovine corticotrophin releasing factor (oCRF), bromocriptine or TRH. The concentrations of ACTH were grossly elevated and alpha-MSH levels ranged from undetectable to higher than the normal range. In seven of eight subjects there was a rapid corticotrophic response, but no change in the alpha-MSH level, following oCRF. This response was delayed in one subject. Following oCRF injection, the plasma oCRF profile was variable but circulating oCRF was detectable even at the end of the experiment in all cases. There was no significant change in circulating ACTH or alpha-MSH following either bromocriptine or TRH. Cultured tumour cells from one case of Cushing's disease showed a corticotrophic response but no change in alpha-MSH to oCRF and the response was enhanced by vasopressin. Bromocriptine added to the same tumour depressed ACTH secretion without affecting the output of alpha-MSH. The present data suggest that the tumours in these subjects are responsive to oCRF and arise from corticotrophs rather than melanotrophs.

Adrenocorticotropic Hormone↗
PubMed1986

Rapid improvement in visual field defects following bromocriptine treatment of patients with non-functioning pituitary adenomas.

The role of bromocriptine in the treatment of non-functioning pituitary tumours is not yet defined. Patients with these tumours who present with visual field defects usually undergo immediate surgery. Three consecutive patients are reported: each had rapid improvement in their visual field defects following bromocriptine 7.5 mg/d before surgery. Histological and immunohistochemical examination confirmed that their tumours were non-functioning chromophobe adenomas. Their responses indicate that bromocriptine may have a role in the management of some patients with non-functioning pituitary tumours.

Adenoma, Chromophobe↗
PubMed1987

Normal growth and pubertal development during bromocriptine treatment for a prolactin-secreting pituitary macroadenoma.

An 11-year-old male presented with a 2-year history of headache and lethargy. Serum PRL was elevated at 14,000 mU/l and computerized tomography showed a pituitary macroadenoma. Visual fields and fundi were normal and the testes showed early pubertal changes. There was normal responsiveness of serum cortisol but absence of GH response to hypoglycaemia. After bromocriptine therapy for 4 months serum PRL had fallen to 90 mU/l and the tumour was not visible on repeat computerized tomography. After 7 months treatment, repeat pituitary function testing showed restoration of GH response to hypoglycaemia. Treatment with bromocriptine was continued and there was spontaneous progression of normal puberty; the serum testosterone continued to rise, and height maintained the 50th centile. Bromocriptine therapy should be considered as initial therapy in the management of prolactinomas in prepubertal patients.

Adenoma↗
PubMed1987

A comparison between the effects of SMS 201-995, bromocriptine and a combination of both drugs on hormone release by the cultured pituitary tumour cells of acromegalic patients.

The in-vivo reaction of the plasma GH concentration to the administration of the somatostatin analogue SMS 201-995, bromocriptine and their combination were compared with the in-vitro effects of both compounds and their combination on GH release and the GH tumour cell content of 9 acromegalic patients. Exposure of cultured GH-secreting pituitary tumour cells for 4-96 h to SMS 201-995 showed a variable, but in all instances during longer incubations statistically significant inhibition of GH release, which paralleled the sensitivity of GH secretion to the drug in vivo. This inhibitory effect on GH release was in two of the eight tumours accompanied by a decrease in the GH tumour cell content after 24-72 h of culture. These changes either reflect an inhibition of GH synthesis and/or an increase in intracellular breakdown (crinophagy) of GH and might be the basis for the tumour shrinkage which has been observed in about half of the acromegalic patients during long-term SMS 201-995 therapy. The inhibitory effects of bromocriptine on GH secretion were antagonized by haloperidol, while the inhibitory effect of SMS 201-995 was not affected by the dopamine receptor antagonist. This suggests that the effects of SMS 201-995 and bromocriptine are mediated via separate mechanisms involving different receptors. Additive but no potentiating inhibitory effects of both drugs on GH release were observed in a group of six patients in vivo and in three of six tumours in vitro.

Acromegaly↗
PubMed1990

The effect of cyproheptadine and/or bromocriptine on plasma ACTH levels in patients cured of Cushing's disease by bilateral adrenalectomy.

Cyproheptadine and bromocriptine have been reported to be therapeutic in suppressing ACTH levels in Cushing's disease and Nelson's syndrome. However, there have been only scattered reports of their effect in suppressing raised ACTH levels found in patients cured of Cushing's disease by bilateral adrenalectomy. In order to assess whether these agents could prove beneficial in such patients we studied 12 patients previously treated with bilateral adrenalectomy alone for Cushing's disease before and after 3 weeks of cyproheptadine and/or bromocroptine therapy. All had raised plasma ACTH values but no patient had evidence of a pituitary macroadenoma. Plasma ACTH and cortisol were sampled 2-hourly for 24 h. Neither drug regime led to any change in plasma levels of cortisol for 24 h after a 20 mg dose of oral hydrocortisone. Plasma ACTH (mean +/- SEM) showed a small but significant overall reduction (523 +/- 45 vs 392 +/- 34 ng/l; P less than 0.05) while on bromocriptine alone (5 mg given at 0800 and 1800 h, n = 5). When each time point was analysed individually this reduction was significant at only five out of 13 time points. At 0400 h plasma ACTH (mean +/- SEM) was 758.4 +/- 298.1 vs 380.2 +/- 166.6; 0600 h, 795 +/- 288.7 vs 477.8 +/- 191.7; 1200 h, 266.8 +/- 106.2 vs 187.0 +/- 80.3; 1400 h, 470.0 +/- 239.0 vs 302.0 +/- 135.9; 1600 h, 548.6 +/- 262.5 vs 394.2 +/- 178.5 ng/l (P less than 0.05). There was no significant change in plasma ACTH during treatment with the combination of bromocriptine and cyproheptadine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1987

Involvement of sympathetic nervous system inhibition in the hypotensive effect of bromocriptine in spontaneously hypertensive rats.

The hypotensive effect of bromocriptine in young (6 week old) spontaneously hypertensive rats (SHR) was studied. Blood pressure and plasma norepinephrine level in bromocriptine-treated SHR were significantly lower than those in vehicle-treated SHR after 3 weeks of treatment (5 mg/kg per day, i.p.), while no significant decrease of blood pressure or plasma norepinephrine level was observed after 2 weeks of treatment. These results suggest the involvement of sympathetic nervous system inhibition in the hypotensive effect of bromocriptine in SHR.

Aging↗