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PubMed1984

Studies in constitutionally tall adolescents. II. Effects of bromocriptine on growth hormone secretion and adult height prediction.

After previous demonstration of paradoxical GH responses to TRH and oral glucose loading tests in some constitutionally tall adolescents, we studied the effects of a small dose of bromocriptine (5 mg/day) on GH secretion and adult height prediction. In 10 patients, each of whom had a substantial plasma GH increase after TRH injection, bromocriptine reduced or suppressed this abnormal response. In 4 of these patients who also had paradoxical GH increases after glucose loading, bromocriptine suppressed this abnormality in 2. Predicted adult height was reduced in 10 of the 12 patients after 6-12 months of treatment. This reduction resulted either from a decrease in growth velocity, an increase in skeletal maturation rate, or both. Since no side effects were noticed we suggest that bromocriptine may be a valuable alternative to sex steroid treatment to limit final height in excessively tall adolescents.

Adolescent↗
PubMed1984

Perivascular fibrosis in prolactinomas: is it increased by bromocriptine?

Prolonged treatment of patients with pituitary prolactinomas with bromocriptine may increase the consistency of the tumor thereby making selective extirpation more difficult. We made quantitative determinations of the amount of perivascular fibrous tissue in prolactinomas on random electron micrographs, comparing a group of 21 patients treated with bromocriptine for periods longer than 3 months and a control group of 21 patients who did not receive bromocriptine. Statistical analysis of the data showed a significant increase of perivascular fibrous tissue in the treated group (P less than 0.002). We suspect that this fibrosis is a consequence of the rapid shrinkage of prolactinoma cells caused by bromocriptine. Presumably, this cell shrinkage causes enlargement of the extracellular and perivascular spaces which are filled by the deposition of collagen, producing a more dense consistency of the adenoma.

Adenoma↗
PubMed1984

Necrotic changes in prolactinomas after long term administration of bromocriptine.

Six prolactinoma patients were studied endocrinologically and their tumors were examined histologically after long term bromocriptine therapy. In patient 1 with a large prolactinoma, a marked reduction in size and a remarkable decrease in elevated serum PRL levels occurred after bromocriptine treatment for 8 months. The histological findings consisted of two components, i.e. shrunken island-like cell nests and acellular spaces. Some degenerative and necrotic tumor cells, hyaline substance, and fibrosis were observed with light and electron microscopy in these acellular spaces. Island-like cell nests consisted of atrophic cells having disproportionally scanty cytoplasm. The same histological findings were observed in four other patients. However, in another patient whose tumor decreased in size only slightly during bromocriptine therapy, the specimen had few acellular spaces. Thus, long term bromocriptine treatment of patients with prolactinomas may result in necrosis of some adenoma cells in some patients.

Adolescent↗
PubMed1984

Human menopausal gonadotropin/human chorionic gonadotropin-induced ovarian hyperstimulation with transient hyperprolactinemia: steroidogenesis enhanced during bromocriptine therapy in monkeys.

To examine the role of gonadotropin-induced hyperprolactinemia on reproductive function, 17 euprolactinemic ovulatory monkeys were given extended fixed dose regimens of human menopausal gonadotropin (hMG) (12 days), followed by hCG the next day, and some animals then received bromocriptine. All animals were given hMG/hCG from day 3 (D3) until D14, with hCG on D15; those in group I (n = 12) received no further therapy, while those in group II (n = 5) received bromocriptine (0.25 mg/kg X day, im) daily from the day of hCG administration until menses. Ovarian hyperstimulation developed to various degrees in all animals. Based on serum estradiol (E2) levels, 13 were high responders (E2, greater than 1000 pg/ml), 2 were medium responders (E2, 500-1000 pg/ml), and 2 were low responders (E2, 150-500 pg/ml). In group I, transient hyperprolactinemia occurred in the luteal phases in 8 of the 12 animals compared to the follicular phase levels in the same animals (P less than 0.01). In group II, bromocriptine treatment in the luteal phase prevented hyperprolactinemia, but there was no change in the menstrual cycle or luteal phase lengths; however, significant luteal phase increases in progesterone (P less than 0.005) and E2 (P less than 0.02) secretion occurred during bromocriptine therapy. Deliberate hMG/hCG studies in euprolactinemic women seem indicated to learn whether women so treated experience estrogen-progesterone-induced hyperprolactinemia like that in monkeys and, if so, to determine its consequences on the reproductive process.

Animals↗
PubMed1987

The effects of bromocriptine, thyrotropin-releasing hormone, and gonadotropin-releasing hormone on hormone secretion by gonadotropin-secreting pituitary adenomas in vivo and in vitro.

The characteristics and dynamics of hormone secretion in vivo and in vitro were investigated in six patients with gonadotropin-secreting pituitary adenomas. All six tumors secreted and contained FSH and different combinations of LH, beta-LH, and alpha-subunit. In addition, immunohistochemical examination of the pituitary tumor tissue showed staining with both LH and FSH in three and either LH or FSH in the other three tumors. TRH and GnRH stimulated hormone secretion in vivo and in vitro, and they also increased the hormone content of the cultured tumor cells. Bromocriptine significantly inhibited hormone release and reduced the hormone content of the tumor cells. In vivo, 2.5 mg bromocriptine significantly suppressed plasma hormone levels; the inhibiting effect on alpha-subunit concentrations was in general more marked than that on LH and FSH. We conclude that hormone release by gonadotropin-secreting pituitary adenomas can be stimulated by TRH and GnRH and inhibited by bromocriptine. Most of these tumors synthesize FSH, but there is a wide variation in the production of LH, beta-LH, and alpha-subunits. The sensitivity of hormone release to bromocriptine suggests that chronic therapy with this drug might have a beneficial effect on pituitary tumor size.

Adenoma↗
PubMed1987

Bromocriptine treatment in adolescent boys with familial tall stature: a pair-matched controlled study.

Recently, bromocriptine has been proposed as a novel agent for the treatment of excessively tall stature in adolescents. To further test its value, we treated nine boys, aged 10.0-15.4 yr, for 1 yr with bromocriptine (7.5 mg/day). A paradoxical plasma GH response to TRH was demonstrated in four of eight boys before and in five boys after 6 months of bromocriptine treatment. At the onset of therapy, the mean adult height prediction was 202.2 +/- 4.3 (+/- SD) cm (Bayley-Pinneau), 202.1 +/- 4.7 cm (TW Mark II), and 198.6 +/- 5.3 cm (Roche-Wainer-Thissen). After 1 yr of therapy, the mean adult height prediction had changed by -4.5 +/- 2.6 cm (Bayley-Pinneau), -3.4 +/- 2.2 cm (TW Mark II), and -2.6 +/- 1.2 cm (Roche-Wainer-Thissen). These reductions were solely due to a decrease in growth velocity and not to an increased skeletal maturation rate. To substantiate these findings, each treated boy was pair-matched with an untreated tall boy so that their chronological and skeletal ages differed by less than 1 yr. After 1 yr of follow-up, height predictions in the treated boys compared with those in the matched control boys gave significantly reduced results with the Bayley-Pinneau and the Roche-Wainer-Thissen, but not with the TW Mark II, method. Because of this discrepancy it is uncertain whether final height in tall boys will really be reduced by treatment with bromocriptine.

Adolescent↗
PubMed1987

Lack of bromocriptine-induced reduction of predicted height in tall adolescents.

Fifteen girls and five boys with excessive predicted adult height (chronological age, 10.1-14.6 yr; bone age, 11.0-14.0 yr) were treated with bromocriptine (two doses; 2.5 mg/day) to reduce their final height. After a mean treatment period of 1.14 yr (range, 0.6-1.75 yr) we did not find a reduction of predicted adult height [difference, -0.5 +/- 3.5 (+/- SD) cm according to Bayley and Pinneau's tables (P = NS) and +0.2 +/- 2.5 (+/- SD) cm according to the method of Tanner (P = NS)]. Mean peak plasma GH concentrations after TRH administration before and during bromocriptine were 51.5 +/- 49.4 and 58.5 +/- 50.7 mU/L, respectively. The wide range of the GH values may be explained by physiological variation in this age group. After ingestion of 2.5 mg bromocriptine a significant increase in plasma GH occurred within 3 h in six adolescents tested. Our results do not support the concept that bromocriptine may reduce predicted adult height in tall adolescents by decreased GH secretion or acceleration of skeletal maturation.

Adolescent↗
PubMed1991

A comparison of the efficacy and safety of pergolide and bromocriptine in the treatment of hyperprolactinemia.

UNLABELLED: Pergolide is a synthetic ergoline derivative with highly potent long-acting PRL-lowering activity, allowing therapy of hyperprolactinemia with a once daily administration of the drug. The results of two open-label, randomized controlled multicenter clinical trials are reported. Pergolide (taken once a day), was compared with bromocriptine (taken two to four times daily) regarding efficacy and safety in the reduction of PRL levels, the cessation of galactorrhea and amenorrhea, the improvement in sexual function, and tumor shrinkage in hyperprolactinemia without (trial I; 61 patients) and with radiologically evident pituitary tumors (trial II; 96 patients). Both drugs were equally effective in lowering PRL levels in both trials. A median optimal dose of 50 micrograms pergolide and 5 mg bromocriptine/day suppressed PRL levels in the 61 patients of trial I by more than 80%. During the 24-week investigational period galactorrhea disappeared in 96% and 87% of patients, whereas menstruation returned in 90% and 96% of patients, respectively. An equally high efficacy (optimal median dose: 75-100 micrograms pergolide, 7.5-10 mg bromocriptine daily) was observed in trial II, although the resumption of menses was less frequent than in the patients of trial I (50% and 58% of patients, respectively). Sexual dysfunction improved similarly on both drugs in about half the patients. In addition, tumor shrinkage occurred to a similar extent with both drugs. A high incidence of adverse events was noted especially at the initiation of therapy with both compounds: nausea, dizziness, vomiting, asthenia, headache, and decrease in blood pressure occurred at a similar incidence and extent during the use of pergolide and bromocriptine. Patients in trial I treated with pergolide reported a slightly higher incidence of fever, vasodilatation, and flu syndrome. CONCLUSIONS: in these 24-week studies comprising a total of 157 hyperprolactinemic patients, a once daily administration of pergolide was shown to be as safe and effective as the two to four times daily ingestion of bromocriptine. Longer-acting dopamine agonists like pergolide that can be taken once daily, are likely to increase the ease to adherence to the therapeutic regimen. This might result in a higher compliance to medical treatment of hyperprolactinemia.

Adult↗
PubMed1992

Effects of the dopamine agonist CV 205-502 in human prolactinomas resistant to bromocriptine.

In 21 patients with prolactinomas resistant to bromocriptine, we studied the effects of CV 205-502 on PRL hypersecretion and tumor mass, as assessed by consecutive computed tomography examinations. Cell culture studies were performed in 9 of such tumors. In 11 patients (group I; 52%) with a mean baseline plasma PRL level of 468 +/- 160 micrograms/L (+/- SE), normal PRL values were achieved after 1-6 months of treatment with 0.1-0.5 mg/day CV 205-502. Tumor size was reduced by 25% or more in 6 of 11 patients. In group II (n = 10), PRL levels (948 +/- 538 micrograms/L at baseline) were reduced by 48% after treatment with 0.1 mg/day CV 205-502. A progressive increase in the daily dose up to 0.5 mg did not further improve the partial reduction of PRL. No reduction in tumor size was observed in this group. The cell culture studies showed that 1) a brief exposure to both drugs provoked PRL suppression lasting 3 days; 2) in group I, CV 205-502 suppressed PRL release more efficiently than bromocriptine, with a maximal inhibition of 72% at 10(-9) mol/L; and 3) in group II, CV 205-502 only achieved a 26% inhibition of PRL release at 10(-8) mol/L, superimposable to that of bromocriptine. These data indicate that in at least half of such adenomas resistant to bromocriptine, CV 205-502, probably due to its higher affinity toward the D2 dopamine receptor, can overcome such resistance.

Adult↗
PubMed1978

Bromocriptine-induced behavioral hypersensitivity: implications for the therapy of parkinsonism.

Bromocriptine (CB-154) is a direct-acting dopamine agonist of proven clinical efficacy in parkinsonism. The capacity of bromocriptine to induce receptor site hypersensitivity was investigated utilizing a behavioral model in guinea pigs. Following 4 weeks of bromocriptine treatment, animals demonstrated a subsequent long-lasting hypersensitivity to amphetamine and apomorphine. The data suggest that chronic use of bromocriptine can induce receptor site hypersensitivity. These results may be an indication that, because of a similar propensity to side effects during chronic therapy, direct-acting dopamine agonists will offer no long-term advantage over current antiparkinsonian drugs. The observed phenomena suggest that chronic dopaminergic agonism may not be an ideal therapy for parkinsonism.

Animals↗
PubMed1979

The role of bromocriptine in the treatment of parkinsonism.

Fifty-three patients with parkinsonism, either with intractable symptoms despite optimum-dosage levodopa therapy or with adverse effects from levodopa limiting its usefulness, were treated with bromocriptine, with gradually increasing doses until benefit or adverse effect was encountered. All were initially maintained on optimal levodopa therapy. Improvement was seen in 26 patients, of whom 19 (36 percent of the total 53 patients) had sustained improvement. Effective doses of bromocriptine ranged from 5 to 90 mg per day. Improvement occurred in all categories of clinical problems, including patients who lost some benefit from chronic levodopa therapy as well as those with adverse effects from levodopa. A high incidence (70 percent) of adverse effects of bromocriptine limited the usefulness of this drug. Since one cannot predict which patients might benefit from bromocriptine, this drug is worth a trial in patients not doing well on levodopa therapy if other means to improve their condition are not successful.

Aged↗
PubMed1982

Lisuride versus bromocriptine treatment in Parkinson disease: a double-blind study.

Twenty-eight parkinsonian patients were studied in a double-blind, crossover comparison of lisuride and bromocriptine. All but two patients completed the study, with each drug adjusted to an optimal dose (mean daily intake of 4.5 mg for lisuride and 56.5 mg for bromocriptine). Treatment with each drug was given for 7 to 10 weeks; three assessments were made at biweekly intervals with optimal dose levels. Conventional antiparkinsonian medications, including levodopa, were not changed. Efficacy and adverse effects were assessed by objective and subjective techniques. The only significant difference was slightly better control of akinesia with bromocriptine. There was considerable variability in the optimal dose of each drug, though the clinical profile of lisuride was quite similar to that of bromocriptine.

Adult↗
PubMed1982

Bromocriptine: low-dose therapy in Parkinson disease.

In a double-blind trial with a placebo phase, low-dose bromocriptine therapy (average dose, 15 mg per day) produced a significant improvement in 25 idiopathic parkinsonian patients. Tremor and bradykinesia were equally and significantly improved in both the levodopa-treated and the de novo patients. Rigidity was most improved in the levodopa-treated subjects. Age was not a factor in determining the dose of bromocriptine or the degree of improvement. Adverse effects occurred in 30% but were mild and dose-dependent. Four subjects, unable to tolerate initial doses of bromocriptine, withdrew from the trial. A low initial dose (1 mg per day) and slow escalation in dosage produced an optimal, though delayed improvement. Low-dose bromocriptine therapy is effective, does not induce significant dyskinesia nor on-off phenomenon, and is probably an alternative to levodopa as a drug of first choice in Parkinson disease.

Aged↗
PubMed1995

Bromocriptine treatment of nonfluent aphasia.

Using a double-blind, placebo-controlled, crossover design, we studied the effect of bromocriptine (15 mg daily) in 20 men with chronic nonfluent aphasia. The study was conducted over a 28-week period in two phases. In phase I, the patients received either bromocriptine or placebo; in phase II the treatments were crossed over. We evaluated each patient's language and nonverbal cognitive skills at the beginning and end of each phase and 6 weeks after completion of phase II. When compared with placebo treatment, bromocriptine did not significantly improve the patient's speech fluency, language content, overall degree of aphasia severity, or nonverbal cognitive abilities. Based on these results, bromocriptine is not recommended as monotherapy for the treatment of chronic nonfluent aphasia.

Adult↗
PubMed1993

Nasal mucosal congestion after treatment with bromocriptine.

Nine women were given bromocriptine a few days after delivery in order to inhibit lactation. Nasal airway resistance to airflow (NAR) was recorded and blood samples were taken before treatment with bromocriptine, 2 to 3 hours after the first dose of this drug, and after 3 to 5 days on this treatment. All the women had increased nasal congestion after bromocriptine and NAR rose significantly. The prolactin, estradiol, and progesterone hormone levels decreased significantly, but no significant difference was found in the levels of thyroid-stimulating hormone (TSH) and vasoactive intestinal polypeptide (VIP). The bromocriptine effect may be caused by different mechanisms.

Adult↗
PubMed1984

[The response of ovarian function to HMG-HCG and bromocriptine therapies in hyperprolactinemic patients].

Plasma hormonal changes were analysed in patients with hyperprolactinemia who conceived following Bromocriptine therapy. Following the administration of HMG-HCG and Bromocriptine, serial plasma samples were collected from the cases. Plasma levels of FSH, LH, prolactin (PRL), estrone (E1), estradiol (E2), 17-hydroxyprogesterone (17-P), 20 alpha-dihydroprogesterone (20 alpha-P), progesterone (P) were determined simultaneously using specific radioimmunoassays. Pretreatment PRL levels, 180--420 ng/ml, were normalized by 7.5--12.5 mg/day of Bromocriptine treatment causing a rapid decrease in plasma PRL, reaching a plateau within several days. The first LH surge at midcycle after the start of the Bromocriptine treatment was established at 10--50 days. In the patients the first mid-cycle LH surge was observed, but the luteal phase was definitely short, as demonstrated by plasma progestins levels. The results from the present longitudinal studies on hyperprolactinemia revealed characteristic changes accompanied by the restoration of the hypothalamic-pituitary-ovarian function during the treatment period.

Adult↗
PubMed1985

[The mechanism of induction of ovulation by bromocriptine in euprolactinemic anovulation--the role of occult hyperprolactinemia in anovulation].

It has been well documented that ovulation was induced by Bromocriptine treatment in euprolactinemic anovulation. The present study has been carried out to clarify the underlying mechanism. 28 patients with euprolactinemia (PRL less than 25 ng/ml) were treated with a 5 mg daily administration of Bromocriptine. Ovulation was induced in 13 cases, which were determined by their BBT charts. In the ovulated cases, PRL secreting capacities were increased, determined by TRH administration. On the other hand, PRL secreting capacities were normal in the anovulated cases. The studies of the circadian secretion of PRL revealed that a nocturnal hyperprolactinemic state occurred for several hours in the ovulated cases, which was not seen in the anovulated cases. From these results, the mechanism of induction of ovulation by Bromocriptine in euprolactinemic anovulation exists on the suppression of the increased PRL secreting capacity, which may be related to the occulted hyperprolactinemia at night. Ovulated cases by Bromocriptine are seemingly euprolactinemia, but in truth they may be a kind of hyperprolactinemia.

Adult↗
PubMed1999

Long-term treatment with bromocriptine of a plurihormonal pituitary adenoma secreting thyrotropin, growth hormone and prolactin.

A 48-year-old female presented with acromegaly, amenorrhea and hyperthyroidism associated with high serum free T4 levels and measurable TSH concentrations. The administration of GHRH induced significant increases in GH, PRL and TSH. Conversely, intravenous infusion of dopamine or oral administration of bromocriptine effectively inhibited GH, PRL and TSH secretion. Serum alpha-subunit levels were neither affected by GHRH, dopamine nor bromocriptine. Transsphenoidal surgery was performed and immunostaining of the tissue showed that the adenoma cells were positive for GH, PRL or TSH. The patient was treated with bromocriptine at a daily oral dose of 10 mg after surgery. Serum TSH were initially suppressed but returned within reference intervals with persistent normalized free T4 levels. Serum PRL became undetectable and GH levels were stable around 6 ng/ml except the periods of poor drug compliance, when serum TSH, GH and PRL levels rose considerably. The patient was followed-up for 10 years without any change in the residual adenoma tissues as detected by magnetic resonance imaging. These findings suggest that long-term bromocriptine therapy is effective in treating the hypersecretory state of a plurihormonal adenoma secreting TSH, GH and PRL.

Acromegaly↗