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PubMed2001

In-vitro and in-vivo evaluation of a matrix-controlled bromocriptine mesilate-releasing vaginal ring.

The aim of this study was to evaluate the in-vitro release rates and in-vivo effectiveness of a controlled release, intravaginal dosage form of bromocriptine mesilate. The dimeticone (poly(dimethylsiloxane)) elastomer vaginal ring contained 3 mg bromocriptine mesilate and low molecular weight gelatin in a ratio of 1:3, and 10% propylene glycol. The daily release rate of the drug was designed to be 10% of the total administered dose and was confirmed with release experiments under sink conditions. The effect of the vaginal ring preparation on plasma prolactin level in the rabbit was investigated over a 10-day period. The results showed that the vaginal ring of bromocriptine mesilate significantly decreased the plasma prolactin level of the test group (P < 0.001-0.05) compared with the control and placebo groups. It was concluded that bromocriptine mesilate was effectively absorbed from rabbit vagina and that this controlled release intravaginal ring preparation of bromocriptine mesilate was effective in decreasing the plasma prolactin level in rabbits for ten days.

Administration, Intravaginal↗
PubMed1980

Long-term efficacy of bromocriptine in Parkinson disease.

Twenty-eight patients with Parkinson disease (PD) were treated with bromocriptine for at least 2 years (mean, 2.8 years; range, 2 to 5 years). All of them had first been treated with levodopa (alone or combined with carbidopa, as Sinemet) for 7.4 years (range, 1 to 10 years). At the time bromocriptine was started, all were showing increasing disability. In these patients, attempts to increase levodopa resulted in adverse effects, and attempts to decrease levodopa resulted in increased parkinsonism. Bromocriptine (mean daily dose, 56 mg) was added to levodopa and resulted in improvement of at least one stage (Hoehn and Yahr scale) in 21 of the patients. After 2 years, five of these patients continue to maintain this improvement. The remaining patients, although there has been deterioration, maintain some of their original improvement. Bromocriptine, when added to levodopa, results in improvement that is maintained, in part, for at least 2 years. The ratio of bromocriptine to levodopa has to be periodically readjusted.

Bromocriptine↗
PubMed1984

Severity of Parkinson's disease and the dosage of bromocriptine.

In view of reports that low-dose bromocriptine (15 mg or less daily) therapy is effective in Parkinson's disease, we undertook a retrospective study of 79 patients with Parkinson's disease to evaluate factors that affect the optimal daily dose of bromocriptine in subjects whose intake of levodopa was decreased as bromocriptine was introduced. Doses of bromocriptine 15 mg or less daily were seldom therapeutic; doses of over 15 mg, up to 30 mg, were appropriate for patients with mild, early disease. Those with more severe symptoms of longer duration usually required larger doses. The optimal daily requirement of bromocriptine was correlated to the severity and duration of the illness, but not to the age of the patient.

Adult↗
PubMed1985

Cerebrospinal fluid rhinorrhea during treatment with bromocriptine for prolactinoma.

A 47-year-old man exhibited loss of libido and impotence in association with plasma hyperprolactinemia and a pituitary mass with downward extension of the tumor to the sphenoid sinus and to the suprasellar cisterns. Bromocriptine, 15 mg daily, reduced the hyperprolactinemia as well as tumor size. After 8 months on this therapy, the patient developed overt CSF liquorrhea. Five days after discontinuation of bromocriptine, the CSF rhinorrhea stopped, and when bromocriptine was given again 2 weeks later, CSF rhinorrhea returned within 3 days. We believe this phenomenon to be due to retraction of tumor by bromocriptine exposing a defect in the sella floor. Transient occurrence of CSF rhinorrhea can be considered as a consequence of tumor regression in patients on bromocriptine. The possibility of this complication, especially in patients with downward extension of tumor, should be noted.

Bromocriptine↗
PubMed1984

[The effects of dopamine agonist (bromocriptine) on the secretion of pituitary gonadotropins and ovarian sex steroids in normally cycling women].

To investigate the effects of bromocriptine on the secretion mechanism of pituitary gonadotropins and ovarian sex steroids, 5 mg of bromocriptine was administered to four normally cycling women in the follicular, pre-ovulatory, mid-luteal or menstrual phase, respectively. Blood samplings were taken from two hours before until six hours after the administration every 15 min. by an intravenous indwelling catheter. Serum FSH, LH, prolactin, estradiol and progesterone were determined by RIA, and the changes of basal levels and the pulsatile patterns of these hormones were analysed in each of the four phases. Serum prolactin levels decreased significantly (p less than 0.005) from two hours after the administration of bromocriptine and remained in a very low range in all phases of the cycles until the end of the experiments. The basal levels of FSH showed a significant decrease in the pre-ovulatory and mid-luteal phases two to six hours after the administration (p less than 0.025 approximately p less than 0.005). Also the basal levels of LH showed a significant decrease in the follicular, pre-ovulatory and mid-luteal phases two to six hours after the administration (p less than 0.05 approximately p less than 0.005). However, no significant change was observed in the amplitude or the frequency of the pulsatile patterns of FSH and LH in all phases of the menstrual cycles. The serum levels of estradiol did not show marked changes by the administration of bromocriptine, but the serum levels of progesterone were significantly decreased in the mid-luteal phase two to six hours after the administration (p less than 0.005). These facts suggest that bromocriptine acts mainly on the pituitary rather than the hypothalamus to decrease the serum levels of gonadotropins, and also may have some role in the steroidogenesis of the ovary.

Bromocriptine↗
PubMed1985

[The effects of bromocriptine on the pulsatile pattern and the circadian profile of gonadotropins and testosterone secretion in normal adult men].

To investigate the effects of bromocriptine on the secretion mechanism of pituitary gonadotropins and testosterone, 5 mg of bromocriptine was administered to five young adult men who were normal in their endocrinological states. Blood samplings were taken from two hours before until six hours after the administration every 15 min., and after that, blood samplings were continued until 21 hours every one hour by an intravenous indwelling catheter. Serum FSH, LH, prolactin and testosterone levels were determined by RIA, and the changes of the pulsatile patterns of FSH and LH, and the circadian profile of these hormones by the administration of bromocriptine were analysed. Serum prolactin levels decreased significantly (p less than 0.005) from two hours after the administration of bromocriptine and remained in a very low range until the end of the experiment. The basal levels of FSH showed a significant decrease from two to six hours after the administration (p less than 0.005). Also the basal levels of LH showed a significant decrease from two to six hours after the administration (p less than 0.005). However, the basal levels of serum FSH and LH did not show significant decreases after that until the end of the experiment. No significant change was observed in the amplitude or the frequency of the pulsatile patterns of FSH and LH until six hours after the administration of bromocriptine. The serum levels of testosterone were also significantly decreased from two to six hours after the administration (p less than 0.005), but they did not show a significant decrease after that until the end of the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Effects of bromocriptine and tamoxifen on growth and hormone receptor levels of 7,12-dimethylbenz(a)anthracene-induced mammary tumors in rats.

The role of prolactin (PRL) and estrogen in the growth of 7,12-dimethylbenz(a)-anthracene (DMBA)-induced rat mammary tumors was investigated. Tumor growth was suppressed by both bromocriptine and tamoxifen. Combined administration of ovine PRL and tamoxifen attenuated the inhibitory action of tamoxifen on tumor growth. Serum PRL levels were decreased by both bromocriptine and tamoxifen administration. Estrogen receptors (ER) in tumor tissues were decreased in number by tamoxifen, but not by bromocriptine. Progesterone receptors (PgR) in DMBA-induced mammary tumors were abolished by tamoxifen and significantly reduced by bromocriptine. Combined administration of ovine PRL with tamoxifen attenuated the inhibition of PgR induced by tamoxifen alone, while ER remained undetectable. Specific PRL binding to the liver was significantly reduced by treatment with bromocriptine, tamoxifen and tamoxifen plus ovine PRL, whereas PRL receptors in mammary tumor were not influenced by these drugs. These results suggest that PRL may stimulate DMBA-induced tumor growth independently of ER and that a part of the inhibiting effect of tamoxifen on tumor growth may be explained by the decreased PRL secretion.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1992

Beneficial effects of high daily dose bromocriptine treatment in Cushing's disease.

Treatment with a high daily dose bromocriptine was evaluated in 6 Cushing's disease patients (4 females and 2 males; aged 23 to 56 years). The highest doses administered were 40 mg to patient 1, 55 mg to patient 2, 35 mg to patient 3, 25 mg to patient 4, 25 mg to patient 5, and 17.5 mg to patient 6. The former 3 cases, 2 (patients 1 and 2) of whom were previously reported and further followed up, showed clinical and biochemical improvement with the regimen. Patient 1 who obtained remission with 40 mg/day has been on remission for further 14 months with a total of 36 months. Patient 2, who had a reduction in pituitary tumor size with 35 mg daily, relapsed thereafter. The therapy, however, resolved the paradoxical responses of plasma ACTH and cortisol to arginine. Readministration of bromocriptine resulted into another clinical and biochemical improvement with 45 to 55 mg/day. Patient 3, a relapsed case after a remission with reserpine plus pituitary irradiation, showed an improvement in the 24-h urinary free cortisol excretion with 35 mg/day. Patient 4 was the only case who had a marked decrease in plasma cortisol (basal; 16.3, nadir; 1.9 micrograms/dl) after a single-dose bromocriptine test among the 5 cases tested. The patient had favorable response with 25 mg/day for 2 months but the dose was not increased after an escape. Patient 5 received the drug in 4 occasions, 7.5 to 25 mg/day, in combination with several agents, which failed to induce clinical remission. The last patient did not respond to a maximum dose of 17.5 mg/day. These observations suggest that, regardless of the result of a single-dose bromocriptine test, treatment with a high daily dose of bromocriptine, 35 mg or more, may be necessary to obtain a favorable clinical response and normal cortisol secretion.

Adrenocorticotropic Hormone↗
PubMed1979

Effect of bromocriptine (CB-154) on oestrogen-induced prolactin release.

In order to study the interaction between oestrogens and bromocriptine on PRL release, we evaluated the ability of bromocriptine (CB-154) to counteract the oestrogen-induced PRL release in four hyperprolactinaemic amenorrhoeic women. Bromocriptine acutely administered induced a similar percentage of PRL decrease in the same patient before and after oestrogen administration. When bromocriptine was chronically administered, contemporary oestrogen injection did not affect PRL release. These results show that bromocriptine is able to block the release of PRL induced by oestrogens, suggesting an interaction between oestrogens and DA-mimetic compounds on PRL release.

Adult↗
PubMed1979

Persisting suppression of prolactin secretion after long-term treatment with bromocriptine in patients with prolactinomas.

The effect of bromocriptine withdrawal after long-term treatment on prolactin levels has been investigated in thirty-seven patients with prolactinomas. In ten patients with macroprolactinomas and post-operatively excessively high prolactin levels persisting suppression of prolactin secretion after bromocriptine withdrawal has been observed. This effect was not observed in patients with microprolactinomas or macroprolactinomas with only moderately elevated prolactin levels. The degree of persisting suppression correlated to the height of prolactin levels before treatment and to the duration of bromocriptine therapy. No correlation was found between the rise of prolactin levels after bromocriptine withdrawal and withdrawal time. It is suggested that the persisting suppression of prolactin levels is a sequence of reduction in tumour size. This anti-proliferative action of bromocriptine seems to be specific for the prolactin secreting cells in macroprolactinomas with high proliferation rate and high prolactin turn-over. These findings offer new possibilities in the management of patients with macroprolactinomas.

Adenoma↗
PubMed1982

Effect of bromocriptine and metergoline in the treatment of hyperprolactinaemic states.

The effects of bromocriptine or metergoline treatment were evaluated in 80 hyperprolactinaemic patients (62 women and 18 men). The patients were subdivided into 4 groups: group A) 16 women with idiopathic hyperprolactinaemia; group B) 19 women with untreated Prl-secreting microadenomas; group C) 27 women with unsuccessfully operated prolactinomas; group D) 18 men with unsuccessfully treated macroprolactinomas. Sixty-eight patients were given bromocriptine (2.5-20 mg/day) for 3-58 months and 33 patients were given metergoline (4-16 mg/day) for 3-19 months. Bromocriptine and metergoline were equally effective in the treatment of functional hyperprolactinaemia and of untreated microadenomas, while bromocriptine showed a more potent Prl-lowering effect than metergoline in patients with higher Prl levels and large prolactinomas; both drugs restored the gonadal function to a similar extent, though metergoline was effective in some cases, even in the absence of full Prl suppression. Bromocriptine seems to exert an antitumoral effect, as documented by CT scan in some patients with macroadenomas, but the precise role of both drugs with respect to dose, length of treatment and effectiveness after withdrawal needs to be evaluated further.

Adenoma↗
PubMed1983

The role of prolactin in the inhibitory action of bromocriptine on growth hormone secretion in acromegaly.

UNLABELLED: Bromocriptine treatment results in clinical improvement and inhibition of plasma GH levels in only part of the acromegalic patients. The possible role of the simultaneous presence of Prl and GH in GH-secreting pituitary adenomas was investigated with regard to the inhibitory action of bromocriptine on GH secretion and the paradoxical increase of GH release in reaction to TRH. Surgically obtained pituitary tumour tissue from 35 consecutive acromegalic patients was studied immunohistochemically. In 21 patients no Prl was present in the tumour tissue. These patients had normal plasma Prl levels. In the other 14 patients Prl was present in the tumour tissue. Hyperprolactinaemia was found in 10 of these 14 patient. Plasma GH levels from 2 till 10 h after the administration of 2.5 mg bromocriptine measured before operation were significantly more suppressed in the patients with mixed GH/Prl-containing than in those with pure GH-containing pituitary adenomas, being 38 +/- 4% and 65 +/- 4% of basal values, respectively (P less than 0.01). The response of GH to TRH, however, did not differ significantly between the two groups. CONCLUSIONS: 1. In about 70% of patients with 'mixed' GH/Prl containing adenomas, hyperprolactinaemia is present. 2. The simultaneous presence of Prl and GH in a GH-secreting pituitary tumour increases the sensitivity of GH secretion to bromocriptine. 3. The plasma Prl level is of value to predict which patients with acromegaly are likely to respond to bromocriptine with an inhibition of GH secretion.

Acromegaly↗
PubMed1995

Octreotide, but not bromocriptine, increases circulating insulin-like growth factor binding protein 1 levels in acromegaly.

Twenty-three patients with active acromegaly underwent serum sampling for growth hormone (GH), insulin and insulin-like growth factor binding protein 1 (IGFBP-1) after placebo or single doses of octreotide or bromocriptine. Integrated 24-h serum GH levels decreased by 90% after octreotide and 49% after bromocriptine. A statistically significant correlation between the course of GH levels after octreotide and bromocriptine was observed (p < 0.001). Octreotide, but not bromocriptine, induced a significant increase in integrated 24-h serum IGFBP-1 levels to 37.4 times the baseline values. Bromocriptine caused a non-significant increase in integrated 24-h serum IGFBP-1 levels, which argues against a direct regulatory effect of GH on IGFBP-1 production in acromegaly. In conclusion, octreotide induces in acromegaly the production of IGFBP-1, which occurs independently of the number of somatostatin receptors on the GH-secreting pituitary adenoma. The supposed inhibitory effect of IGFBP-1 on the biological effect of IGF-1 might result in an additional clinical benefit in acromegalic patients as compared to treatment directed at the pituitary level.

Acromegaly↗
PubMed1989

Effect of pentobarbitone sodium and bromocriptine on follicular oestradiol production in the rat.

Injection of an ovulation-blocking dose of pentobarbitone sodium given in the early afternoon of pro-oestrus in rats decreased follicular oestradiol production in vitro the next day (2.42 +/- 0.11 ng/4 h/follicle in pro-oestrous rats, 0.49 +/- 0.04 ng/4 h/follicle in pentobarbitone-treated rats). Pentobarbitone, given 1 day earlier (at dioestrus II), prevented the increase in oestradiol production that normally occurs between di-oestrus II and pro-oestrus. Injection of a subovulatory amount of hCG (0.5 i.u.) given after pentobarbitone injection inhibited the decrease in follicular oestradiol production induced by pentobarbitone. The pentobarbitone-induced decrease in oestradiol production was also prevented by bromocriptine (1 mg) given at di-oestrus II (15:00 h) and pro-oestrus (09:00 h). Bromocriptine is an effective inhibitor of prolactin secretion and this suggests therefore that the decrease in follicular oestradiol production after pentobarbitone is due to the preovulatory surge of prolactin. However, pretreatment with bromocriptine also inhibited the effect of pentobarbitone on oestradiol production when pentobarbitone was given at di-oestrus II. Moreover, when ergocornine (another inhibitor of prolactin secretion) was used instead of pentobarbitone to block ovulation, follicular oestradiol production was also decreased the next day. In contrast to bromocriptine, ergocornine was not able to prevent the pentobarbitone-induced decrease in follicular oestradiol production. These results indicate that the decrease in follicular oestradiol production after pentobarbitone injection is due to inhibition of the serum concentrations of LH rather than the preovulatory surge of prolactin. How bromocriptine (but not ergocornine) prevents the pentobarbitone-induced decrease in oestradiol production is not clear.

Animals↗
PubMed1987

13 trisomy born to a mother treated with bromocriptine: incidental or not?

A case of 13 trisomy born to a mother treated with bromocriptine is described. She, 27 years old, was treated with bromocriptine (5 mg/day) as a galactorrhea amenorrhea syndrome with hyperprolactinemia (basal 34-122 ng/ml). After the treatment for about a month, disappearance of galactorrhea and occurrence of menstruation were observed. She became pregnant on the second ovulation. On the 34th week she got a male 13 trisomy (47, XY, +13) baby with premature delivery. The baby died 11 hr after his birth. After the first delivery, bromocriptine was readministered. Following the induced abortion on the second pregnancy, she borned a healthy baby on the third pregnancy in spite of taking bromocriptine. This case of 13 trisomy might be incidental. However, the effect of bromocriptine on chromosome should be further evaluated in detail.

Adult↗
PubMed1984

Effects of bromocriptine and naloxone on plasma levels of prolactin, LH and FSH during suckling in the female rat: responses to gonadotrophin releasing hormone.

The roles of dopamine and the endogenous opiate peptides in the mediation of the inverse relationship between prolactin and gonadotrophin secretion during lactation were studied by comparing the effects of bromocriptine and naloxone on plasma levels of prolactin, LH and FSH during suckling in the female rat. The effects of exogenous gonadotrophin releasing hormone (GnRH) on the LH and FSH responses to bromocriptine and naloxone were also assessed. In control animals (saline), there was a marked fall in LH levels and a large increase in prolactin levels within 15 min of suckling. In response to GnRH (25 ng) there was a small progressive increase in LH levels reaching a maximum at 45 min. Both bromocriptine (500 micrograms) and naloxone (500 micrograms) markedly suppressed the suckling-induced prolactin surge when administered in two separate groups of animals. However, despite the bromocriptine-induced suppression of prolactin levels, there was no increase in LH levels which remained low throughout the suckling period. Naloxone (500 micrograms), however, induced a twofold increase in LH levels within 15 min suggesting that an enhanced opiate rather than dopaminergic activity may be responsible for the suppression of GnRH and hence gonadotrophin secretion during suckling. This is supported by the finding that whereas combined bromocriptine (500 micrograms) and GnRH (25 ng) treatment suppressed the suckling-induced prolactin rise and also induced only a small progressive increase in LH (similar to GnRH alone), combined naloxone (500 micrograms) and GnRH (25 ng) treatment induced a sharp sixfold increase in LH levels within 15 min while at the same time markedly suppressing prolactin levels. None of these drug treatments affected the levels of FSH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Hormone concentrations, mammary development and milk yield in goats given long-term bromocriptine treatment in pregnancy.

Ten British Saanen goats were treated daily with 5 mg bromocriptine intramuscularly from week 8 of pregnancy until week 20 (day 140). By comparison with untreated control goats (n = 8), concentrations of prolactin in plasma were suppressed throughout the treatment period and remained significantly lower until 3 days prepartum, parturition occurring on day 153 +/- 0.7 (mean +/- S.E.M., n = 10). Growth hormone concentrations were low, but the incidence of levels exceeding 1 microgram/l was increased in bromocriptine-treated goats. Plasma concentrations of placental lactogen, progesterone and oestrone sulphate were unaffected. The accumulation of pre-colostrum in the udder (lactogenesis stage I) was not affected by bromocriptine treatment in goats carrying twin fetuses, but in goats with single kids it was delayed by about 4-6 weeks to week 17 of pregnancy. Secretion could not be expressed from the udder and the concentration of alpha-lactalbumin in plasma remained low. Udder volume was significantly reduced in week 15-16 but not week 20-21 of pregnancy by bromocriptine treatment. Milk yields after 50 or 203 days of lactation were not significantly different from those in control goats. Placental lactogen concentrations in late pregnancy and udder volume in week 20-21 were the only variables measured which correlated with milk yield post partum. It is concluded that in vivo placental lactogen is an effective mammotrophic hormone, although less potent than prolactin as evidenced by the delay in lactogenesis stage I in bromocriptine-treated goats bearing single kids.

Animals↗
PubMed1987

Influence of bromocriptine and oestrogen on prolactin synthesis, secretion and tumour growth in vivo in rats.

The effects of diethylstilboestrol implants and bromocriptine administration on serum prolactin concentrations, prolactin messenger RNA (mRNA) and pituitary tumour weight were examined. Intact female Fischer 344 rats were implanted s.c. with 10 mg diethylstilboestrol (DES) under light anaesthesia. All animals except the control group carried the implant for 7 weeks at which time the rats were subdivided into five groups: A, control; B, DES for 7 weeks; C, DES for 7 weeks followed by withdrawal of DES for 1 week; D, DES for 7 weeks followed by withdrawal of DES and administration of bromocriptine for 1 week; E, DES for 8 weeks with concurrent administration of bromocriptine during the last week. Serum concentrations of prolactin were measured by radioimmunoassay, prolactin mRNA concentrations were measured by dot-blot hybridization and sodium dodecylsulphate-polyacrylamide gel electrophoresis of the in-vitro translated mRNA. Pituitary growth was estimated by changes in pituitary weight and assessed by light and electron microscopic examination. Treatment with DES dramatically increased serum prolactin concentrations and prolactin mRNA and induced pituitary tumour formation as shown by histological changes. Withdrawal of DES for 1 week did not lead to a decrease in pituitary tumour weight but was accompanied by a decrease in serum prolactin concentrations and prolactin mRNA from peak concentrations although they remained significantly increased above controls. Treatment with bromocriptine after DES implants were removed led to a significant reduction in pituitary tumour weight and a decrease in serum prolactin concentrations and prolactin mRNA. Histology of the pituitary tumour after the bromocriptine treatment showed pituitary cells similar to those from normal animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗