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PubMed1984

Effects of bromocriptine on pituitary organelle marker enzyme activities in lactating and postlactating rats: selective activation of lysosomal prolactin proteolytic activity.

Effects of the dopamine agonist 2-bromo-alpha-ergocryptine (bromocriptine) on plasma and pituitary PRL and enzyme activities in lactating and postlactating rats have been investigated. Lactating rats which had been suckling their young for 3 days were given a single sc injection of bromocriptine or solvent. The treated and control animals were divided into 2 further groups. One group (lactating rats) was permitted to suckle their pups for a further 12 or 24 h; the young were removed from the other group (postlactating rats). Homogenates were prepared from the anterior pituitaries and assayed for organelle marker enzyme activities. When 0.5-500 micrograms bromocriptine were administered to lactating rats for 24 h, pituitary PRL was increased by all doses, but only the 500-micrograms dose significantly reduced plasma PRL. Total protein was unchanged, lysosomal acid PRL proteolytic activity increased 8-fold, N-acetyl-beta-glucosaminidase and beta-glucuronidase (lysosomes) were unchanged, acid phosphatase (lysosomes and endoplasmic reticulum) was increased by three of four doses, 5'-nucleotidase and alkaline phosphatase (plasma membrane) were increased 4-fold, neutral-alpha-glucosidase (endoplasmic reticulum) and malate dehydrogenase (mitochondria) were unchanged, and catalase (peroxisomes) was significantly increased. Bromocriptine (500 micrograms) administration to lactating and postlactating rats for 12 and 24 h significantly decreased the pituitary DNA but not the total protein content of the pituitaries in all animals. The lysosomal acid PRL proteolytic activity and the lysosomal enzyme activities, N-acetyl-beta-glucosaminidase and beta-glucuronidase, were increased by suckling withdrawal alone. Acid PRL proteolytic activity was further increased (to 18-fold) by coadministration of bromocriptine, whereas the increase in the activities of the other lysosomal marker enzymes was blocked. Malate dehydrogenase activity (mitochondria) was also increased by litter removal and blocked by bromocriptine. The activity of the plasma membrane markers 5'-nucleotidase and alkaline phosphatase were increased by litter removal, and bromocriptine further increased both enzyme activities. The activity of neutral-alpha-glucosidase (endoplasmic reticulum) was unchanged by any treatment. The results demonstrate that bromocriptine produces significant changes in the activities of lysosomal marker enzymes, particularly acid PRL proteolytic activity, as well as marker enzymes of plasma membranes and other organelles in pituitaries of lactating and postlactating rats.

5'-Nucleotidase↗
PubMed1990

Bromocriptine increasingly suppresses the in vitro gonadotropin and alpha-subunit release from pituitary adenomas during long term culture.

Prolonged treatment with bromocriptine may lead to a decrease in tumor size in patients with a gonadotroph, alpha-subunit-secreting, or clinically nonfunctioning pituitary adenoma. The effectiveness of the treatment, however, may depend on its duration. We investigated the effects of prolonged incubation with bromocriptine on the release and intracellular hormone and alpha-subunit concentrations in 10 such adenomas in vitro. The release of FSH, LH, alpha-subunit, or a combination of these was demonstrated in 7 tumors. Bromocriptine significantly suppressed this release in 6 tumors. In 5 tumors bromocriptine had an inhibitory effect on gonadotropin and/or alpha-subunit release which increased with duration of culture. Withdrawal of bromocriptine during the culture period led to a recovery of gonadotropin or alpha-subunit release in the 2 tumors in which it was tested. Intracellular hormone and alpha-subunit concentrations in 3 of 4 tumors cultured for 4 or more weeks were significantly lower in bromocriptine-treated than in untreated cells. We conclude that 1) bromocriptine can suppress the in vitro release of gonadotropins and alpha-subunit from the majority of clinically nonfunctioning, gonadotroph, and alpha-subunit-secreting pituitary adenomas; 2) during prolonged incubation of these tumors with bromocriptine, this drug has a time-dependent increasing inhibitory effect on the release and synthesis of gonadotropins and alpha-subunit, which eventually may lead to decreased intracellular concentrations of these glycoproteins.

Adenoma↗
PubMed1986

Attenuated development of hypertension by chronic administration of bromocriptine in Doca-salt hypertensive rats.

The aim of the study was to investigate whether or not the development of hypertension is influenced by chronic treatment with bromocriptine and/or domperidone. Rats treated with DOCA-salt were divided into 4 groups: control with vehicle, bromocriptine, bromocriptine with domperidone, and domperidone. Increased blood pressure by DOCA-salt treatment was significantly suppressed by treatment with bromocriptine and this bromocriptine suppression was significantly blocked by treatment with domperidone. Increased urinary excretion of norepinephrine by DOCA-salt treatment was significantly suppressed by bromocriptine and the inhibiting effect of bromocriptine disappeared with domperidone. In the four groups of rats, there were significant correlations between systolic blood pressure and urinary excretion of norepinephrine, systolic blood pressure and urinary excretion of epinephrine, and urinary excretion of dopamine and sodium. These results suggest that the chronic effect of bromocriptine is to suppress development of DOCA-salt hypertension, mainly through peripheral mechanisms which are involved in the decreased release of norepinephrine.

Animals↗
PubMed1998

[Comparative studies on antiparkinsonian agents, talipexole and bromocriptine, evaluated by contralateral rotational behavior in unilaterally nigral-lesioned rats].

The stimulating effect of antiparkinsonian drugs, talipexole and bromocriptine, on the striatal postsynaptic dopamine receptors were studied by measuring contralateral rotational behavior in rats. The nigro-striatal dopamine system of rats was degenerated by unilateral injection of 6-hydroxydopamine (6-OHDA, 8 micrograms/rat) into substantia nigra. By subcutaneous administration, talipexole at 0.16 mg/kg and bromocriptine at 10.24 mg/kg induced significantly increased rotational behavior to the contralateral direction to the lesioned side. The onset of the effect was 30 min for talipexole and 90 min for bromocriptine. By intragastric administration, talipexole at 0.4 mg/kg and bromocriptine at 20.48 mg/kg significantly increased the rotational behavior, and the onset of the effect was 60 min for talipexole and 180 min for bromocriptine. Rotational behavior induced by talipexole was suppressed by a D2 antagonist, sulpiride (40 mg/kg, s.c.), but not by a D1 antagonist, SCH23390 (1 mg/kg, s.c.). In contrast, rotational behavior induced by bromocriptine was suppressed by both sulpiride and SCH23390. These results indicated that when the nigrostriatal dopaminergic functions are disrupted, talipexole stimulates the striatal postsynaptic dopamine receptors at much lower doses than bromocriptine. Also it was indicated that the stimulating effect of talipexole is solely mediated by dopamine D2 receptors, whereas the effect of bromocriptine is mediated by both D1 and D2 receptors.

Administration, Oral↗
PubMed1986

[Histological changes and operative findings of pituitary adenomas after bromocriptine treatment].

Twenty-eight patients with various types of pituitary adenomas were studied endocrinologically and neuroradiologically. We observed the changes of tumor size during bromocriptine treatment. After various periods of bromocriptine therapy, we operated on these tumors and examined then histologically. One of 5 patients with nonfunctioning adenomas improved remarkably in his visual field and acuity after 7-month bromocriptine therapy. The pathological findings disclosed remarkable changes in tumors composed of shrunken island-like cell nests and acellular spaces. These shrunken island-like cell nests were composed of tumor cells whose cytoplasmic volume decreased and whose nuclear chromatin clumped. In acellular spaces, there were irreversibly destructed tumor cells, hyaline substances, tumor cell debris and collagen fibrils. One of 8 cases of acromegalies showed a remarkably reduced tumor on CT with clinical improvement after treatment with bromocriptine for 10 months. This patient's serum growth hormone titer was raised by an abnormal response to intravenously injected TRH (thyrotropin releasing hormone), and his serum prolactin was abnormally high. Therefore, this tumor was thought to be a mixed adenoma with growth hormone secreting and/or prolactin secreting cells. Histological examinations disclosed cell shrinkage of tumor cells. Interestingly, there were scanty fibrotic changes in this tumor in spite of the long term bromocriptine therapy. In 15 cases of prolactinomas, the larger the tumor size and the longer the period of the bromocriptine therapy, the more fibrosis was seen. Under a period of bromocriptine therapy longer than 3 months, the fibrotic changes of tumor progressed, and this made more difficulty in selective adenomectomy even in the case of intrasellar adenomas. Therefore we thought that transsphenoidal surgery could successfully be done within 3 months during continuation of bromocriptine therapy.

Acromegaly↗
PubMed1986

Long-term bromocriptine therapy and predictive tests in acromegaly.

The value of predictive tests in bromocriptine therapy and the effects of long-term bromocriptine therapy were investigated in acromegalic patients. In 72 acromegalic patients, there was a tendency for patients with a plasma GH response to TRH or with an elevated basal plasma PRL level, but without a plasma GH response to LHRH, to have a plasma GH response to bromocriptine, though statistical analysis did not reveal a significant difference. Acute and chronic effects of bromocriptine were significantly interrelated, while the chronic effect of bromocriptine and abnormal plasma GH response to TRH or elevated plasma PRL levels were not, in 18 acromegalic patients. These results suggest that the acute bromocriptine test is a better predictor than the TRH test and plasma PRL levels for evaluating the effects of chronic bromocriptine therapy. To maintain the low plasma GH levels, increasing doses of bromocriptine were needed in most patients, and failure to control the elevated GH level despite increasing doses was observed in 2 of 18 patients.

Acromegaly↗
PubMed1989

The combination therapy with bromocriptine and cyproheptadine in patients with acromegaly.

The therapeutic efficacy of the combination of cyproheptadine and bromocriptine was studied in 15 patients with active acromegaly showing incomplete GH suppression in response to bromocriptine therapy alone. The mean basal plasma GH was 31.3 +/- 5.5 micrograms/L, and it decreased to 19.0 +/- 3.9 micrograms/L during the single bromocriptine therapy (10 to 20 mg for 2 to 21 months). When cyproheptadine (12 to 16 mg for 8 to 52 months) was added to bromocriptine therapy, plasma GH decreased further (9.4 +/- 3.0 micrograms/L: vs pretreatment, P less than 0.001; vs bromocriptine treatment, P less than 0.005), and GH normalization was obtained in 8 patients. The plasma somatomedin-C levels in these 8 patients (0.3-1.8 U/ml) were within the normal range during the combination therapy. Plasma GH responses to TRH or GHRH were markedly suppressed in 6 patients during the combination therapy compared to pretreatment or during bromocriptine treatment. In addition, a clear reduction in the tumor size was observed in 4 of 7 previously untreated patients during the combination therapy. In conclusion, cyproheptadine has therapeutic efficacy in acromegalic patients who showed incomplete GH suppression in response to treatment with bromocriptine alone. Following the cyproheptadine and bromocriptine combination therapy tumor shrinkage was observed in some patients.

Acromegaly↗
PubMed1985

Effects of bromocriptine on hormone production and cell growth in cultured rat pituitary cells.

Rat pituitary adenoma cells (GH3) that spontaneously synthesize and secrete both prolactin (Prl) and growth hormone (GH) were used in this study. Bromocriptine (5 X 10(-5) mol/l), a dopamine (DA) agonist, induced a rapid reduction in Prl and GH secretion with maximum effect (approximately 60%) after 15 min of treatment. Bromocriptine also inhibited Prl and GH production in a time- and dose-dependent manner with ED50 at 4 X 10(-6) mol/l and 7 X 10(-6) mol/l, respectively. Maximum effect was obtained at 5 X 10(-5) mol/l of bromocriptine which after 24 h of treatment reduced the production of Prl and GH by approximately 70 and approximately 50%, respectively. After 9 days of treatment both Prl and GH production was reduced by more than 95%. Bromocriptine also reduced cellular growth rate. The ED50 was approximately 1 X 10(-5) mol/l and the maximum effect (greater than 50%) was observed at 5 X 10(-5) mol/l. All effects of bromocriptine were reversible upon cessation of treatment. The antiproliferative effect of bromocriptine was also observed using a rat hepatoma cell line (MH1C1) and a human epithelial cell line (HE), suggesting a non-receptor mediated growth inhibition at high concentrations of the drug. In conclusion, the inhibitory effect of bromocriptine on secretion and production of both Prl and GH in GH3 cells occurs at a lower concentration than its effect on cell proliferation. The pharmacological effects of bromocriptine in vivo on Prl and GH producing adenomas may be explained by an action directly at the pituitary level.

Adenoma↗
PubMed1987

The rapid diagnosis of sensitivity or resistance to dopamine agonists with depot bromocriptine.

Some patients with hyperprolactinaemia are unable to tolerate even low doses of oral bromocriptine. In such cases, it is difficult to predict whether serum prolactin might be normalized if higher doses could be tolerated, or whether true resistance to bromocriptine is present. We have investigated 8 such patients who were subjected to a dopamine infusion (4 micrograms/kg per min for 4 h), followed by an injection of 50 mg of depot bromocriptine on a separate occasion. Serum prolactin was normalized in 4 patients during dopamine, and in 6 patients 12-48 h following depot bromocriptine. The 2 patients who failed to respond to depot bromocriptine also failed to respond to high oral doses of bromocriptine, while the remaining 6 patients were successfully transferred to oral bromocriptine without adverse reactions after the depot preparation was administered, and with a normalization of serum prolactin. It is concluded that depot bromocriptine may represent a better predictor of true unresponsiveness to dopamine agonist therapy than a dopamine infusion, and may also allow for initiation onto oral therapy of previously intolerant patients.

Administration, Oral↗
PubMed1996

Prolactinomas resistant to bromocriptine: long-term efficacy of quinagolide and outcome of pregnancy.

Resistance to bromocriptine, defined as the absence of normalization of prolactin (PRL) levels despite a 15-30 mg daily dose of bromocriptine during at least 6 months, has been observed in 5-17% of the prolactinomas according to the literature. The recent availability of a new potent dopamine agonist, quinagolide, prompted us to analyze its long-term therapeutic effects in 28 patients with prolactinomas resistant to bromocriptine. Before bromocriptine, their PRL levels were 520 +/- 185 micrograms/l (mean +/- SEM) and decreased to 291 +/- 154 micrograms/l after a 6-21 month period of bromocriptine treatment. All the women (N = 20) remained amenorrheic and hypogonadism was not improved in men (N = 8). Subsequently, after 1 year of 150-300 micrograms/day quinagolide, 12/28 patients of the present series recovered normal gonadal function and their initial mean baseline PRL value (404 +/- 180 micrograms/l) was 16 +/- 2 micrograms/l after 1 year of treatment. A significant tumor shrinkage was observed in 5/8 macroadenomas (62%). During the 3-year follow-up period under quinagolide, a similar good control was achieved in these patients, with the exception of one man presenting with a secondary rise of PRL under quinagolide. In contrast, 15 other patients (one patient interrupted quinagolide at 6 months because of poor tolerance) were not normalized under 150-450 micrograms/day quinagolide. Their initial PRL levels (606 +/- 298 micrograms/l) were reduced to 343 +/- 187 micrograms/l (versus 463 +/- 265 micrograms/l under bromocriptine after the same duration of treatment). Despite such a partial inhibitory effect of quinagolide, 7/12 women resumed menstrual cycles and three pregnancies occurred. In no case was any tumor shrinkage noticed during the 3-4-year follow-up. Three patients even presented, after 2 years of quinagolide treatment, with a secondary rise of PRL values associated with a further tumor growth in two patients. During the 3-year follow-up period, nine pregnancies occurred in seven women. In five women, after quinagolide withdrawal, the plasma PRL baseline values ranged from 52 to 158 micrograms/l and from 65 to 192 micrograms/l, respectively, at the first trimester and at the end of uneventful pregnancies. In contrast, in two women a rapid increase of PRL (240-400 micrograms/l) correlated with tumor growth during the first trimester. Such a tumor progression was blocked by quinagolide treatment but not by bromocriptine. These data, although observed in a limited series, justify the careful follow-up of pregnancies in this subclass of patients at risk. Finally, in the whole population, long-term control of hyperprolactinemia by quinagolide was obtained in 11/28 patients (39%) previously resistant to bromocriptine, and 15/20 women (75%) resumed normal gonadal function with a quinagolide daily dose of 300 micrograms in most of them.

Aminoquinolines↗
PubMed2001

Comparison of the effects of cabergoline and bromocriptine on prolactin levels in hyperprolactinemic patients.

OBJECTIVE: It is well known that bromocriptine has a suppressive effect on the prolactin release in hyperprolactinemic patients. But it also has some adverse effects. The new, long-acting dopaminergic drug, cabergoline, has been reported to be an effective agent in these patients. However, there are relatively few reports comparing the beneficial and adverse effects of these drugs in the treatment of hyperprolactinemic patients. Therefore, here we studied and compared the efficacy and tolerability of cabergoline with bromocriptine in hyperprolactinemic patients. PATIENTS: Seventeen patients (7 with microprolactinoma, 4 with macroprolactinoma, 6 with idiopathic hyperprolactinemia) were given bromocriptine at a dose of 2.5 mg (or 5 mg for macroprolactinomas) twice daily, and 17 patients (8 with microprolactinoma, 4 with macroprolactinoma, 5 with idiopathic hyperprolactinemia) were given cabergoline at a dose of 0.5 mg twice weekly for 12 weeks. RESULTS: At the end of the study, the prolactin reduction was significantly greater in the cabergoline group than in the bromocriptine group (-93 vs. -87.5 %, respectively, p < 0.05). Normalization of prolactin levels was achieved in 10 of 17 patients (59%) in the bromocriptine group, and in 14 of 17 patients (82%) in the cabergoline group (p = 0.13). Two patients (50%) with macroprolactinoma in the bromocriptine group and three patients (75%) with macroprolactinoma in the cabergoline group demonstrated a normalization of their serum prolactin levels. Adverse events were noted in 53% of bromocriptine patients and in 12% of cabergoline patients (p < 0.01). CONCLUSION: These data indicate that cabergoline is a very effective agent for lowering the prolactin levels in hyperprolactinemic patients and that it appears to offer considerable advantage over bromocriptine in terms of efficacy and tolerability.

Adult↗
PubMed1987

Prolactin-secreting adenomas: the preoperative response to bromocriptine treatment and surgical outcome.

Controversy exists regarding the effects of bromocriptine on the success of transsphenoidal surgery for patients with prolactinomas. Various studies on this drug have reported adverse effects, improvement, and no effect upon the subsequent surgical outcome. The authors have retrospectively reviewed the case histories of 55 patients with immunocytochemically confirmed prolactin-secreting pituitary adenomas operated on by a transsphenoidal approach between 1981 and 1985. All patients had received bromocriptine in a variety of doses and for variable durations prior to surgery. Thirty-nine patients were women and 16 were men, with an age range of 8 to 72 years. Basal prolactin levels prior to bromocriptine treatment ranged from 38 to 100 ng/ml in 11 patients, from 101 to 200 ng/ml in 12, and greater than 200 ng/ml in 29. The "cure" rates were 54%, 58%, and 38%, respectively. Thirty-one patients had microadenomas, with a postoperative cure rate of 68%; 12 had diffuse expansive adenomas, with a 17% cure rate; and 12 had grossly invasive tumors, with a 17% cure rate. A response to preoperative bromocriptine therapy was defined as a return of the basal prolactin level to normal: 18 patients were responders and 29 were hyporesponders; in eight the data were not available. The postoperative cure rate was 50% for the responders and 31% for the hyporesponders. Taking into account the distribution of tumor type, there was no actual difference in outcome between the responder and the hyporesponder groups. The total bromocriptine dose received preoperatively was nearly identical for all groups. No significant differences in the frequency or extent of fibrosis, calcification, or prolactin immunoreactivity were observed in the 55 patients when compared with 26 control prolactinomas not treated with bromocriptine. It is concluded that short-term bromocriptine treatment does not adversely affect surgical outcome in any of the prolactin-secreting adenoma groups, nor does response or lack of response to bromocriptine predict surgical outcome.

Adenoma↗
PubMedDate not supplied

A phase II study of bromocriptine in patients with androgen-independent prostate cancer.

Prolactin is an important physiological regulator of prostate development and growth in preclinical models. In prostate cancer there is strong evidence that prolactin exerts a trophic effect independent of testosterone. In addition, patients with prostate cancer that have an elevated prolactin level correlated with a poorer prognosis. Based on these data, we evaluated the clinical effect of prolactin suppression using bromocriptine in patients with androgen-independent prostate cancer. We conducted an open-label phase II trial of bromocriptine in patients with progressive metastatic prostate cancer. Basal and thyrotropin releasing hormone (TRH)-stimulated prolactin levels were utilized as biological endpoints for determining the dose of bromocriptine. All patients continued to receive complete androgen blockade. Thirteen patients were enrolled (median age 69.5 years). There were no complete or partial responses associated with bromocriptine in 11 of the evaluable patients. The mean duration of bromocriptine treatment was 8.2 weeks (2-14 weeks). One patient had a clinically insignificant decrease in prostate-specific antigen (PSA) and another patient had a 19.9% decrease in PSA with progression of a soft tissue mass. The vast majority of patients (10 of 11) had suppression of prolactin with a bromocriptine dose of 2.5 mg three times a day. One patient required a dose adjustment due to inadequate suppression, with a final maintenance dose of bromocriptine 12.5 mg per day resulting in complete suppression. No serious treatment-related toxicities were observed. The most common complications noted were nausea, headaches, dizziness, and fatigue. Our data showed that 2.5 mg three times per day of bromocriptine suppressed prolactin in 90% of the patients. Furthermore, this dose appears to be well tolerated.

Adenocarcinoma↗
PubMed1990

Alpha-2 adrenergic activity of bromocriptine and quinpirole in chicken pineal gland. Effects on melatonin synthesis and [3H]rauwolscine binding.

In the pineal gland and retina of chickens, serotonin N-acetyl-transferase (NAT) activity and melatonin content are modulated by different receptors, alpha-2 adrenergic receptors in pineal gland and D2-dopamine receptors in retina. The effect of two D2-dopamine receptor agonists, bromocriptine and quinpirole (LY 171555), on melatonin synthesis in these tissues was investigated. Systemic administrations of bromocriptine and quinpirole decreased nocturnal NAT activity and melatonin content of both pineal gland and retina. Bromocriptine was equipotent in the two tissues, whereas quinpirole was approximately 100-fold more potent in retina than in pineal gland. In pineal gland, the suppressive effects of bromocriptine and quinpirole on NAT activity were blocked by yohimbine, a selective alpha-2 adrenergic receptor antagonist, but not by spiperone, a D2-dopamine receptor antagonist. In contrast, bromocriptine- and quinpirole-induced decreases of the enzyme activity in retina were antagonized by spiperone, and not affected by yohimbine. The nocturnal increase of NAT activity of pineal glands in vitro was inhibited with an order of potency clonidine greater than bromocriptine greater than quinpirole. Additionally, bromocriptine and quinpirole displaced the specific binding of [3H]rauwolscine, an alpha-2 adrenergic receptor antagonist, to membranes from chicken pineal gland, with potencies comparable to those observed for inhibition of NAT activity in vitro. It is suggested that bromocriptine and quinpirole, in addition to their D2-dopaminergic activity, can stimulate alpha-2 adrenergic receptors in pineal gland of chicken.

Animals↗
PubMed1991

Increased circulating levels of bromocriptine after vaginal compared with oral administration.

OBJECTIVE: To compare the circulating levels of bromocriptine after oral and vaginal administration of the drug. DESIGN: Experimental PARTICIPANTS: Seven ovulatory female volunteers and one hyperprolactinemic patient. INTERVENTIONS: Ovulatory volunteers were randomized to receive either oral or vaginal bromocriptine (2.5 mg). In a second session, the subjects were crossed-over to bromocriptine by the alternate route. An additional hyperprolactinemic patient received vaginal bromocriptine only. MAIN OUTCOME MEASURE: Serum bromocriptine and prolactin (PRL) levels were measured hourly for 12 hours in the normal volunteers and for 10 hours in the hyperprolactinemic patient. RESULTS: Circulating bromocriptine levels were significantly higher after vaginal bromocriptine after the 7th hour (P less than 0.05). The reduction in serum PRL was significantly greater after oral administration between 2 and 6 hours. CONCLUSIONS: Vaginally administered bromocriptine may result in a reduction in the overall dose required, thereby improving compliance without compromising therapeutic efficacy.

Administration, Oral↗
PubMed1991

Effect of bromocriptine on sperm function in vitro and in vivo.

Vaginal bromocriptine is an effective method for the treatment of hyperprolactinemia, but it is unknown whether bromocriptine applied vaginally can interfere with sperm function. Thus, we sought to determine the effects in vitro and in vivo on sperm directly exposed to bromocriptine. Ten semen specimens from normal donors were diluted with Ham's F-10 medium and incubated with 0, 0.01, 0.1, and 1.0 mmol/L bromocriptine solution or diluent without bromocriptine. Computerized semen analysis revealed a 31% decrease in sperm motility, a 24% decrease in sperm average path velocity, and a 33% decrease in sperm average straight line velocity only using 1.0 mmol/L of bromocriptine (P less than .05). In addition, eight women with hyperprolactinemia and infertility who were receiving vaginal bromocriptine consented to a postcoital test. Five became pregnant and delivered normal infants. Four of the five women who had a postcoital test had six, eight, ten, and ten motile sperm per high-power field and one had one to two motile sperm per high-power field. Because sperm function was preserved enough to result in fertilization and term pregnancy, the clinical importance of the in vitro findings is probably minimal and it can be concluded that vaginal bromocriptine can be used in women with infertility due to hyperprolactinemia.

Administration, Intravaginal↗
PubMed1981

[Bromocriptine therapy].

1. The study of bromocriptine and its effects has opened up new perspectives on the highly sophisticated neuroendocrine control mechanisms and the role of neurotransmitters. 2. As a specific prolactin inhibitor, bromocriptine is the treatment of choice in many cases of hyperprolactinemia in female and male. There is ample evidence that with bromocriptine a reduction of pituitary tumor size (particularly in prolactin-secreting tumors) can be achieved. 3. One highly specific use of bromocriptine, and which involves virtually no problems, is inhibition of puerperal lactation. 4. Bromocriptine is effective and useful in the treatment of acromegaly. While it may restore growth hormone levels to normal in mild and selective cases, it may be helpful in controlling severe cases in which surgical or radiotherapeutic approaches have failed to achieve satisfactory results. 5. As a dopamine agonist, bromocriptine offers a new possibility of treating parkinsonism. It may be given alone or, as is preferable in many cases, in combination with submaximal doses of levodopa. 6. Side effects are sometimes only observed on initiation of bromocriptine therapy, sometimes occur only during chronic therapy, and may occasionally necessitate interruption of the treatment. Sometimes continuation of therapy leads to tolerance of unwanted effects. Patients should be informed before the start of bromocriptine treatment about the possibility of side effects. With proper instruction on the manner in which the drug should be taken, many adverse reactions can be avoided or diminished.

Acromegaly↗
PubMedDate not supplied

Bromocriptine for induction of ovulation in hyperprolactinemic amenorrhea.

Hyperprolactinemia is a frequent finding in infertile women with amenorrhea. Bromocriptine is the drug of choice for treatment of hyperprolactinemic amenorrhea. This dopamine agonist is very effective in normalizing raised prolactin levels. Ovulatory menstrual cycles and fertility are then rapidly restored. Bromocriptine therapy represents a major advance in the treatment of anovulatory infertility. Prolactin-secreting pituitary adenomas are common causes of hyperprolactinemia. Neither surgery nor irradiation reliably provides the definitive cure that had been hoped for in patients with prolactin-secreting pituitary tumours. Experience with medical treatment has revealed that induction of ovulation with bromocriptine is remarkably safe both in patients with microtumours and those with macrotumours without suprasellar extension. In the future, it is possible that even the larger macrotumours with suprasellar can be safely managed by medical therapy with bromocriptine. During pregnancy, pituitary tumour complications may arise in women with prolactinomas. However, data accumulated during recent years have shown that induction of ovulation and pregnancy by bromocriptine is remarkably safe in women with both micro- and macroprolactinomas. The risk of permanent sequelae due to rapid tumour enlargement during pregnancy is exceedingly small in properly investigated and carefully supervised women with prolactinomas. Bromocriptine is clearly a must for every infertility clinic. The value of bromocriptine in the treatment of normoprolactinemic amenorrhea, polycystic ovarian disease, luteal insufficiency and ovulatory infertility is not yet proven. However, bromocriptine is extremely effective in normalizing hyperprolactinemia and undoubtedly the drug of choice for treatment of female infertility due to hypersecretion of prolactin.

Adenoma↗