Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Bromocriptine”

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

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

At least 217 records · Page 12Linked to original sources
PubMed1994

Effect of bromocriptine and SMS 201-995 on growth of human somatotrophic and non-functioning pituitary adenoma cells in vitro.

The effect of the dopamine agonist bromocriptine and the somatostatin analog SMS 201-995 on growth of 12 human somatotrophic and 13 non-functioning adenoma cell cultures was investigated. When adenoma cells were maintained in medium supplemented with 5% fetal calf serum, cell counts of 10 of 12 somatotrophic cultures increased to 145 +/- 6 and 171 +/- 9% (mean +/- SD) and in 12 of 13 non-functioning cell cultures up to 125 +/- 12 and 217 +/- 15% after 3 days of incubation. In most cases bromocriptine and SMS 201-995 dose dependently (1 nmol/l to 10 mumol/l) inhibited adenoma cell growth but there was only (1, 10 mumol/l) a significant inhibitory effect at high doses of both drugs. A 1 mumol/l concentration of bromocriptine decreased cell counts of 5 of 12 somatotrophic cell cultures (range 84 +/- 3 to 76 +/- 6% vs control = 100%) and in 5 of 13 non-functioning cell cultures (range 85 +/- 4 to 71 +/- 7%). A 10 mumol/l concentration of bromocriptine decreased cell counts in all 12 somatotrophic (range 87 +/- 1 to 61 +/- 8%) and in 12 of 13 non-functioning adenoma cultures (range 87 +/- 6 to 57 +/- 3%). Bromocriptine specifically inhibited growth because its effect could be reversed by the dopamine D2-receptor antagonist haloperidol. Both 1 and 10 mumol/l SMS 201-995 significantly decreased cell counts in three of six somatotrophic (87 +/- 3 to 38 +/- 3%) cell cultures. In two of five cases growth of non-functioning adenoma cultures was suppressed by 1 mumol/l SMS 201-995, and in four of five cases by 10 mumol/l (86 +/- 3 to 74 +/- 4%). The growth inhibitory effect of both bromocriptine and SMS 201-995 was not just due to an effect on growth of fibroblasts contaminating the adenoma cell cultures, because it could be observed also when adenoma cells were maintained in a D-valine-supplemented medium that suppresses fibroblast growth. In summary, both bromocriptine and SMS 201-995 at high doses were able to inhibit cell growth of cultured somatotrophic and non-functioning adenomas in vitro. However, the mechanism of this inhibitory effect is not yet well understood.

Adenoma↗
PubMed1986

Inhibitory effects of bromocriptine on mammary development and function in lactating mice.

Five experiments were conducted. In the first, the plasma prolactin concentration of lactating mice was significantly reduced 3, 6 and 12 h after a single injection of 0.2 mg bromocriptine at 09.00 h, but recovered to normal levels at 24 h. A second injection at 17.00 h (i.e. total dose of 0.4 mg) completely prevented this recovery. Prolactin concentration was also reduced after the s.c. implantation of a solid pellet of bromocriptine. Once daily injections of bromocriptine for 7 days starting 1-day prepartum (early lactation group) or on day 5 of lactation (established lactation group) significantly reduced milk yield, assessed from the weight gain of the litter or estimated by a tritiated water dilution procedure. In early lactation the degree of inhibition was positively related to the size of the suckling litter (three pups, no inhibition; nine pups, 16.4% inhibition; 14 pups, 40.8% inhibition), but in established lactation an inhibition of 25-30% was observed, regardless of litter size. Twice-daily injections and s.c. implants of bromocriptine both reduced milk yield by a greater amount (approximately 45%), but in no case was secretion completely suppressed. The inhibitory effect of bromocriptine was prevented by the simultaneous administration of ovine prolactin (0.4 mg). Lactogenesis was apparently not affected by bromocriptine treatment. At the end of the early lactation treatment period, the mammary glands of bromocriptine-treated animals were significantly smaller and contained fewer cells than those of controls, but this was not the case in animals treated during established lactation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Bromocriptine-induced reduction of body fat in pigs.

An experiment was conducted with 36 crossbred finishing pigs (18 male castrates and 18 females) to evaluate the effect of bromocriptine implants on growth, feed intake, feed efficiency, plasma urea nitrogen (PUN) and carcass characteristics. Three levels of bromocriptine (0, 5 and 10 mg/[pig.d]) were administered, via implants at the base of the ear, to six (two replicates of three) male castrates or to six (two replicates of three) intact female pigs (2 x 3 factorial arrangement of treatments). Average initial weight of pigs at the time of implantation was 89.7 kg, and the implants remained in the pigs for 28 (replicate 1) or 30 (replicate 2) d prior to slaughter. Gain, feed intake and efficiency of feed utilization were not affected (P greater than .10) by bromocriptine. Plasma urea nitrogen was lower in female pigs administered 10 mg bromocriptine; bromocriptine did not affect PUN of male pigs (gender x bromocriptine, P less than .08). Tenth rib fat thickness and average backfat thickness were lower (P less than .06) and percentage of muscling was higher (P less than .06) in pigs implanted with bromocriptine. Female pigs had less 10th rib fat but larger loin eye areas and a greater percentage of muscling than male pigs.

Adipose Tissue↗
PubMed1994

Positive response to compound CV 205-502 in hyperprolactinemic patients resistant to or intolerant of bromocriptine.

The clinical effects of CV 205-502, a potent and non-ergot-derived dopamine agonist, were investigated in 24 selected patients with hyperprolactinemia previously treated with standard oral bromocriptine, the slow-release oral form of bromocriptine (BRC-SRO) and/or the long-acting injectable form of bromocriptine (BRC-LAR); 14 were chosen because of their resistance to treatment and ten because they were intolerant of the different forms of bromocriptine. A macroprolactinoma was present in seven patients and a microprolactinoma in ten, whereas seven had no radiological images of a pituitary tumor and were classified as having non-tumoral hyperprolactinemia. All the 24 patients were treated with CV 205-502 at a daily dose of 0.075-0.6 mg for 3-12 months. All the patients had gonadal dysfunction and galactorrhea. Basal serum prolactin values ranged from 70 to 1677 ng/ml. CV 205-502 was effective in 11 of the 14 patients resistant bromocriptine, BRC-SRO and BRC-LAR; serum prolactin levels became normal within 6 months and a tumor shrinkage was obtained in five of the seven macroprolactinomas. In general, the drug was effective and well tolerated. Only three patients (two resistant and one intolerant) manifested nausea, vomiting and postural hypotension. In conclusion, this study shows that CV 205-502 is effective in bromocriptine-resistant hyperprolactinemic patients. Furthermore, CV 205-502 has insignificant and tolerable side-effects in patients intolerant of bromocriptine. CV 205-502 can, therefore, be considered a useful and effective drug, and an interesting therapeutic alternative to the ergot-derived dopamine-agonist drugs in use today.

Administration, Oral↗
PubMed1996

Nasal spray administration of bromocriptine: pharmacology and effect on serum prolactin level in puerperal women.

This study was aimed at investigating the absorption of nasally administered bromocriptine and its effect on serum prolactin level. Fifteen physiologically hyperprolactinemia women who had asked to discontinue breast feeding received a single nasal spray administration of 0.8 mg bromocriptine. Serum prolactin levels were measured by radioimmunoassay at 30 and 15 min before drug administration, at the time of administration and at 15, 30, 60, 120, 240, 480 and 720 min after administration; bromocriptine was radioimmunoassayed in only five of the patients from time 0 to 720 min after administration. Serum bromocriptine levels increased rapidly after administration, reached a maximum at 120 min and thereafter declined slowly over the subsequent 10 h. As the bromocriptine level increased there was a decline in the serum prolactin level. The first significant decline in serum prolactin level compared with the baseline level occurred at 30 min after administration and the level continued to decrease significantly until time 120 min. Four hours after administration the mean serum prolactin level was within the normal assay range. The maximum decline in serum prolactin level was reached at 720 min after administration. Correlation analysis between serum bromocriptine and prolactin concentrations yielded a significant negative value between times 0 and 120 min after administration. There was no significant change in mean orthostatic systolic or diastolic blood pressure or in mean heart rate. Only one patient complained of headache and dizziness; another experienced mild transient nausea, and none had vomiting. Ten patients (66.67%) reported light endonasal burning and an unpleasant taste which subsided after a few minutes; no patient showed nasal irritation at nasal examination. In conclusion, nasal administration of 0.8 mg bromocriptine was effective in reducing the serum prolactin level for more than 12 h after administration without inducing significant side-effects.

Administration, Intranasal↗
PubMed2000

Effects of bromocriptine administration during the follicular phase of the oestrous cycle on prolactin and gonadotrophin secretion and follicular dynamics in merino monovular ewes.

Two experiments using Spanish Merino ewes were conducted to investigate whether the secretion of prolactin during the follicular phase of the sheep oestrous cycle was involved in the patterns of growth and regression of follicle populations. In both experiments, oestrus was synchronized with two cloprostenol injections which were administered 10 days apart. Concurrent with the second injection (time 0), ewes (n = 6 per group) received one of the following treatments every 12 h from time 0 to 72 h: group 1: vehicle injection (control); group 2: 0.6 mg bromocriptine (0.03 mg per kg per day); and group 3: 1.2 mg bromocriptine (0.06 mg per kg per day). In Expt 1, blood samples were collected every 3 h from 0 to 72 h, and also every 20 min from 38 to 54 h to measure prolactin, LH and FSH concentrations. In Expt 2, transrectal ultrasonography was carried out every 12 h from time 0 until oestrus, and blood samples were collected every 4 h to measure prolactin, LH and FSH concentrations. Ovulation rates were determined by laparoscopy on day 4 after oestrus. Bromocriptine markedly decreased prolactin secretion, but did not affect FSH concentrations, the mean time of the LH preovulatory surge or LH concentrations in the preovulatory surge. Both doses of bromocriptine caused a similar decrease in LH pulse frequency before the preovulatory surge. The highest bromocriptine dose led to a reduction (P < 0.01) in the number of 2-3 mm follicles detected in the ovaries at each time point. However, bromocriptine did not modify the total number or the number of newly detected 4-5 mm follicles at each time point, the number of follicles > 5 mm or the ovulation rate. In conclusion, the effects of bromocriptine on gonadotrophin and prolactin secretion and on the follicular dynamics during the follicular phase of the sheep oestrous cycle indicate that prolactin may influence the viability of gonadotrophin-responsive follicles shortly after luteolysis.

Analysis of Variance↗
PubMed2001

Central bromocriptine-induced tachycardia is reversed to bradycardia in conscious, deoxycorticosterone acetate-salt hypertensive rats.

A central dopaminergic origin has been demonstrated for the bromocriptine-induced tachycardia in conscious, normotensive rats. The present study investigated the effect of bromocriptine on heart rate and the principal site of action of this agonist in conscious, deoxycorticosterone acetate-salt hypertensive rats, in which altered central dopaminergic activity has been previously reported. Intravenous administration of bromocriptine (150 microg/kg) increased heart rate (49+/-5 beats/min.) in uninephrectomized control rats, while it induced a significant bradycardia (50+/-6 beats/min.) in deoxycorticosterone acetate-salt hypertensive rats. In the latter animals, intravenous (500 microg/kg) or intrathecal (40 microg/rat at T9-T10) pretreatment with domperidone, a selective dopamine D2 receptor antagonist that does not cross the blood-brain barrier, reduced partially, but significantly, the bradycardiac responses to bromocriptine (reduction of about 44% and 48% of the maximal effect, respectively). In contrast, the bromocriptine-induced bradycardia was fully abolished by intravenous pretreatment with metoclopramide (300 microg/kg), a dopamine D2 receptor antagonist that crosses the blood-brain barrier, or by combined pretreatment with intravenous and intrathecal domperidone. These results indicate that, in deoxycorticosterone acetate-salt hypertensive rats, bromocriptine decreases rather than increases heart rate, an effect that is mediated partly through a peripheral D2 dopaminergic mechanism and partly through stimulation of spinal dopamine D2 receptors. They further support the concept that, in normotensive, conscious rats, the central tachycardia of bromocriptine appears to predominate and to mask the bradycardia of this agonist at both peripheral and spinal dopamine D2 receptors.

Animals↗
PubMed1990

Attenuating effect of bromocriptine on cysteamine anticarcinogenesis of stomach cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine.

The effect of bromocriptine on inhibition by cysteamine of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine was investigated in inbred Wistar rats. After 25 weeks of p.o. treatment with N-methyl-N'-nitro-N-nitrosoguanidine, rats were given injections every other day: cysteamine (50 mg/kg body weight); cysteamine (50 mg/kg body weight) plus bromocriptine (0.5 or 0.25 mg/kg body weight); or bromocriptine (0.5 or 0.25 mg/kg body weight). In week 52, the group treated with cysteamine showed a significantly decreased incidence of gastric cancers. Concomitant treatment with bromocriptine at 0.5 but not at 0.25 mg/kg body weight significantly attenuated the inhibitory effect of cysteamine on gastric carcinogenesis. Administration of bromocriptine alone at either dosage had no influence on gastric carcinogenesis. The labeling index of the antral mucosa was significantly reduced in rats treated with cysteamine and significantly higher in those treated concomitantly with bromocriptine at 0.5 mg/kg body weight than in those treated with cysteamine alone. These findings indicate that cysteamine suppressed gastric carcinogenesis and that bromocriptine at high dosage attenuated this inhibition. These findings also suggest that dopamine is involved in the mechanism of inhibition of gastric carcinogenesis by cysteamine.

Animals↗
PubMed1989

The behavioral toxicity of bromocriptine in patients with psychiatric illness.

Dopamine agonists may be useful in the treatment of neuroleptic-induced hyperprolactinemia and movement disorders; it is a treatment approach that has been avoided for fear of inducing or exacerbating psychotic symptoms. The risks of giving dopamine agonists to psychiatric patients have been well documented in the literature. To further evaluate the psychotogenic effects of bromocriptine, a dopamine receptor agonist, we conducted a double-blind study in which 16 psychiatrically stable patients were treated for tardive dyskinesia with neuroleptics plus high doses of bromocriptine (N = 11) or placebo (N = 5) for 10 weeks. The diagnoses included schizophrenia, schizoaffective disorder, and major depression with psychotic features. Patients were evaluated weekly with the Brief Psychiatric Rating Scale and the Clinical Global Impression Scale during the 10-week treatment phase and for 8 weeks after medication was withdrawn. There were no statistically significant differences between active and placebo groups in behavioral ratings at baseline, week 10, and week 18. These results are compared with the findings of previous studies in which bromocriptine was given to psychiatric patients. Although the literature suggests that bromocriptine can induce or exacerbate psychosis in psychiatric patients, this occurs primarily in those with a psychotic diathesis and who are not currently receiving neuroleptic medication. Other important factors include the dose of bromocriptine, duration of treatment, and the clinical state of the patient at the time bromocriptine treatment is initiated. These results suggest that bromocriptine can be safely used in patients at risk for psychotic illnesses as long as patients are clinically stable and maintained on neuroleptics.

Adult↗
PubMed1987

Long-term treatment with high-dosage bromocriptine in advanced Parkinson's disease.

Long-term follow-up indicated that levodopa as a replacement therapy merely improves the parkinsonian symptoms, and does so for only a limited number of years. The reason for this tachyphylaxis or declining efficacy in levodopa therapy and the increasing number and intensity of various distressing difficulties in the management of Parkinson's disease, such as dyskinesias and on-off phenomena, is the main subject of many recent studies. It is still widely accepted that levodopa provides the best therapeutic tool for Parkinson's disease. Bromocriptine, an ergot derivative, is the main clinically used dopamine agonist, and it has been established as a valuable adjunct in the treatment of Parkinson's disease. Bromocriptine is most useful in patients with a declining efficacy of levodopa treatment, in patients with diurnal oscillations in motor performance, especially in patients with wearing-off phenomena, and in patients with onset and end-of-dose dyskinesias. The question of bromocriptine dosage, required to obtain an optimal benefit and a decreased rate of late adverse reactions, is quite controversial. The trend has been to lower daily dosage of bromocriptine, i.e., low doses suffice in patients with mild, early disease. Higher doses of bromocriptine seem to be required in patients with severe parkinsonian deficits. In this retrospective study of 8 years experience with high dosage of bromocriptine in levodopa response-losing parkinsonian patients, the adjunction of bromocriptine had a clear-cut but short-lasting beneficial effect on the disability scores.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Pleuropulmonary disease during bromocriptine treatment of Parkinson's disease.

Pleuropulmonary disease has been observed in eight patients with Parkinson's disease treated with bromocriptine or its related compound, mesulergine. The pleuropulmonary changes included pleural effusions, pleural thickening, and parenchymal lung disease. The patients developed symptoms from nine months to four years after starting treatment with bromocriptine that varied in dosage from 22 to 50 mg daily, while the patient receiving mesulergine was taking 6 mg daily. No other cause was found for the pleuropulmonary changes. In six patients the medication was discontinued with subsequent clinical, physiologic, and radiologic improvement. In two patients bromocriptine treatment was continued for one to two years, and in one patient there was further physiologic and radiologic progression of the pleuropulmonary changes. These findings suggest a causal relationship between bromocriptine treatment and pleuropulmonary disease. We recommend a chest roentgenogram and pulmonary function evaluation prior to bromocriptine treatment with follow-up studies if the patient develops respiratory symptoms. Physicians prescribing bromocriptine should be aware of this side effect to ensure early recognition and prompt withdrawal of bromocriptine therapy.

Aged↗
PubMed1986

Bromocriptine: long-term low-dose therapy in Parkinson's disease.

Low-dose bromocriptine therapy (average dose 14.5 mg/day at 2 years) produced significant improvement in 25 of 39 parkinsonian patients. Bradykinesia was less in de novo subjects; tremor and rigidity improved most in the levodopa subjects. Five of six patients improved after a low-dose bromocriptine drug "holiday." After the addition of bromocriptine any reductions in levodopa dosage were small, with repeated cuts made gradually over months preventing the deterioration commonly seen with larger sudden reductions in levodopa dosage. Five patients withdrew because of intolerable adverse effects, two because of worsening response. Adverse effects were mild and generally dose dependent, and in some patients they disappeared without reduction in continuing bromocriptine therapy. Eighty percent of those who tolerated bromocriptine maintained response over 2 years. Bromocriptine did not induce dyskinesia, the wearing-off response, or the on-off phenomenon in de novo subjects and was used as a first choice drug in these parkinsonian patients. Best results were obtained from a combination of bromocriptine and levodopa.

Adult↗
PubMed1984

[How do we explain the antihypertensive effect of bromocriptine? Clinical and experimental contribution].

The mechanism of the antihypertensive properties of bromocriptine was investigated in dog and man. In anaesthetized dogs, bromocriptine induced a decrease in the pressor responses to adrenaline or phenylephrine and reduced the hypotensive properties of clonidine. In 6 hypertensive patients with Parkinson's disease, chronic treatment with bromocriptine (46.4 +/- 12.0 mg/day) elicited both a significant decrease in blood pressure and an improvement of extrapyramidal symptoms. During bromocriptine therapy, domperidone (60 mg/day during 1 month), a specific peripheral dopaminergic antagonist was introduced. The drug did not change the levels of blood pressure (before domperidone: 150.8 +/- 22.5/79.9 +/- 8.9 mmHg after domperidone: 150 +/- 17.3/87.5 +/- 12.9 mmHg). These results confirm the antihypertensive properties of bromocriptine and demonstrate that, beside their dopaminergic properties, the drug also possesses mixed alpha 1 and alpha 2 adrenolytic actions. These two properties may contribute to the mechanism of the antihypertensive effects of bromocriptine. These data also show that domperidone can be used in bromocriptine-treated hypertensive parkinsonians without side effects on blood pressure.

Adrenergic alpha-Antagonists↗
PubMed1984

Mechanism of the depressor effect of bromocriptine in the spontaneously hypertensive rat.

Bromocriptine, a dopamine (DA) agonist which passes the bloodbrain barrier, has been shown to have a depressor effect in the spontaneously hypertensive rat of the Okamoto strain. To elucidate the mechanism of this depressor effect, the responses of mean arterial blood pressure and plasma epinephrine (EP), norepinephrine, prolactin and renin activity to i.v. administration of bromocriptine (500 micrograms/kg), alone and after pretreatment with i.v. metoclopramide, a DA antagonist which crosses the blood-brain barrier, and domperidone, a DA antagonist which does not cross the blood-brain barrier, were examined in conscious unrestrained spontaneously hypertensive rats. Metoclopramide attenuated the depressor action of bromocriptine in a dose-related manner, but domperidone had no effect. Neither metoclopramide nor domperidone given alone altered mean arterial blood pressure. Bromocriptine given alone decreased plasma prolactin and increased plasma EP without altering plasma norepinephrine or plasma renin activity. Pretreatment with either metoclopramide or domperidone completely blocked the EP-stimulating effects of bromocriptine. Neither DA antagonist given alone had an effect on plasma EP, norepinephrine or plasma renin activity; both agents stimulated prolactin release. These results suggest that the depressor action of i.v. administered bromocriptine is mediated mainly through a central dopaminergic mechanism rather than by peripheral effects and that plasma EP responses to bromocriptine do not directly contribute to its depressor action.

Animals↗
PubMedDate not supplied

[Puerperal inhibition of lactation with metergoline or bromocriptine].

In a controlled, randomised, prospective, clinical study, the effect of prolactin suppression and clinical course of the lactation suppressors Bromocriptine and Metergoline were investigated. During 7 months 150 patients were studied. 81 of those patients, who did not nurse, were treated by Bromocriptine (primary lactation suppression: n = 62, secondary suppression: n = 19) and 69 of the patients were treated by Metergoline (primary suppression: n = 54, secondary suppression: n = 15). The drugs were administrated orally to all subjects, dosed 2 x 2.5 mg/d of Bromocriptine for 14 days and 3 x 4 mg/d of Metergoline for 10 days, starting in average after 13 hours. Puerperal suppression of prolactine were compared with randomised breast feeding subjects (n = 30). In Bromocriptine treated women the average plasma prolactin level decreased from 78.4 +/- 22 ng/ml to 17.0 +/- 3.3 ng/ml during five days of treatment. In Metergoline treated women the plasma prolactin level decreased from 129.7 +/- 15.1 ng/ml to 56.9 +/- 10.0 ng/ml during the first days of treatment. Prolactin level of breast feeding subjects decreased from 233.6 +/- 21.4 ng/ml to 185.8 +/- 23.7 ng/ml during the same period (p < 0.05). There is no statistical significancy of clinical difference of both drugs, but a statistical trend was seen. With Bromocriptine treated women were suppressed efficiently in 71 of 81 cases, 10 refused. Refusals were divided in two quality levels, level I with subjects with moderate complaints and little puerperal lactation, level II with subjects with considerable complaints including strong puerperal lactation. With Metergoline suppressed women, treatment was efficiently in 51 of 69 cases, but refusals of level I were observed in 11 cases and refusals of level II were observed in 7 cases. The results show that Bromocriptine and Metergoline are effective on suppression of lactation. Under the current drug dose of Metergoline an advantage of Bromocriptine were observed. Only further studies could investigate, whether an adaptation of drug dose would improve the clinical efficiency of Metergoline.

Administration, Oral↗
PubMed1976

A comparison between amantadine and bromocriptine using the stereotyped behaviour response test (SBR) in the rat.

Amantadine (100 mg/kg), apomorphine (2.5-10 mg/kg) and bromocriptine (10-50 mg/kg) all produced stereotyped behaviour in the rat. Apomorphine was rapid in onset and of short duration, amantadine was slower to reach a maximum and bromocriptine had a delayed onset of 50 min and a prolonged action. Amantadine and bromocriptine were antagonised by pimozide (1 mg/kg for 30 min) suggesting an action on dopamine receptors, and by D,L-alpha-methyl-p-tyrosine (150 mg/kg for 3 h) suggesting an indirect action. Amantadine, though not bromocriptine, antagonised apomorphine and amantadine also reversed the SBR due to bromocriptine. Pretreatment of rats with p-chlorophenylalanine (100 mg/kg twice daily for 2 days) had no effect on bromocriptine. The significance of these results is discussed with reference to the proposed mechanism of action of bromocriptine and to the use of multiple drug therapy in Parkinsonism.

Amantadine↗
PubMed1993

Prolactin-secreting macroadenomas in adolescents. Response to bromocriptine therapy.

OBJECTIVE: To report five cases of prolactin (PRL)-secreting macroadenomas in adolescents, including their presentations and responses to bromocriptine mesylate treatment. PATIENTS: Five adolescents (three females and two males) aged between 12.5 and 17 years were diagnosed as having PRL-secreting macroadenomas at the pediatric endocrine service at New York University Medical Center between 1987 and 1989. Presenting complaints included visual field deficits, gynecomastia, and amenorrhea, both primary and secondary. All patients demonstrated some feature of hypogonadism or pubertal arrest. Diagnostic criteria included an elevated serum PRL level (mean, 1670 micrograms/L; range, 610 to 3700 micrograms/L) and visualization of a pituitary tumor that measured greater than 1 cm by either a computed tomographic scan or magnetic resonance imaging (mean size, 2.7 cm; range, 1.4 to 4 cm). INTERVENTIONS: Each patient was treated with bromocriptine mesylate at an oral dose of 7.5 mg/d. The patients continued with that treatment for the duration of the study period. MEASUREMENTS AND RESULTS: Anterior pituitary function was evaluated in four of five patients before treatment. All four were growth hormone deficient. Three patients were also gonadotropin deficient. Thyrotropin (thyroid-stimulating hormone) and corticotropin (adrenocorticotropic hormone) deficiencies were demonstrated in three patients who had multiple pituitary deficits. Follow-up testing included serial PRL measurements and radiographic imaging of tumor size. All patients demonstrated a marked decrease in PRL levels, as well as in tumor size (mean shrinkage, 70%). The three patients who initially had visual field deficits showed significant improvement of vision with bromocriptine therapy. Follow-up study of anterior pituitary function showed significant improvement with bromocriptine treatment in three patients. CONCLUSIONS: Bromocriptine was quite effective in the shrinkage of PRL-secreting macroadenomas in all our patients. It is a noninvasive treatment that can preserve and restore vision, as well as pituitary function, which is integral to continued growth and sexual maturation of the adolescent. Bromocriptine is preferable to surgery or radiation in the treatment of PRL-secreting macroadenomas in the adolescent.

Adolescent↗
PubMed1984

Comparative effects of tamoxifen and bromocriptine on prolactin and pituitary weight in estradiol-treated male rats.

Male ACI rats were treated with estradiol to induce hyperprolactinemia and pituitary hypertrophy and hyperplasia. Animals received estradiol alone or with tamoxifen or bromocriptine for 4, 8, or 12 weeks. Estradiol treatment resulted in time-dependent increases in pituitary wet weight and serum prolactin concentrations. Tamoxifen completely blocked the increase in both variables; bromocriptine decreased but did not prevent time-dependent increases. Animals were also treated for 8 weeks with estradiol alone, followed by 4 weeks with estradiol and tamoxifen or bromocriptine. Neither compound reversed the hyperprolactinemia, although the pituitary wet weight of animals treated with bromocriptine was slightly but significantly reduced. These findings suggest that in this model if treatment is initiated simultaneously with estrogen stimulation, tamoxifen is more effective than bromocriptine at the doses studied; and, if therapy is initiated subsequent to the establishment of estrogen-induced hyperprolactinemia and pituitary hyperplasia, bromocriptine is more effective than tamoxifen at the doses studied.

Animals↗