Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Bromocriptine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 955 records · Page 53Linked to original sources
PubMed1981

Bromocriptine inhibits colony formation by rat pituitary tumor cells in a double-layered agar clonogenic assay.

In order to assess the possible antiproliferative action of bromocriptine on pituitary tumors, the effects of the drug on colony formation were studied using GH3 cells grown in double-layered agar. Bromocriptine (300 nM) clearly inhibited both the number of colonies arising from single tumor cells as well as the size of the tumor cell colonies (p less than 0.001). The drug did not inhibit colony formation by cells derived from 2 non-pituitary tumors. The data show that this dopamine agonist blocks proliferation of rat pituitary tumor cells in vitro and lend further support to the preliminary clinical observations of an anti-tumor effect of bromocriptine in man.

Animals↗
PubMed2003

Successful pregnancy after bromocriptine therapy in an anovulatory woman complicated with ovarian hyperstimulation caused by follicle-stimulating hormone-producing plurihormonal pituitary microadenoma.

Gonadotropin-producing pituitary adenomas are extremely rare in reproductive-age women. We report here a case of gonadotroph microadenoma with ovarian hyperstimulation. It was found in a 29-yr-old infertile Japanese woman with enlarged multicystic ovaries. The patient had an elevated basal serum estradiol level (up to 6755 pM, or 1840 pg/ml). Serum FSH and prolactin were mildly elevated (15.4 IU/liter, 1.4 nM or 31.4 ng/ml), whereas LH was low (0.5 IU/liter). The FSH level was paradoxically elevated in response to TRH administration. Dynamic magnetic resonance imaging revealed a pituitary microadenoma. Daily administration of bromocriptine, a dopamine agonist, normalized the ovarian size, and the patient ovulated naturally. She conceived after 3 months of bromocriptine therapy and delivered a normal child. She underwent elective transsphenoidal pituitary surgery, 3 yr after the delivery. Immunostaining of the resected tumor showed that 80% and less than 5% of the tumor cells stained for FSH-beta and prolactin, respectively. Furthermore, RT-PCR suggested that dopamine type 2 receptor was expressed in the adenoma. Gonadotroph microadenoma should be considered in women with spontaneous ovarian hyperstimulation, even if they have no neurological symptoms or marked pituitary enlargement. In such cases, bromocriptine therapy may be an alternative to pituitary surgery.

Adenoma↗
PubMed1976

Prolactin and testosterone: independent circulating levels in hyperprolactinemic and normoprolactinemic amenorrhea. The effect of prolactin suppression by bromocriptine.

In order to elucidate the pituitary regulation of the female testosterone secretion, we studied by radioimmunoassay the circulating prolactin (PRL) and testosterone-dihydrotestosterone (T-dT) levels in 12 hyperprolactinemic and 12 normoprolactinemic patients with secondary amenorrhea. After the basal levels had been recorded, each patient was given bromocriptine for two weeks, 2.5 mg twice daily, and repeat estimations of the PRL and T-dT levels were done. We found no significant difference in the basal T-dT levels between normoprolactinemic and hyperprolactinemic patients, and no significant correlation between the PRL and T-dT levels in either group. Although the PRL levels of the hyperprolactinemic patients were greatly suppressed by bromocriptine, the T-dT levels showed no systematic change. In normoprolactinemic patients, the T-dT concentrations were somewhat lower during bromocriptine treatment, but the difference from basal levels was not statistically significant (0.05 less than P less than 0.1). Our results suggest that in patients with secondary amenorrhea PRL does not interfere directly with T-dT secretion, or vice versa.

Adult↗
PubMed1976

Bromocriptine increases plasma estradiol-17 beta concentration in amenorrhea patients with normal serum prolactin.

In a series of 23 patients bromocriptine increased the plasma estradiol-17 beta level from 44.0 +/- 9.5 (mean +/- SE) to 144.1 +/- 31.8 pg/ml after 3 - 5 weeks' treatment (p less than 0.01). In normoprolactinemic patients (N = 12) the level increased from 59.6 +/- 16.3 to 186.5 +/- 50.5 pg/ml (p less than 0.05), and in hyperprolactinemic patients (N = 11) the corresponding values were 27.0 +/- 6.2 and 97.8 +/- 34.6 pg/ml (p less than 0.05). Bromocriptine treatment did not significantly alter the FSH and LH levels. The results suggest that bromocriptine treatment induces endocrine recovery also in patients whose clinical findings give no indication of prolactin suppression.

Amenorrhea↗
PubMed1979

A pregnancy in an acromegalic woman during bromocriptine treatment: effects on growth hormone and prolactin in the maternal, fetal, and amniotic compartments.

An unexpected 20-week-old pregnancy was found in a young acromegalic who had been treated with 10 mg bromocriptine/day for 10 months. The drug was continued throughout the period of gestation. No growth of the pituitary adenoma was noticed. The intrauterine development of the fetus was normal. Bromocriptine therapy had no discernible effect on the expected patterns of secretion of placental hormones, but inhibited completely the increase of PRL in the serum of the mother. Maternal plasma GH concentrations were very high in spite of the treatment and progressively declined after delivery. The plasma GH level was normal in the child, but PRL was very low at birth and increased in the following days. The expected high PRL concentration was found in the amniotic fluid. This case study suggests that bromocriptine crosses the human placenta and affects the fetal pituitary, maternal GH does not influence fetal or amniotic GH, and amniotic fluid PRL correlates poorly with either maternal or fetal blood levels and is not affected by bromocriptine.

Acromegaly↗
PubMed1980

Dopaminergic mechanisms and luteinizing hormone secretion. I. Acute administration of the dopamine agonist bromocriptine does not inhibit luteinizing hormone release in hyperprolactinemic women.

The concept that domapinergic mechanisms control LH secretion by modulation of gonadotropin-releasing hormone (GnRH) has been recently investigated in man. Since hyperprolactinemia is associated with increased hypothalamic dopamine turnover (which may reflect increased dopaminergic activity), inhibition of GnRH by dopamine in this situation would be maximal. Additional stimulation of dopamine receptors by a dopamine agonist would not be expected to result in further inhibition of LH release. Twelve hyperprolactinemic women were studied on 2 days during which measurements of serum PRL and LH were made over 11.5 h. Day 1 served as a control for day 2 when 2.5 mg of the dopamine agonist bromocriptine were administered orally at 0900 h. While serum PRL and LH levels on day 1 showed small fluctuations (+/- 10%), serum PRL on day 2 fell by 82%. Serum LH concentrations on day 2 remained unchanged. The demonstration or the efficacy of bromocriptine in lowering PRL levels documents the expected increase in dopaminergic tone; however, the lack of effect of bromocriptine in surpressing LH release suggests that either there is already maximal endogenous inhibition of GnRH in hyperprolactinemic women or, alternatively, that dopaminergic mechanisms are unimportant in the control of LH secretion.

Adult↗
PubMed1983

alpha-Subunit and gonadotropin responses to luteinizing hormone-releasing hormone in hyperprolactinemic women before and after bromocriptine.

alpha-Subunit and gonadotropin responses to a LHRH infusion (0.2 micrograms/min) for 4 h were studied in eight hyperprolactinemic amenorrheic women, ages 23-40, and in five normal women in the early follicular phase of the menstrual cycle. Basal alpha-subunit and LH concentrations were comparable to normal women; however, basal FSH concentrations were significantly (P less than 0.05) lower. Peak serum alpha, LH, and FSH concentrations during the LHRH infusion were significantly higher than controls (P less than 0.01, P less than 0.05, and P less than 0.01, respectively). Gel chromatography of serum confirmed the presence of both free alpha-subunit and intact LH which had normal biological activity. Six of the women were restudied in the early follicular phase of the cycle after return of normal ovulatory function and normalization of serum PRL concentrations. During bromocriptine therapy, peak serum alpha, LH, and FSH concentrations decreased significantly (P less than 0.02, P less than 0.05, and P less than 0.001, respectively) and were comparable to control subjects. The changes in serum alpha and gonadotropin responses to the LHRH infusion during bromocriptine therapy occurred independently of the serum estradiol concentrations. Abnormalities in the regulation of alpha-subunit and gonadotropin secretion are present in hyperprolactinemia. These abnormalities reverse with bromocriptine therapy and may occur independently of changes in gonadal steroids.

Adult↗
PubMed1984

Use of bromocriptine in a patient with generalized resistance to thyroid hormone.

A 50-yr-old man with a large goiter had elevated serum levels of T4 (22 micrograms/dl), T3 (228 ng/dl), and free T4 (6.6 ng/dl), a high 24-h 131I-thyroidal uptake (69%), and an elevated TSH level (3.6 microU/ml), as well as hyperresponsiveness of TSH to TRH (peak TSH, 47 microU/ml). Normal serum alpha-subunit concentrations and sella turcica films mitigated against the presence of a pituitary tumor. A normal basal metabolic rate and minimally elevated concentration of testosterone-estradiol binding globulin were consistent with generalized resistance to thyroid hormone. Mild lactotroph resistance was also present. The patient was given bromocriptine for 16 months (2.5-10 mg daily). Basal serum TSH levels decreased (less than 0.3-2 microU/ml), as did the TSH response to TRH; serum T4 levels (14-17 micrograms/dl); and 24-h 131I-thyroidal uptake (28%) were reduced. Serum T3 levels, however, changed little. The thyroid gland decreased to normal size, and the basal metabolic rate and testosterone-estradiol binding globulin remained normal. Bromocriptine was stopped for 4 months. Serum TSH increased to 4.5 microU/ml; T4 and T3 increased to 27 micrograms/dl and 328 ng/dl; the patient became clinically mildly hyperthyroid. Thus, bromocriptine in this patient was useful in decreasing TSH secretion and decreasing goiter size, while maintaining clinical euthyroidism. Only a small amount of TSH was necessary to maintain iodine uptake and thyroid hormone synthesis and secretion in a responsive thyroid gland. We speculate that this patient may be secreting a highly bioactive form of TSH and/or have increased thyroid sensitivity to TSH.

Bromocriptine↗
PubMed1984

Bromocriptine therapy for hyperthyroidism due to increased thyrotropin secretion.

We describe a patient with TSH-induced hyperthyroidism successfully treated with bromocriptine. A 25-yr-old woman was found to have hyperthyroidism due to excessive TSH secretion; no pituitary tumor was found. Her serum T4 level ranged between 21.9 and 25.9 micrograms/dl and that of T3 between 283 and 314 ng/dl. Serum TSH was between 5 and 9 microU/ml with an exaggerated response to TRH. Basal metabolic rate was +26 to +38%. Serum PRL was also elevated (79 ng/ml). Administration of bromocriptine for 4 months decreased serum TSH and PRL levels to normal with a concomitant fall in levels of serum T3 and T4. Regression of the clinical manifestations of hyperthyroidism occurred during bromocriptine drug therapy. These results suggest that reduction in hypothalamic dopaminergic tone may have contributed to the inappropriately increased TSH secretion in the patient.

Adult↗
PubMed1984

Reduction of follicle-stimulating hormone (FSH) secretion in FSH-producing pituitary adenoma by bromocriptine.

An FSH-secreting pituitary adenoma was demonstrated in a 32-yr-old man who presented with unilateral optic atrophy without any clinical or laboratory evidence of hypogonadism. Semen analysis was normal, although basal FSH levels were markedly elevated (greater than 80 mIU/ml). He had normal plasma LH levels and no other detectable endocrine abnormalities. Administration of GnRH elicited delayed and sustained FSH and brisk LH responses. Administration of TRH resulted in TSH and PRL responses and unexpected FSH and LH elevations. Two surgical operations resulted in temporary reduction of plasma FSH levels, but it increased later concomitant with CT demonstration of tumor growth. After pituitary irradiation, no reduction in FSH levels occurred. A single dose of 5 mg bromocriptine elicited a significant reduction in FSH levels from 137 to 64 mIU/ml. Long term treatment with 15 mg/day bromocriptine resulted in further reduction of FSH level, to 36.4 mIU/ml, without any change in tumor size. This finding implies that bromocriptine could be an adjunctive therapy or an alternative to other modes of treatment in patients with these rare tumors.

Adenoma↗
PubMed1985

Bromocriptine as primary therapy for prolactin-secreting macroadenomas: results of a prospective multicenter study.

To assess the effectiveness of bromocriptine in reducing the size of PRL-secreting macroadenomas with extrasellar extension, we conducted a prospective multicenter trial in patients without prior radiotherapy, applying a standard protocol of treatment and tumor size evaluation. Basal serum PRL levels [1441 +/- 417 (+/- SEM) ng/ml for women; 3451 +/- 1111 ng/ml for men] fell in all patients and to 11% or less of basal values in all patients but 1. Normal PRL levels were reached in 18 of the 27 patients. In 13 patients (46%), tumor size was reduced by greater than 50%, in 5 patients (18%) by about 50%, and in 9 patients (36%) by approximately 10-25%. The extent of tumor size reduction did not correlate with basal PRL, nadir PRL, percent fall in PRL, or whether PRL levels reached normal. However, a reduction in PRL levels always preceded any detectable change in tumor size. In 19 patients, reduction in tumor size was evident by 6 weeks, but in the other 8, such reduction was not noted until the 6 month evaluation. In the 4 patients in whom bromocriptine was discontinued at the end of 1 yr, tumor reexpansion occurred in 3. Visual fields improved in 9 of the 10 patients in whom they were abnormal. Because of the excellent results found in most of the patients in this series, we suggest that therapy with bromocriptine should be considered as initial management for patients with PRL-secreting macroadenomas.

Adenoma↗
PubMed1987

Role of dopamine in the regulation of growth hormone secretion: dopamine and bromocriptine augment growth hormone (GH)-releasing hormone-stimulated GH secretion in normal man.

The role of the dopaminergic system and its interaction with GH-releasing hormone (GHRH) in the regulation of GH secretion was investigated in normal men in two complementary studies. The men were given continuous iv infusions of 0.15 M saline (5 h), dopamine (4 micrograms/kg X min; 1 h), GHRH (2 ng/kg X min; 2 h), and GHRH (2 ng/kg X min; 2 h) plus dopamine (4 micrograms/kg X min; 1 h) on four separate occasions, and serum GH responses were measured. In a second study, on separate days, placebo or bromocriptine (2.5 mg/dose) was administered, and GH and PRL responses to a single iv GHRH dose were measured. A continuous infusion of dopamine and GHRH on separate days stimulated GH secretion in all subjects. The mean integrated GH secretion was 13.2 +/- 3.1 (+/- SEM) ng/mL X h during the dopamine infusion and 14.7 +/- 4.6 during GHRH, compared with 1.7 +/- 0.4 during the saline infusion. The combination of GHRH and dopamine resulted in the greatest stimulation of GH secretion (29.8 +/- 5.7 ng/ml X h; P less than 0.05 vs. 3 other study days). The oral dopamine agonist bromocriptine also augmented GHRH-stimulated GH secretion. Integrated GH secretion after a single iv injection of GHRH following two doses of bromocriptine was 160 +/- 29.5 ng/ml X h compared with 81.3 +/- 22.2 after placebo (P = 0.04). We suggest that these findings are compatible with the hypothesis that dopamine inhibits hypothalamic somatostatin secretion, which then allows for a greater stimulatory effect of GHRH.

Adult↗
PubMed1991

The efficacy and tolerability of CV 205-502 (a nonergot dopaminergic drug) in macroprolactinoma patients and in prolactinoma patients intolerant to bromocriptine.

We studied the effect of CV 205-502 in 12 patients with macroprolactinomas and 8 patients with PRL-secreting tumors, who were selected because of previous repeatedly shown intolerance to bromocriptine in even small doses. We also investigated serum insulin-like growth factor-I (IGF-I) levels before and during CV 205-502 therapy. In 12 macroprolactinoma patients followed for 1 yr, 0.075-0.450 mg CV 205-502 lowered PRL levels by 91.2 +/- 5.4%. Only 3 of the patients had transient side-effects of nausea, dizziness, or fatigue. In eight patients with PRL-secreting tumors who were bromocriptine intolerant, CV 205-502 (0.075-0.300 mg daily) lowered PRL levels by 80.2 +/- 6.3%. Four of these patients showed transient side-effects (nausea, fatigue, and/or tachycardia). None of the patients discontinued therapy. There was a close correlation between pretreatment circulating PRL levels and tumor size, expressed in cubic millimeters. The decrease in pituitary tumor size after 52 weeks of CV 205-502 therapy (-74 +/- 6%) was also correlated with the decrease in PRL levels (P less than 0.01). In four patients with hypopituitarism, lowered IGF-I levels did not change during CV 205-502 therapy. However, in seven previously untreated patients with macroprolactinoma and normal CV 205-502 is a potent dopaminergic drug, which effectively controls PRL secretion and induces tumor shrinkage. At the doses used in our study, it causes only mild and transient side-effects in a minority of patients and can also be used to treat hyperprolactinemic patients who have shown intolerance to bromocriptine therapy.

Adult↗
PubMed1996

Development of acromegaly during treatment of hyperprolactinemia with bromocriptine: an unusual acidophil stem cell adenoma.

We present clinical details of a patient with a 20-yr history of amennorhea, a pituitary tumor, elevated PRL levels, and initially undetectable GH. Bromocriptine failed to fully suppress PRL, and there was no tumor shrinkage. Within 7 months of starting bromocriptine treatment, the patient developed clinical and biochemical signs of acromegaly. At surgery, a stem cell adenoma was excised. The mechanisms by which bromocriptine may have resulted in the development of acromegaly in this patient are discussed.

Acromegaly↗
PubMed2006

A randomized, double-blind trial of bromocriptine efficacy in nonfluent aphasia after stroke.

The authors assessed the efficacy of bromocriptine in nonfluent aphasia after stroke in a 16-week, randomized, double-blind, placebo-controlled clinical trial conducted from June 2002 to April 2004. In all 38 patients after 4 months of treatment, improvement in both the bromocriptine and placebo treatment groups was observed (p < 0.001). The analysis of repeated-measures analysis of variance revealed bromocriptine did not improve nonfluent aphasia.

Adult↗
PubMed1976

Studies with bromocriptine. Part 1. "On-off" phenomena.

A dopaminergic agonist, bromocriptine, has been studied in patients with idiopathic parkinsonism complicated by severe "on-off" phenomena induced by levodopa. In a "blind" self-evaluating within-patient comparison, fluctuations in clinical state still occurred when levodopa (with or without carbidopa) was replaced with bromocriptine, but they were significantly reduced in frequency. The observation that on-off phenomena can be induced by bromocriptine complicates interpretation of these episodes in terms of pharmacokinetics of levodopa. There may be variations in receptor sensitivity or alterations in the influence of unidentified neurophysiologic mechanisms that modulate striatal output.

Bromocriptine↗
PubMed1976

Studies with bromocriptine. Part 2. Double-blind comparison with levodopa in idiopathic parkinsonism.

A double-blind crossover study was performed in 12 patients with idiopathic parkinsonism to compare their response to bromocriptine with their response to previous optimal drug treatment, including levodopa. There was a 26 percent overall improvement with bromocriptine; rigidity, tremor, and facial expression showed the greatest response. Seven of eight patients who were taking levodopa at the beginning of the study was taken off the drug completely. Adverse reactions were transient and dose-dependent. Bromocriptine promises to be an effective new therapeutic agent in the treatment of idiopathic parkinsonism.

Aged↗
PubMed1979

Bromocriptine and dopaminergic function in Huntington disease.

The cerebrospinal fluid (CSF) content of homovanillic acid (HVA) was assayed in 10 patients with Huntington disease. On doses of less than 40 mg of bromocriptine daily, there was clinical improvement and the CSF HVA concentration increased. On higher doses of bromocriptine, chorea worsened and the CSF HVA concentration decreased. Bromocriptine at low dosage seems to act as a partial dopamine antagonist, with phenothiazine-like effects, and at higher doses it acts as a direct dopamine-receptor stimulating agent.

Adult↗