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PubMed1989

Bromocriptine therapy for non-functioning pituitary adenoma.

Over a 6-year period, 25 patients with non-functioning pituitary adenomas were treated with bromocriptine, while 18 other patients with this condition underwent surgery as the first therapeutic modality. The medically treated group, consisting of those patients without alarming eye symptoms, was analysed in retrospect. Eight of these patients had previously undergone surgery and radiotherapy. Bromocriptine was used in a dose of 5 to 22.5 mg per day; the mean duration of treatment was 18 months. For 11 patients, radiological findings obtained during the year before treatment with bromocriptine revealed progression in five cases and stable tumour size in the others. Three of the five patients with progression showed tumour size reduction during bromocriptine therapy while no further growth occurred in the other two. When medication was stopped in one responding patient, the tumour grew again. One other patient, without pretreatment radiological investigation, exhibited tumour size reduction during bromocriptine therapy, and one patient exhibited radiological progression during the study period. In one case visual fields improved and in one other deteriorated without parallel changes in tumour size on computerized tomography. The favourable reactions were equally divided between the groups with and without previous radiotherapy. We conclude that bromocriptine is rarely capable of reducing the size of non-functioning pituitary adenomas (16% in this series). However, pituitary adenomas exhibiting recent growth may be sensitive to this drug, leading to size reduction or growth arrest.

Adenoma↗
PubMed1990

A double-blind study comparing a new non-ergot, long-acting dopamine agonist, CV 205-502, with bromocriptine in women with hyperprolactinaemia.

Twenty-two hyperprolactinaemic women were randomly allocated to two groups and treated with bromocriptine or the new, non-ergot, long-acting dopamine agonist, CV 205-502. The study was double-blind for 6 months. Four patients in the bromocriptine group, but none in the CV 205-502 group, discontinued the study because of adverse reactions. Adverse reactions in those receiving the new drug were milder and more transient than with bromocriptine. With once-daily doses of 0.075 mg CV 205-502, eight of 11 women achieved normal PRL concentrations after 8 weeks treatment (median (95% confidence limits), 352 (70-987) mU/l) compared with two of nine receiving a divided daily dose of 5 mg bromocriptine (1802 (1205-4438) mU/l) (P less than 0.002). With doses of 0.075-0.15 mg of CV 205-502, 10 of 11 women achieved normal PRL concentrations at 24 weeks compared with three of the remaining seven women on doses of 5-10 mg of bromocriptine. Regular menstrual bleeding was restored and galactorrhoea relieved in the majority of patients, with marginally greater efficacy with CV 205-502. CV 205-502 is highly effective for the long-term treatment of hyperprolactinaemia. It is better tolerated than bromocriptine, is effective in a once-daily dose, appears to be safe, and provides a valuable alternative to the dopamine agonist drugs in use today.

Adult↗
PubMed1991

Withdrawal of bromocriptine after long-term therapy for macroprolactinomas; effect on plasma prolactin and tumour size.

The present study describes the effect on plasma prolactin values and tumour size of bromocriptine withdrawal in 12 patients who had been treated for macroprolactinomas for a period of 3.5-7 (mean 4.9) years. Pretreatment plasma prolactin values ranged from 12,000 to 210,000 (mean: 66,000) mU/l. Immediately before bromocriptine withdrawal plasma prolactin values were in the normal range (less than 350 mU/l for men; less than 450 mU/l for women). Bromocriptine treatment was associated with tumour reduction in all cases. The following observations were made upon withdrawal of bromocriptine: (1) In 11 patients hyperprolactinaemia redeveloped although plasma prolactin levels remained below 600 mU/l in two of these patients during a follow-up period of 1 year. In the other nine patients bromocriptine treatment was reinstituted after 4-12 weeks. (2) Hyperprolactinaemia was associated with tumour reexpansion in one case and increased density of the tumour in two cases. (3) In one patient plasma prolactin remained undetectable during a follow-up period of 1 year and no tumour re-expansion was found. It is concluded that tumour regrowth is uncommon and of small extent after cessation of long-term bromocriptine treatment for macroprolactinomas.

Adult↗
PubMedDate not supplied

Effects of bromocriptine on pancreatic secretion in the isolated, blood-perfused pancreas of the dog.

Effects of bromocriptine on the secretion of pancreatic juice were investigated with dog isolated, blood-perfused pancreas. Bromocriptine (1-10 mg) caused dose-dependent increases in the secretion of pancreatic juice. However, bromocriptine did not affect the perfusion blood flow rate. The secretory response to bromocriptine was inhibited by pretreatment with a dopamine antagonist, sulpiride, but not by phentolamine, propranolol, atropine, metiamide, indomethacin or tetrodotoxin. Bromocriptine caused a dopamine-like secretion of the pancreatic juice containing a high concentration of bicarbonate but had little effect on protein output. These results suggest that bromocriptine increases pancreatic secretion stimulating directly on pancreatic dopamine receptors.

Animals↗
PubMed1986

Ultrastructural localization of prolactin in estrogen-induced prolactinoma of the rat pituitary. Experimental models for the human prolactinomas and the effects of bromocriptine.

In order to establish the experimental model for human prolactinomas and its bromocriptine treatment, estrogen-induced prolactinoma was produced in the female Wistar rats, in which daily bromocriptine treatment was given for a week, 3 days or 1 day (24 hours). The prolactinoma was produced by giving 5 mg estrogen depot every four weeks. The rats were killed at 4, 12, 20, and 24 weeks after the initial injection of the estrogen. By immunoelectron microscopy, in the estrogen induced prolactinoma, PRL was localized in well developed lamellar or whorling rough endoplasmic reticulum (RER) and Golgi saccules. In the rats treated with bromocriptine for a week, the serum PRL levels were lowered and the atrophied cytoplasm was filled with secretory granules containing PRL. These data were comparable to those of the human prolactinomas and the present experiment will serve as an animal model for studying the morphofunctional changes of human prolactinomas induced by bromocriptine treatment. The experiment with bromocriptine treatment for 24 hours supported the proposed mechanism that bromocriptine evokes inhibition of exocytosis followed by continuous granule formation in Golgi complexes and subsequently lowers synthesis of PRL.

Animals↗
PubMed1987

The effect of bromocriptine in benign prostatic hypertrophy and vesicosphincteric dynamics.

Four studies were carried out on 66 patients in order to examine the effect of bromocriptine in benign prostatic hypertrophy (BPH) and to clarify its mechanism of action. Two studies were clinical: the first was a double-blind, controlled trial (lasting 6 months) in which bromocriptine 5 mg/day was compared with placebo, and the second was an open study to evaluate the effect of bromocriptine 5 mg on patients with acute retention due to BPH. The other two studies were designed to investigate the action of the drug on vesicosphincteric dynamics. These were double-blind, controlled, parallel trials, one comparing bromocriptine at dosages of 2.5 and 5 mg with placebo 90 min after administration, and the other comparing bromocriptine 5 mg/day with placebo after 15 days' administration in post-prostatectomy patients. Bromocriptine had a favourable effect on patients with BPH but no effect on cases of acute retention. The urodynamic studies suggested that the drug affected urethral sphincteric mechanisms specifically. The weight and volume of the prostate remained unchanged after administration of the drug, so that any clinical response was not due to a direct effect on the gland itself.

Bromocriptine↗
PubMed1975

A study of the effect of bromocriptine on serum oestradiol, prolactin, and follicle stimulating hormone levels in puerperal women.

Nine normal women were examined in the first 11 days of the puerperium. Serum prolactin, oestradiol and follicle simulating hormone (FSH) levels were measured and the FSH response to 100 mug of intravenously administered follicle stimulating hormone/lutenizing hormone-releasing hormone (LH/FSH-RH) was assessed on day 1 post partum in five subjects and on days 4 (two subjects), 6 and 7 post partum in the other four subjects. Bromocriptine therapy was given to six of these women and four to seven days after the start of such therapy, when prolactin levels had fallen to normal non-pregnant levels, these women were retested. Before bromocriptine treatment, the basal FSH levels were unmeasurable in six and low in one other of the nine subjects. After bromocriptine treatment, the basal FSH levels were measurable in four out of six patients and were higher than in the untreated patients (P less than 0-01). The FSH response to LH/FSH-RH was unmeasurable in eight out of nine before treatment, which is less than the response seen in 26 normal men and women (P less than 0-01). There was also no discernible FSH response to LH/FSH-RH after treatment with bromocriptine. Before treatment with bromocriptine, the serum prolactin levels were elevated in all nine women but were within the normal range for non-pregnant women after three days of bromocriptine therapy. Thus postpartum gonadotrophin suppression seemed to depend on high prolactin levels and at least part of the antigonadotrophic action of prolactin seemed to be at pituitary level.

Bromocriptine↗
PubMed1985

Effects of bromocriptine on parkinsonism. A nation-wide collaborative double-blind study.

The effects of bromocriptine in patients with Parkinson's disease manifesting various problems in levodopa therapy were tested in a double-blind manner with the collaboration of 59 institutions. The slow and low principle was in part adopted. Either bromocriptine or placebo was added to levodopa. Twenty-nine % of the bromocriptine-treated patients (n = 108), in contrast to 14.8% of the placebo-treated (n = 108), showed either marked or moderate improvement (P less than 0.05). Twenty to 37% improvement was noted in most of the symptoms studied in those treated with bromocriptine. The significant superiority of bromocriptine was also noted in the effects on wearing-off phenomena and frozen gait. No irreversible side effects were noted. It is concluded that bromocriptine is useful in patients who are manifesting various difficulties in levodopa therapy. Our results are comparable to those using higher maintenance doses. Dopamine antagonistic actions were not observed. This is unlike the case with experimental animals.

Bromocriptine↗
PubMed1999

Bromocriptine test in the evaluation of patients with syncope of unknown aetiology. A case-control study.

The aim of the present study was to evaluate, through a case-control study, the specificity of the upright tilt test with bromocriptine as a marker of neurally mediated syncope of unknown aetiology. We have compared upright tilt test with bromocriptine (2.5 mg p.o.) in patients with syncope of unknown aetiology and controls. A total of 23 patients and controls matched by age and sex had upright tilt test with bromocriptine. The upright tilt test procedure consisted of 10 min in supine position, 10 min of 60 degree head-up tilt and a further 10 min with the subject supine; this procedure was performed in baseline condition and 60, 120, 180 and 240 min after the administration of bromocriptine. The protocol end points were the development of syncope or presyncope in association with hypotension with or without bradycardia. A positive response to bromocriptine test was found in 78% (95% CI, 61% to 95%) of patients and in 13% (95% CI, 0% to 26%) of controls (P<0.001). No significant differences were detectable among patients and controls showing a positive response to the test. Bromocriptine test seems to be a useful alternative tool for the diagnosis of neuromediated syncope also suggesting that dopaminergic supersensitivity may, at various and to varying degrees, play a role in the pathogenesis of syncopal episodes.

Adolescent↗
PubMed1983

Bromocriptine in the prevention of alcohol abuse.

In a double-blind trial comprising 50 chronic alcoholics, randomized in two parallel groups, bromocriptine was compared with placebo on psycho-social variables in the prevention of alcohol abuse for 6 months. The overall effects on the abuse situation, social functioning, social belonging and psychic status were significantly bettered by bromocriptine. Craving was reduced from strong to very mild, indicating a distancing effect of bromocriptine on dependency. Neurotic states and depressive reactions were significantly improved by bromocriptine, as were social situation, motivation and personal insight. Global evaluation of bromocriptine treatment was beneficial in most patients, with a substantial reduction in the number of patients abusing alcohol. Our results indicate that bromocriptine may affect the craving.

Adult↗
PubMed1980

Metabolite involvement in bromocriptine-induced circling behaviour in rodents.

Bromocriptine and apomorphine produced identical circling responses in rodents with medial forebrain bundle lesions. Rotation induced by bromocriptine, but not by apomorphine, was inhibited by prior treatment with reserpine or alpha-methyl-p-tyrosine suggesting a requirement for intact presynpatic events. Bromocriptine-induced circling also was inhibited by the catecholamine re-uptake blockers nomifensine and desmethylimipramine, supporting the role of presynaptic mechanisms. Bromocriptine-induced circling, but not apomorphine circling, was reduced by pre-treatment with SKF 525A, an inhibitor of monooxygenase enzymes, suggesting metabolite involvement in the turning response. This compound prolonged hexobarbitone sleeping times and zoxazolamine paralysis times in mice. These indices of drug metabolizing activity also were prolonged by pre-treatment with desmethylimipramine while nomifensine prolonged only hexobarbitone sleeping times and alpha-methyl-p-tyrosine had no effect on either index. The data suggest that a metabolite of bromocriptine may be of importance in causing circling and that uptake of bromocriptine (or a metabolite) into presynaptic catecholamine terminals may be necessary.

Amphetamine↗
PubMed1988

Dopamine-mediated behaviours produced in naive mice by bromocriptine plus SKF 38393.

The ability of bromocriptine and SKF38393 (2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine) to produce some dopamine-mediated behaviours has been assessed in mice. Soon after injection, SKF38393 produced moderate increases in grooming and sniffing which were not very intense, while bromocriptine (with or without SKF38393) inhibited all grooming behaviour. Bromocriptine alone also depressed rearing and sniffing in the first hour and SKF38393 alone was without effect on rearing, but the combination produced a marked increase in the incidence of both rearing and sniffing, both of which behaviours appeared to be stereotyped. When bromocriptine-induced locomotor stimulation was peaking about 3 h after injection, as measured in automated activity cages in previous studies, there was an increase in sniffing and rearing, the incidence of which was unaffected by the addition of SKF38393, perhaps due to the shorter duration of action of SKF38393 than of bromocriptine. The data indicate that the D-1 agonist SKF38393 can qualitatively and quantitatively alter the behavioural spectrum produced by the D-2 agonist bromocriptine.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1997

Contribution of cytochrome P450 3A pathway to bromocriptine metabolism and effects of ferrous iron and hypoxia-re-oxygenation on its elimination in the perfused rat liver.

The contribution of the cytochrome P450 3A pathway to bromocriptine metabolism, and the effects of ferrous iron and hypoxia-re-oxygenation on its elimination, were evaluated with the perfused rat liver. Outflow profiles of bromocriptine after bolus administration were estimated by moment analysis and dispersion model analysis. Kinetic parameters were not significantly changed by troleandomycin, a P450 3A inhibitor. The inhibition of bromocriptine metabolism by troleandomycin was 5.7 +/- 2.4%. These findings indicate that cytochrome P450 3A does not play an important role in bromocriptine elimination with the perfused rat liver. Elimination rate constant (ka) values were significantly increased by ferrous iron perfusion or hypoxia-re-oxygenation. Free-radical generation can, therefore, affect bromocriptine elimination. Our observations suggest that bromocriptine might be eliminated by scavenging of free radicals in the liver.

Amitrole↗
PubMed1992

Acute administration of bromocriptine abolishes the hyperprolactinemic response induced by submaximal exercise in man.

The effective control of hypophysial prolactin (PRL) secretion with a pharmacological agent is a prerequisite for the investigation of the role of hyperprolactinemia observed during exercise. Using bromocriptine, a potent inhibitor of PRL secretion, this study established the proper experimental conditions whereby any significant increase in plasma PRL level can be prevented and basal circulating levels maintained during physical exercise. On three occasions at weekly intervals, 15 male adults, separated into two groups, exercised on an ergocycle (40 min at 65% VO2max) either 1 or 3 h after ingesting either placebo or 1.25 or 2.50 mg of bromocriptine mesylate (Parlodel; Sandoz Canada Inc., Dorval, Qué.). Under all conditions, the plasma PRL elevation observed during exercise after placebo was prevented by the administration of bromocriptine. Resting plasma PRL levels were maintained when exercise was performed 1 h after bromocriptine ingestion, but were significantly reduced when exercise was performed 3 h after administration of either bromocriptine dosages. Considering the primary and secondary effects observed, 1.25 mg of bromocriptine administered 1 h before exercise provides suitable experimental conditions to investigate the role of the increase in plasma PRL during physical exercise.

Administration, Oral↗
PubMed1993

Bromocriptine redirects metabolism and prevents seasonal onset of obese hyperinsulinemic state in Syrian hamsters.

Bromocriptine redirects metabolism and prevents seasonal onset of the obese hyperinsulinemic state in Syrian hamsters. Metabolic and hormonal effects of bromocriptine were studied in seasonally obese female Syrian hamsters, Mesocricetus auratus. Daily injections of bromocriptine and vehicle (controls) were made at light onset (10:14-h light-dark cycle) for 10 wk. After 9 wk of treatment blood samples were taken every 4 h during a day for assays of hormones, glucose, triglyceride, and fatty acids, and after 10 wk of treatment, tests were carried out to measure insulin-stimulated glucose disposal during a hyperinsulinemic clamp, lipid mobilization (rate of glycerol appearance), protein turnover (lysine flux and deamination), and body composition (deuterium dilution). Bromocriptine reduced percent body fat by 53% and increased percent lean body mass by 8%. It also decreased triglyceride levels by 52% and plasma free fatty acid concentration during the dark-near light onset by 49% and glycerol appearance by 25%. Protein synthesis and catabolism were increased by 62 and 56%, respectively, and deamination of amino acid was decreased by 53% by bromocriptine. Bromocriptine reduced plasma concentration of insulin throughout the day, especially at light onset, by 78% without change in baseline glucose level and markedly decreased steady state plasma glucose (by 40%) during a continuous infusion of insulin and glucose. It also reduced the nocturnal plasma concentration of prolactin by 90%, cortisol by 70%, and thyroid hormones (thyroxine and triiodothyronine) by 50% and dramatically altered the circadian profiles of these hormones and insulin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Nine-year follow-up study of bromocriptine monotherapy for Parkinson's disease.

A 9-year nationwide study of bromocriptine monotherapy and combination therapy with bromocriptine and levodopa in Parkinson's disease is reported. Eleven patients were on bromocriptine monotherapy, 35 patients were on combined treatment of bromocriptine and levodopa for a certain time during a 9-year period. Maintenance doses of bromocriptine at the end of the 9th year in the two groups were 11.1 mg/day in the monotherapy and 12.7 mg/day in the combination therapy group with levodopa. Changes in Hoehn and Yahr's grading between the time of trial start and the end of 108 months' treatment revealed that 5 of 11 cases in the monotherapy group remained in the same stages, the other 2 cases improved in condition from stage II to I, and another 4 deteriorated compared with pretreatment grade. On the other hand, 20 of 35 cases in the combination-therapy group reached more advanced stages, 3 patients moving to stage V. Four of them, however, improved, and 11 did not change at the end of 9 years of treatment. Although it is difficult to prove the neuroprotective effect of a dopamine receptor agonist, our long-term nation-wide collaborative studies will help us to answer the question of how bromocriptine works in pharmacokinetic aspects.

Aged↗
PubMed1991

A nationwide collaborative study on the long-term effects of bromocriptine in patients with Parkinson's disease. The fourth interim report.

The interim results of the nationwide collaborative study on the long-term effects of bromocriptine in patients with Parkinson's disease are reported. Four years ago, two prospective clinical studies were started to evaluate the long-term effects of bromocriptine in Parkinson's disease. The first was to investigate the long-term effects of bromocriptine monotherapy and the second to see the long-term effects of a combination therapy of bromocriptine with levodopa. Patients who had never been treated with levodopa were placed on bromocriptine monotherapy, and those who had been treated with levodopa for not more than 5 years were allocated randomly to either the combination or the levodopa group. Two hundred and eighty-six patients were enrolled in the former study and 416 in the latter. Among the 286 patients, 164 continued for further observation at the end of the fourth year, and 74 of them were still being treated with bromocriptine monotherapy. However, in 78, levodopa had to be added. Among the 416 patients in the second study, 216 were allocated to the combination group and 200 to the levodopa control group. At the end of the fourth year, 130 in the former and 140 in the latter group remained for further observation. In all three groups, a gradual loss of efficacy was noted. The rate of efficacy loss appeared largest in the monotherapy group and smallest in the combination group. Effects on tremor and rigidity are still maintained, but effects on akinesia and gait were lost by the end of the fourth year in all groups. Wearing-off and dyskinesias seem to be better managed by the combination therapy. The incidence of wearing-off was very small in the monotherapy group. No serious side effects were encountered except for 1 patient who died of pulmonary fibrosis in the combination group.

Bromocriptine↗
PubMed1993

The effects of CV205-502 in patients with hyperprolactinaemia intolerant and/or resistant to bromocriptine.

CV205-502 is a new non-ergot dopamine agonist currently being studied for the treatment of hyperprolactinaemia. We have assessed the effects of CV205-502 on prolactin secretion and the clinical consequences of hyperprolactinaemia in 16 patients with hyperprolactinaemia who had previously been unsuccessfully treated with bromocriptine. These patients had been either intolerant of and/or resistant to the effects of bromocriptine. Sixteen patients, all women in an age range between 20 and 49 years (mean 31.5 years), were treated for periods of between 8 and 52 weeks with doses of CV205-502 ranging from 0.075 to 0.3 mg taken once daily at night. Seven out of 10 of the patients, who were intolerant of bromocriptine, tolerated CV205-502 better with fewer side effects although the nature of the side effects was similar to that associated with bromocriptine. Only 1 patient from this group stopped taking CV205-502 due to side effects. Six of 11 patients exhibiting bromocriptine resistance showed a significant reduction in the degree of hyperprolactinaemia but normoprolactinaemia was achieved in only 1. Galactorrhoea ceased in 2 of 6 patients, menstruation resumed in 6 of 11 patients presenting with amenorrhoea, and 2 patients conceived. In patients with bromocriptine intolerance and/or resistance, CV205-502 is useful as a second line treatment.

Adult↗