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PubMed1996

[The therapy of a macroprolactinoma with the intramuscular application of a long-acting bromocriptine preparation].

HISTORY AND CLINICAL FINDINGS: Three years ago, a now 26-year-old woman with secondary amenorrhoea was found to have a prolactinoma which was treated with bromocriptine. However, because of side effects and psychosocial problems she took the drug only irregularly. There were no neurological symptoms and the visual fields were normal. Her weight was 97 kg and her height 168 cm. INVESTIGATIONS: Without treatment the serum prolactin concentration was 6978 microU/ml, while other endocrine parameters were unremarkable. Cranial computed tomography showed a suprasellar adenoma (craniocaudal diameter 1.0 cm). TREATMENT AND COURSE: Renewed treatment with bromocriptine (5 mg three times daily) brought prolactin concentration to within normal limits, but then rose again to at least 52,600 microU/ml when the patient took the drug irregularly, and the tumour grew to 2.8 cm. As the obesity (her weight now 120 kg) made neurosurgical intervention very risky a treatment trial with long-acting bromocriptine preparation (50 mg bromocriptine every 28 days intramuscularly), was undertaken. Serum prolactin concentration, measured at the end of the 28-day period, rapidly fell (6470 microU/ml after 3 months). Radiological examination indicated significant tumour shrinkage ( < 1.0 cm after 2 years). CONCLUSION: Repeated intramuscular administration of bromocriptine was an effective, well tolerated alternative (but not yet licensed in Germany) to oral dopamine agonists in the treatment of macroprolactinoma.

Adult↗
PubMed1990

Effects of bromocriptine at parturition in the tammar wallaby, Macropus eugenii.

Female tammar wallabies were treated with the dopamine agonist bromocriptine at the end of pregnancy to suppress the peripartum pulse of plasma prolactin. The animals were subsequently observed, and a series of blood samples taken to define the hormonal profiles before and immediately after parturition. Birth was observed in 4/5 control animals and occurred in 8/9 bromocriptine-treated animals. The peripartum peak in plasma PGFM concentrations was not affected by bromocriptine although the pulse of prolactin normally seen at parturition was completely abolished. The timing of luteolysis was apparently unaffected, as plasma progesterone concentrations fell similarly in both treated and control animals immediately after parturition. However, all of the neonates of the bromocriptine-treated animals died within 24 h, possibly because of a failure to establish lactation. Subsequent onset of post-partum oestrus was delayed or absent both in control and in bromocriptine-treated animals, suggesting that the frequent blood sampling and disturbances in the peripartum period interfered with these endocrine processes. It is concluded that both prolactin and prostaglandin can induce luteolysis in the pregnant wallaby, but that the normal sequence of events results from a signal of fetal origin inducing a prostaglandin release from the uterus, which in turn releases a pulse of prolactin that induces a progesterone decline.

Animals↗
PubMed1994

The effects of bromocriptine on lactation and subsequent reproduction in grey kangaroos, Macropus fuliginosus and Macropus giganteus.

Both species of grey kangaroo were tested to determine whether a single exposure to bromocriptine in mid winter will terminate lactation, and whether females that cease to lactate will return to oestrus immediately and give birth early, or at the next summer breeding season. In Experiment 1, 11 lactating western grey kangaroos (Macropus fuliginosus) received injections either of saline (n = 2) or of bromocriptine at dose rates of 0.2, 1.0 or 5.0 mg kg-1 bodyweight (n = 3 per dose). Pouch young of females treated with the highest dose of bromocriptine showed either retarded growth or no growth, but they subsequently survived. In Experiment 2, lactating western (n = 12) and eastern grey kangaroos (M. giganteus) (n = 14) received a single intramuscular injection of saline or approximately 2 mg kg-1 or 4 mg kg-1 Parlodel LA (a long-acting form of bromocriptine) and their young were weighed. Within 3 weeks, the young of all 19 females treated with Parlodel LA had lost weight and 17 had died, whereas only one young, which had not lost weight, was lost from the seven control females. The western grey females did not give birth until the normal summer breeding season but the eastern grey females gave birth 2-4 months early. It is concluded that bromocriptine has potential for the humane control of grey kangaroo populations.

Animals↗
PubMedDate not supplied

Bromocriptine in the treatment of post-polio fatigue: a pilot study with implications for the pathophysiology of fatigue.

Fatigue is the most commonly reported and most disabling of all post-polio sequelae (PPS). Bromocriptine mesylate (Parlodel) was employed in a placebo-controlled trial in five survivors of paralytic polio who continued to report moderate to severe daily fatigue after complying with the conservative treatments prescribed for PPS. Placebo was given for 4 wk followed by increasing doses of bromocriptine mesylate, administered at 12:00 pm for 28 days, which reached a total dose of 12.5 mg/day. Three subjects reported marked symptom improvement on bromocriptine but not on placebo. Their reported difficulty with attention, concentration, word finding, mind wandering, memory, thinking clearly, and fatigue on awakening was significantly negatively correlated with days on bromocriptine but not with days on placebo. Before the drug trial began, responders had clinically impaired performance on neuropsychologic tests of attention and information processing speed, more than twice as many hyperintensities on magnetic resonance imaging of the brain, abnormally low fasting adrenocorticotropic hormone levels, and nearly double the mean plasma prolactin level compared with nonresponders. The implications of these findings for the pathophysiology of fatigue are discussed. A double-blind, placebo-controlled, multicenter study will be needed to confirm bromocriptine's efficacy in treating attentionally and neurophysiologically impaired polio survivors whose severe and disabling fatigue does not respond to conservative therapies.

Adrenocorticotropic Hormone↗
PubMed1984

Low-dose bromocriptine therapy in severe Parkinson's disease.

We present an interim report of an ongoing, single-blind study of the effectiveness and safety of bromocriptine mesylate (Parlodel) in 15 patients, 14 of whom had severe idiopathic Parkinson's disease (Stages 4 and 5 on the Hoehn and Yahr Scale). The patients had never received levodopa, amantadine, or bromocriptine. Gradually increasing doses of bromocriptine were assessed: Initial daily dosage was 1.25 mg, with weekly increments of 1.25 mg/day until either the clinical response was satisfactory or a maximum of 15 mg/day was reached. The patients were on no other antiparkinsonian agents, except trihexyphenidyl HCl (Artane). Response to treatment was scored on the Columbia Scale. The patients discussed in this report had been in the study for varying times, ranging from 1 month to 3 years. Only one patient who entered this study dropped out because his response to bromocriptine was unsatisfactory; he had taken the drug for 2 weeks. No serious adverse reactions were noted with the gradually increasing dosage regimen. Response on the whole was very satisfactory; patients improved by at least two stages on the Hoehn and Yahr Scale. Improvement began within 48 h of onset of treatment with 1.25 mg daily. The preliminary results of this study indicate that low-dose bromocriptine as a first-line drug in severe Parkinson's disease is definitely warranted.

Adult↗
PubMed1995

L-deprenyl as an adjunct to low-dose bromocriptine in early Parkinson's disease: a short-term, double-blind, and prospective follow-up study.

The therapeutic efficacy of L-deprenyl (10 mg daily) as an adjunct to low-dose bromocriptine monotherapy (up to 25 mg daily) in patients with early Parkinson's disease (PD) was evaluated in a double-blind placebo-controlled short-term study (11 patients) and subsequently in a long-term prospective open follow-up (21 patients) until L-dopa was required, over a 4-year period. The combined regimen of bromocriptine plus L-deprenyl produced a mildly significant improvement, as shown by the majority of clinical rating scales used after 6 weeks of sustained treatment (as compared to bromocriptine alone and bromocriptine plus placebo). In the prospective long-term study, a stabilization of the clinical status was observed until 12 months of sustained treatment, whereas after that, a gradual worsening of the scores on all motor rating scales occurred. However, at 24 months, fewer than one third of the patients had required L-dopa, a proportion comparatively smaller than that reported in the literature with bromocriptine alone. This finding could be related to the persistence of initial symptomatic effect of L-deprenyl, but a slowing action on the course of the disease process exerted by the monoamine oxidase typeB (MAO-B) inhibitor cannot be ruled out.

Aged↗
PubMed1985

Tardive dyskinesia: clinical and neuroendocrine response to low dose bromocriptine.

Twelve patients with a long-standing history of moderate to severe symptoms of tardive dyskinesia, which had remained stable for several months, participated in a 6-week trial with bromocriptine. All patients were receiving a concomitant neuroleptic medication and were treated with a low dose of bromocriptine (0.75 to 7.5 mg). Patients showed a modest overall improvement of 16.6%, with a trend for greater improvement in male patients (23.6%). Baseline prolactin levels in the female patients showed a positive correlation with age and duration of tardive dyskinesia symptomatology. Plasma prolactin levels 4 hours following administration of bromocriptine were negatively correlated with the dose of bromocriptine. There appears to be a differential sensitivity for prolactin and growth hormone response to bromocriptine at these low doses in the presence of chronic neuroleptic treatment.

Bromocriptine↗
PubMed1983

Effects of bromocriptine on the circadian rhythm of 18-hydroxycorticosterone and cortisol secretion in essential hypertensives.

This study examines the influence of bromocriptine, a dopamine agonist, on circadian secretory patterns of plasma 18-hydroxycorticosterone (18-OHB) and cortisol in essential hypertension. Patients with sustained essential hypertension were studied after they had reached equilibrium on a constant 150 mmol sodium and 80 mmol potassium intake. Plasma 18-OHB and cortisol determinations were made at 30-min intervals over 24 h during a control and bromocriptine treatment period (bromocriptine, 2.5 mg t.i.d. for five days). Circadian patterns for plasma 18-OHB and cortisol were observed in all patients before and after bromocriptine. Although bromocriptine did not affect the circadian rhythm of 18-OHB and cortisol it did decrease mean 24-h recumbent 18-OHB from 23 +/- 42.2 to 14.3 +/- 1.4 ng/dl. These results suggest that there is a circadian rhythm of both 18-OHB and cortisol secretion in patients with essential hypertension as in normotensives. Dopaminergic mechanisms exert an effect on the quantitative secretion of 18-OHB. However, the circadian rhythm for 18-OHB and cortisol does not appear to be dependent on dopaminergic mechanisms.

18-Hydroxycorticosterone↗
PubMed1991

Contribution of spinal dopamine receptors to the hypotensive action of bromocriptine in rats.

Bromocriptine, a dopamine (DA) receptor agonist, has been reported to have hypotensive effects in anesthetized and conscious normotensive rats but its mechanism of action is still not fully understood. Therefore, we studied the changes in mean arterial blood pressure (MAP) and heart rate (HR) elicited by an intravenous (i.v.) administration of bromocriptine (150 micrograms/kg), in either pentobarbital-anesthetized or conscious normotensive rats, pretreated with either i.v. (0.3 mg/kg) or intrathecal (i.t.) (93 nmol) domperidone, a DA receptor antagonist that does not cross the blood-brain barrier. In these preparations, i.v. administration of bromocriptine elicited dose-dependent decreases in MAP and rises in HR. The hypotensive effect was antagonized partially by i.t. and fully by i.v. domperidone. However, the latter compound did not modify the tachycardia, which could be blocked by propranolol (0.5 mg/kg i.v.). In rats pretreated with the latter beta-adrenoceptor antagonist, bromocriptine produced only a decrease in blood pressure that was inhibited by i.v. and i.t. domperidone. These results suggest that, in anesthetized and conscious normotensive rats, the hypotension induced by systemic administration of bromocriptine is fully mediated by DA2 dopamine receptors, which are located partly within the spinal cord and partly in the peripheral circulation.

Anesthesia↗
PubMed2002

Bromocriptine reverses P-glycoprotein-mediated multidrug resistance in tumor cells.

One of the most important causes of anticancer treatment failure is the development of multidrug resistance (MDR). The main characteristics of tumor cells displaying the MDR phenomena are cross-resistance to structurally unrelated cytotoxic drugs having different mechanisms of action and the overexpression of the MDR1 gene, which encodes a transmembrane glycoprotein named P-glycoprotein (P-gp). This study evaluated whether bromocriptine, a D2 dopaminergic receptor agonist, influenced anticancer drug cytotoxicity and P-gp activity in a P-gp-expressing cell line compared to a non-expressing subline. The K(i) values for P-gp of cyclosporine and verapamil were 1.09 and 540 microM, respectively, and that of bromocriptine was 6.52 microM in a calcein-AM efflux assay using porcine kidney epithelial LLC-PK1 and L-MDR1 cells, overexpressing human P-gp. Bromocriptine at 10 microM reduced the IC50 of doxorubicin (DXR) in K562-DXR from 9000 to 270 ng/ml and that of vincristine (VCR) in K562-VCR from 700 to 0.30 ng/ml, whereas the IC50 values of DXR and VCR in the K562 subline were only marginally affected by these drugs. Bromocriptine restored the anticancer effect of DXR, VCR, vinblastine, vinorelbine and etoposide on MDR-tumor cells overexpressing P-gp. These observations suggest that bromocriptine has the potential to reverse tumor MDR involving the efflux protein P-gp in the clinical situation.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1989

The effects of lisuride, terguride and bromocriptine on intraocular pressure (IOP).

1. The effects of a single oral dose of the dopaminergic agonists lisuride (0.1 mg), terguride (0.25 mg) and bromocriptine (1.25 mg) on IOP were studied in eight normal volunteers using the non-contact tonometer. 2. Considering all post-dose measurements, compared with placebo, bromocriptine and lisuride but not terguride reduced IOP significantly in both eyes. 3. There was no significant difference between the ocular hypotensive effect of bromocriptine and lisuride. 4. Terguride reduced IOP significantly in the left eye at the 3 h time point after drug administration. 5. The result of this study confirms the reported ocular hypotensive effect of bromocriptine and showed that lisuride is as effective as bromocriptine in reducing IOP. 6. To evaluate the clinical importance of these drugs as ocular hypotensive agents other studies are needed using eye drops.

Adult↗
PubMed1976

Bromocriptine potentiation of gastric acid secretion in cats.

Bromocriptine administered both orally and intravenously potentiated gastric acid secretion in response to submaximal pentagastrin stimulation in cats. Bromocriptine did not increase the maximum acid secretion in response to pentastrin, not did it stimulate basal acid secretion. Potentiation was observed in normal and vagotomized animals which precludes involvement of the vagi in the response. The mechanism of action of this compound on the stomach does not appear to be mediated through stimulation of dopaminergic receptors as no potentiation was observed with dopamine infusions. It is argued that the bromocriptine potentiation of gastric acid secretion may be a demonstration of 5-hydroxytryptamine or alpha-adrenergic antagonism. However, the potentiation observed with daily oral bromocriptine treatment had disappeared by the eighth day and may correlate with the disappearance of gastric side effects noted in patients on bromocriptine treatment.

Animals↗
PubMed1987

Long-term treatment of hyperprolactinaemia with bromocriptine: effect of drug withdrawal.

Fifty-one patients with hyperprolactinaemia (23 with macroadenoma, 23 with microadenoma, and five with idiopathic hyperprolactinaemia) were treated with bromocriptine for 2-12 years (4.9 +/- 2.9 years, mean +/- SD). During therapy, the serum PRL levels were suppressed into the normal range in all but five patients. In these five patients, despite the high circulating PRL, gonadal function returned to normal in three, while in the other two gonadotrophin reserve was impaired even before therapy. Gel chromatography showed that one of these patients had a high proportion of a large molecular weight form of PRL. Twenty-four patients received bromocriptine as the sole method of treatment for over 2 years (3.4 +/- 2.3 years). In five out of the 24 subjects (21%), serum PRL remained normal with no clinical symptoms after prolonged drug withdrawal (1-4 years). Twenty-one patients received radiotherapy in conjunction with bromocriptine therapy. Of these 11 had prior surgery. After a follow-up of 6.0 +/- 3.0 years after radiotherapy, serum PRL remained within the normal range in 6 out of 21 subjects (29%), 1-4 years after bromocriptine withdrawal. One of the patients had impaired GH response to insulin hypoglycaemia developing after radiotherapy. We conclude that prolonged bromocriptine treatment is an effective treatment for prolactinomas.

Adenoma↗
PubMed1995

Effectiveness of a long-acting injectable form of bromocriptine in patients with prolactin and growth hormone secreting macroadenomas.

OBJECTIVE: With the development of new long-acting depot preparations of bromocriptine (bromocriptine LAR), we investigated the effectiveness of intramuscular injections of long-acting bromocriptine in patients with prolactin and GH secreting macroadenomas. STUDY DESIGN AND PATIENTS: Fourteen patients with PRL secreting (8 patients) and GH secreting (6 patients) macroadenomas were treated with monthly intramuscular injections of a long-acting and repeatable form of bromocriptine for 3-6 months. A 50-mg monthly dose was administered in the majority of patients with PRL secreting macroadenomas. A 100-mg monthly dose was administered in all patients with GH secreting macroadenomas. MEASUREMENTS: Plasma PRL and/or GH levels were measured 6 and 12 hours after the first injection and then on days 1, 2, 14 and 28 after each injection, up to a maximum period of 6 months. Patients were hospitalized for 48 hours after each injection and were specifically questioned with respect to side-effects. Pituitary imaging with MRI or CT scans was performed in all patients before commencing treatment and was subsequently repeated in 5/8 patients with macroprolactinomas and 5/6 patients with GH secreting macroadenomas after the completion of a 6-month course of treatment. RESULTS: In all patients with macroprolactinomas, serum PRL levels decreased significantly after their first 50-mg injection with nadir levels obtained by 24-48 hours post injection (12815 +/- 8704 vs 1480 +/- 1859 mU/l; mean +/- SD, P < 0.01). At their latest follow-up, on a 50-mg monthly dose, 4 patients developed normoprolactinaemia (PRL levels < 360 mU/l) while two patients demonstrated a significant reduction in serum PRL levels (70 and 87% or pretreatment values). In two patients, although a substantial decrement of serum PRL levels was achieved 12-24 hours post injection, serum PRL levels increased to pretreatment values by day 14 post injection. Both patients received a higher (100 mg) monthly dose which was partially effective in one patient. In two patients with GH secreting macroadenomas, a sustained decrease of elevated GH levels was observed; in two patients, while a substantial reduction of the elevated serum GH levels was achieved 12-24 hours after the first and subsequent injections, serum GH levels increased to pretreatment values by day 14 post injection; in two patients there was no effect on the elevated serum GH levels. Significant tumour shrinkage (24-50%) was observed in 5/5 patients with PRL secreting macroadenomas assessed at completion of a 6-month course of treatment. Significant tumour shrinkage was also documented in 2/5 acromegalics tested (29 and 46% respectively). CONCLUSION: It is concluded that bromocriptine LAR is an effective treatment in the majority of patients with macroprolactinomas; it is also partially effective in some patients with GH secreting macroadenomas.

Adenoma↗
PubMed2004

Intracerebroventricular injections of prolactin counteract the antagonistic effect of bromocriptine on rabbit maternal behaviour.

To investigate the participation of prolactin in nest-building and maternal behaviour in rabbits, we administered (from pregnancy day 26 to parturition) rabbit prolactin (rbPRL; or vehicle) intracerebroventricularly (i.c.v.) to primiparous animals injected with bromocriptine subcutaneously (s.c.). Control females (given vehicle s.c. and i.c.v.) built a maternal nest (of straw and body hair) in 77% of cases. This proportion decreased to 19% in the bromocriptine-only group (P < 0.05) and increased to 93% in the group given bromocriptine plus rbPRL (P > 0.05). Maternal behaviour (i.e. the adoption of a crouching posture over the litter inside the nest box) was expressed by 77% of control rabbits, 19% of bromocriptine-only animals (P < 0.05) and 57% of females given bromocriptine plus rbPRL (P > 0.05). Values of nonmaternal activities (i.e. scent-marking, ambulation in an open field) were similar among the three studied groups. These results suggest that prolactin, acting in late pregnancy, plays a major role in the stimulation of nest-building and maternal behaviour in rabbits.

Animals↗
PubMed1987

Plasma and pituitary prolactin and blood pressure in bromocriptine-treated spontaneously hypertensive and Wistar-Kyoto rats.

1. The effects on blood pressure (BP) and plasma and pituitary prolactin (PRL) of a 13 day intraperitoneal infusion of bromocriptine delivered by osmotic minipump were investigated in spontaneously hypertensive rats (SHR) and their normotensive controls, the Wistar-Kyoto rats (WKY). 2. In the SHR, a fall in BP which was steepest over the initial few days and sustained up to day 12 was observed in the bromocriptine-treated group compared with the lack of a change in BP observed in the vehicle-treated group. The plasma PRL level taken on day 13 was found to be significantly lower in the bromocriptine-treated group than in the vehicle-treated group. 3. In the WKY, bromocriptine had no significant effect on either BP or plasma PRL. 4. Pituitary PRL content was significantly lower in the SHR than in the WKY. The suppression by bromocriptine treatment was greater in the SHR than in the WKY. 5. These results provide further evidence for a central dopaminergic insufficiency in the SHR and raise the possibility that PRL may, either directly or indirectly by interacting with other factors in the SHR, influence BP.

Animals↗
PubMed1990

Changes in saline and water intakes in bromocriptine-treated genetically hypertensive and normotensive rats.

1. We have previously reported on the effects of a 13-day intraperitoneal infusion of bromocriptine delivered by osmotic pump on blood pressure, plasma and pituitary PRL levels in genetically hypertensive (GH) rats and their normotensive (NT) controls. This paper reports further on that study in describing the changes in saline and water intakes in rats as a result of bromocriptine (BRC) treatment. 2. In the GH rats, bromocriptine did not have any significant effect on saline or water intake. 3. In the NT rats, bromocriptine significantly decreased saline intake and increased water intake. 4. The saline intake in the vehicle-treated GH rats was significantly lower than that in the vehicle-treated NT rats while the water intake was not significantly different. 5. These results indicate that differences exist between the GH and NT rats with regard to their saline and water intakes and their responses to chronic bromocriptine treatment. The changes in saline and water intakes in the GH rats seem to be different from those seen in the spontaneously hypertensive rat in another study.

Animals↗
PubMed1977

Serum prolactin levels and the value of bromocriptine in the treatment of anovulatory infertility.

Basal serum levels of prolactin were measured in 37 infertile anovulatory patients who had failed to conceive on therapy with clomiphene citrate. Twenty of these patients, 16 of whom had galactorrhoea, had elevated basal serum prolactin values which were suppressed to normal or subnormal values during therapy with bromocriptine, the most commonly effective dose being 2.5 mg twice daily. Ovulation, as assessed by urinary oestrogen and pregnanediol measurements, was induced in 17 of these patients with pregnancy in 14. Ovarian responses short of defined criteria for ovulation were induced initially in eight patients, but these progressed to full ovulatory responses in five patients, either on the same or increased doses of bromocriptine. In all the patients who ovaulated, the prolactin levels had been reduced below the mean value for normal women (10.6 ng-ml). The three patients who failed to ovulate all had values higher than this at a dose of bromocriptine reaching 5.0 mg thrice daily. There seemed to be no value in increasing the dose of bromocriptine once ovulation had been achieved. Of the 17 patients with normal basal prolactin values, only one had an unequivocal response to bromocriptine with ovulation and conception, even though the prolactin values in the majority were suppressed to below normal.

Adult↗