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PubMed1984

Effects of bromocriptine and cyproheptadine on basal and corticotropin-releasing factor (CRF)-induced ACTH release in a patient with Nelson's syndrome.

The effects of bromocriptine, a dopamine agonist, and cyproheptadine, a serotonin antagonist, on basal and corticotropin-releasing factor (CRF)-stimulated ACTH release were investigated in a 40-year-old female patient with Nelson's syndrome. Oral administration of either bromocriptine (2.5 mg) or cyproheptadine (8 mg) caused a marked drop in plasma ACTH levels. Intravenous administration of synthetic ovine (o) CRF (50 micrograms) produced an exaggerated response of plasma ACTH. Short-term (3-week) treatment with either bromocriptine (7.5 mg/day) or cyproheptadine (12 mg/day) resulted in a marked suppression of basal ACTH release. Furthermore, a blunted response of plasma ACTH to oCRF was observed after short-treatment with either drug. However, after a longer period of treatment with cyproheptadine (18-week), plasma ACTH levels rose again and hyperresponsiveness to oCRF was restored to the pretreatment levels. These data indicate that synthetic oCRF is a potent secretagogue for ACTH release in a patient with Nelson's syndrome. It is suggested that bromocriptine and cyproheptadine are effective drugs in reducing basal and CRF-stimulated ACTH release, possibly acting at the pituitary level in this case. However, the apparent refractoriness after chronic treatment with cyproheptadine may limit its therapeutic use in the present case.

Adrenocorticotropic Hormone↗
PubMed1977

Bromocriptine treatment in acromegaly: clinical and biochemical effects.

Eight selected patients with active acromegaly and elevated GH levels without other endocrine disturbances were submitted to long-term treatment and acute dose-response trials with bromocriptine. Seven patients showed clinical improvement and lowering of GH levels in response to long-term treatment, however, two of these showed only minor changes in GH levels during the acute dose-response trial. Glucose tolerance and heel pad thickness remained unchanged, while urinary hydroxyproline excretion and blood, plasma and erythrocyte volumes decreased. Using daily doses of 20 mg bromocriptine, side effects were generally minor. Severe vasovagal reactions were, however, observed in two patients, in one at the start of treatment, in the other after ingestion of 25 mg bromocriptine. Bromocriptine represents a valuable treatment alternative in acromegaly, but only long-term treatment will separate responders from nonresponders.

Acromegaly↗
PubMed1978

Response of acromegaly to long term bromocriptine therapy: a biochemical and clinical assessment.

The long term effects of bromocriptine in 12 acromegalics treated for a mean duration of 10.2 months are reported. Seven showed a significant (P less than 0.05) and sustained fall in serum immunoreactive growth hormone (GH) levels throughout 24 h, 6 of whom had a 50% or greater reduction in mean circulating GH during glucose tolerance testing. Only one patient had mean serum GH levels throughout the day suppressed to normal (less than 5 mIU/l) but 3 had suppression of mean serum GH during GTT to normal or very near normal (less than 10 mIU/l). The effective dose was 20 mg daily. Only 4 patients reported any improvement in soft tissue swelling and acral features, which was unrelated to the GH response. Possible reasons for the discrepancy between clinical and biochemical responses are discussed. In 9 of the 12 patients bromocriptine was discontinued and pituitary ablative therapy offered. Three out of 4 patients who underwent trans-sphenoidal hypophysectomy had mean GH levels during GTT reduced to less than 7 mIU/l. In the three who continued bromocriptine treatment GH suppression was maintained at less than 10 mIU/l for up to 3 years but with little change in acral features. Although bromocriptine is safe and was well tolerated it is not as effective as existing forms of pituitary ablative therapy and should be reserved for those cases where ablation is contraindicated or unsuccessful.

Acromegaly↗
PubMed1979

Restoration of oestrogen positive feedback effect on LH release by bromocriptine in hyperprolactinaemic patients with galactorrhoea-amenorrhoea.

Five mg of bromocriptine was administered for 3 weeks to 8 hyperprolactinaemic women with galactorrhoea-amernorrhoea, in whom the response of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to 100 micrograms of iv LH-releasing hormone (LH-RH) had been evaluated. Twenty mg of conjugated oestrogen (Premarin) was injected iv any day between the 10th and 12th day from the initiation of the treatment, and serum LH levels were serially determined for 120 h. Hyperresponse of LH with normal FSH response to LH-RH was observed in most patients. Bromocriptine treatment for 10 to 12 days significantly suppressed mean (+/- SE) serum prolactin (PRL) levels from 65.1 +/- 23.0 to 10.4 +/- 2.0 ng/ml, while LH (12.6 +/- 2.1 to 24.8 +/- 5.9 mIU/ml) and oestradiol (40.1 +/- 7.6 to 111.4 +/- 20.8 pg/ml) levels increased significantly. Patients on bromocriptine treatment showed LH release with a peak at 48 h after injection of Premarin. The mean per cent increases in LH were significantly higher than those in untreated patients with galactorrhoea-amenorrhoea between 32 and 96 h after the injection. The present results seem to suggest that the restoration of LH-releasing response to oestrogen following suppression of PRL by bromocriptine may play an important role in induction of ovulation in hyperprolactinaemic patients with galactorrhoea-amenorrhoea.

Adult↗
PubMed1980

The effect of bromocriptine during early pregnancy in the rat: inhibition of implantation.

The increase in the number of the ovarian LH/hCG-receptors and of serum progesterone concentration during pregnancy in the rat is highly dependent on the presence of prolactin during the luteinization process. Blocking of the hypophyseal prolactin secretion by twice daily injections of 2 microgram/g body weight bromocriptine into rats from the first day of pregnancy onwards prevents the increase in ovarian hCG-binding and progesterone production. Similar results are obtained by application of bromocriptine during the first three days only or either at day 1, 3 or 5 after mating. In all bromocriptine treated rats implantation of blastocysts does not occur. The failure to implant is not due to a teratogenic effect of bromocriptine onto preimplantation embryos, but is probably the consequence of changes of the uterine mucosa caused by the lack of progesterone production in the luteal cells.

Animals↗
PubMed1981

Effects of bromocriptine-induced pregnancy on prolactin-secreting pituitary tumours.

Twenty-eight women with hyperprolactinaemia and amenorrhoea received bromocriptine treatment which resulted in 31 term pregnancies. Bromocriptine treatment was stopped as soon as pregnancy was established. Nineteen of the women had radiological signs of a pituitary tumour. The pregnancies were clinically uneventful in all cases except one who developed headache. Post-partum sellar X-ray showed pregnancy-induced enlargement of the pituitary fossa in 4 of the 28 women. Regression of the radiological changes occurred in 3 of the 4 women within 2 years after the delivery. The women with abnormal sellar X-rays had no difference in the mean prolactin levels before treatment and after pregnancy and lactation while all the women with normal sellae had lower prolactin levels after pregnancy than before. Three women resumed regular spontaneous menstruations after pregnancy and lactation but only one conceived again. Thus, serious pituitary tumour complications are rare in hyperprolactinaemic women with bromocriptine-induced pregnancies. The pregnancy does not worsen the condition. Resolution of hyperprolactinaemia after bromocriptine-induced pregnancy is an unfrequent finding.

Adult↗
PubMed1983

Follow-up of patients with prolactinomas after discontinuation of long-term therapy with bromocriptine.

The effects of bromocriptine discontinuation after a 2 year course of therapy on prolactin (Prl) serum levels and the radiological size of the sella turcica were investigated in 16 women with amenorrhoea-galactorrhoea due to prolactinoma. During therapy, all but 2 patients had normalized serum Prl levels, and 4 women with macroprolactinomas exhibited a reduction in the size of the tumour as documented by CT-scanning and tomography of the sellae. After bromocriptine withdrawal and follow-up during 2 additional years, Prl levels remained normal in 6 patients, 2 of them with microprolactinomas and 4 with macroprolactinoma. The remaining 10 women developed hyperprolactinaemia associated with amenorrhoea and galactorrhoea within 3 months after discontinuation of therapy. No tumour expansion was observed in any case during the 4 year observation period. In the present study bromocriptine treatment seemed to result in permanent cure in 6 out of 16 cases of prolactinomas; nevertheless it is difficult to justify an indefinite medical treatment since the natural history of prolactinoma remains unknown. We presently feel that bromocriptine is more appropriate than neurosurgical transsphenoidal exploration for the primary treatment of prolactinomas. Further investigation is needed before a more definitive conclusion regarding the management of prolactinomas can be reached.

Adult↗
PubMed1984

Metergoline as an alternative to bromocriptine in amenorrhoea.

The results of this study offer further evidence that metergoline is a valuable alternative to bromocriptine in the suppression of excessive prolactin secretion. Forty-nine hyperprolactinaemic and 44 normoprolactinaemic women with amenorrhoea took part in a double-blind trial to compare the efficacy of metergoline 12 mg/day and bromocriptine 7.5 mg/day in restoring menstruation and ovulation. All the women had normal results on conventional tomography of the sella turcica, normal gonadotrophin levels and normal androgen levels. In the hyperprolactinaemic group, metergoline and bromocriptine were equally effective, with 84 and 75% respectively achieving menstruation, and 76 and 67% respectively achieving ovulation, within 4 months. In the normoprolactinaemic group, 47% menstruated and 40% ovulated on metergoline, against comparative figures of 36 and 21% for bromocriptine and 20 and 13% for placebo, but the differences were not statistically significant. Side effects were not a major problem.

Adult↗
PubMed1985

Changes of molecular forms of growth hormone in bromocriptine treated acromegaly in relation to changes of somatomedin-C and clinical response.

Eleven patients with active acromegaly were treated with 10-20 mg bromocriptine daily for a period of 6-9 months. The clinical response was evaluated by a 'clinical and metabolic improvement score'. The biochemical response was evaluated by measurement of both the mean plasma growth hormone (GH) level during the day and the somatomedin-C (Sm-C) concentration. Before and at the end of the treatment period plasma samples were fractionated by Sephadex G-100 chromatography in order to study the effects of chronic bromocriptine treatment on the concentrations of total GH and its different molecular forms. The main observations may be summarized as follows: Three immunoreactive components were observed on Sephadex chromatography corresponding to molecular weight above 100 000 (big-big GH), 40 000-60 000 (big GH) and 20 000-22 000 (little GH). Bromocriptine treatment induced preferentially a reduction of little GH. There was a very good correlation between the decrease of little GH and total GH, and both were significantly correlated with the clinical response. The correlation between the decrease of Sm-C values and that of little and total GH as well as between the decrease of Sm-C and the clinical response was poor. It is concluded that a) measurement of little GH is not superior to the determination of total GH in the assessment of disease activity of bromocriptine treated acromegalic patients; b) both methods are superior to the measurement of plasma Sm-C levels; c) clinical response out of proportion ot the fall of total GH which can be explained by a preferential reduction of little GH, has not been observed in our investigations.

Acromegaly↗
PubMed1985

Changes in computed tomographic findings in microprolactinomas before and after bromocriptine.

Computed tomography (CT) of the pituitary before and after bromocriptine treatment were performed in 10 patients with microprolactinoma. Intrapituitary low densities were demonstrated in 7 out of the 10 patients before bromocriptine. Low densities shrank in size and increased in density after normalization of the plasma prolactin (Prl) level following bromocriptine. At the same time, various degrees of empty sella were demonstrated in these patients and in 2 out of the 3 without noticeable changes before treatment. It was concluded that enhanced CT scans, especially sagittal reconstruction images, were very informative for the diagnosis of microprolactinoma and that bromocriptine reduced the size of the microprolactinoma and often led to empty sella.

Adult↗
PubMed1987

A controlled clinical trial for the effect of bromocriptine on the adrenal contribution in polycystic ovarian disease.

Adrenal involvement in polycystic ovarian disease was assessed by measuring dehydroepiandrosterone sulphate in 20 polycystic ovarian disease patients. The response of dehydroepiandrosterone sulphate to bromocriptine treatment was compared to that of placebo, both being given for one cycle on a double-blind, cross over basis. The mean basal DHEA-S was above the upper limit of the normal range (6793 nmol/l) in three patients. The mean basal dehydroepiandrosterone sulphate in the polycystic ovarian disease group was significantly higher than the mean of the normal control group (P less than 0.01). Dehydroepiandrosterone sulphate showed a significant drop with bromocriptine as compared to placebo (P less than 0.001) and a significant correlation with prolactin both before (P less than 0.001) and after treatment with bromocriptine (P less than 0.001). These findings support the hypothesis of adrenal involvement in polycystic ovarian disease and prove the significant effect of bromocriptine on the adrenal which might be of therapeutic value.

Adolescent↗
PubMed1991

Effect of bromocriptine withdrawal in acromegaly on body composition as assessed by bioelectrical impedance analysis.

To evaluate the effect of bromocriptine withdrawal after dopaminergic long-term treatment (15.0 +/- 6.8 mg/day, mean +/- SD) in 12 acromegalic patients on body composition, bioelectrical impedance was measured before and at the end of two weeks of drug withdrawal. During withdrawal basal hGH and IGF-I increased from 2.5 +/- 1.9 micrograms/l and 2.1 +/- 0.8 kU/l to 9.1 +/- 11.7 micrograms/l and 4.9 +/- 2.2 kU/l, respectively, and the hGH secretion deteriorated significantly both after oral glucose load and in the TRH test, indicating recurrence of active acromegaly. Reactance and resistance decreased by 5 +/- 4 and 23 +/- 19 omega, respectively (p less than 0.01), whereas body weight remained constant (+0.4 +/- 2.1 kg). Bioelectrical impedance analysis indicated evident shifts in body composition, i.e. a significant reduction of body fat (-2.0 +/- 1.7 kg) and a simultaneous increase in both lean body mass (+2.4 +/- 2.2 kg) and total body water (+1.8 +/- 1.6 l). The changes in body composition were related to a combined effect of unsuppressed hypersomatotropism and the lack of bromocriptine actions other than inhibition of hGH secretion (for example stimulation of the renin-angiotensin-aldosterone system by both the recurred hypersomatotropism and the absence of dopaminergic bromocriptine effects). We conclude that bioelectrical impedance analysis is a good additional tool to assess the pathophysiological effects of bromocriptine withdrawal in long-term treated acromegalic patients.

Acromegaly↗
PubMed1991

Dynamics of the acute effects of octreotide, bromocriptine and both drugs in combination on growth hormone secretion in acromegaly.

The separate and combined GH-lowering effects of single doses of octreotide and bromocriptine were assessed in 51 acromegalic patients on 4 occasions each 2 days apart. Patients received sequentially: placebo sc (N = 51), 50 micrograms octreotide sc (N = 51), 2.5 mg bromocriptine po (N = 40) or a combination of both drugs (N = 25). With octreotide, in 28 patients (55%) GH levels were suppressed to less than 5 micrograms/l and 39 of them (76.5%) had a 50% or greater decrease of their basal GH level from 2 to 6 h. During bromocriptine, GH values were suppressed to below 5 micrograms/l in 11 patients (27.5%) and reduced by 50% or more in 21 (52.5%). The combination of both drugs acutely suppressed GH levels to less than 2 micrograms/l in 32%, to less than 5 micrograms/l in 56%, and by more than 50% in 84% of patients. Octreotide produced a stronger and faster suppression of GH levels than bromocriptine in most patients. The combination of both drugs had an additive effect on the lowering of GH levels, especially between 7 and 10 h after drug administration. These results suggest that chronic therapy with a combination of both drugs may be as effective as therapy with higher doses of either compound alone. Albeit transient, octreotide caused a rapid near total suppression of insulin release in the morning, 15 to 45 min after administration. Postprandial glucose rise, between 2 and 3.5 h after breakfast was significantly higher during octreotide than on the control day.

Acromegaly↗
PubMed1992

Invasive mixed growth hormone/prolactin secreting pituitary tumour: complete shrinking by octreotide and bromocriptine, and lack of tumour growth relapse 20 months after octreotide withdrawal.

Octreotide and bromocriptine were used to treat an acromegalic patient harbouring an invasive pituitary tumour secreting growth hormone and prolactin. Octreotide (100 micrograms, subcutaneously, three times daily) and bromocriptine (15 mg orally, daily) rapidly improved clinical signs and symptoms, including diabetes that initially required insulin. Complete control of growth hormone and prolactin secretion was obtained and maintained by this treatment protocol for 12 months without affecting the other pituitary functions. A major tumour shrinkage was apparent by magnetic resonance imaging after six months, and was considered to be complete after 12 months of treatment. Octreotide was then discontinued without any relapse in either growth hormone secretion or tumour growth over a 20-month period following withdrawal. Attempts were made to discontinue bromocriptine, but a maintenance therapy (2.5 mg daily) was required to control rebounds of prolactin hypersecretion. Two months after octreotide withdrawal, acute pancreatitis secondary to cholelithiasis required surgery; this complication was attributed to octreotide (pre-treatment ultrasonography was normal). These findings suggest that combination therapy with octreotide and bromocriptine may be considered in pituitary macroadenomas secreting growth hormone and prolactin. They also emphasize the need for a close monitoring of cholelithiasis, not only during octreotide therapy but also after the drug's withdrawal.

Adenoma↗
PubMed1997

Effects of bromocriptine on serum prolactin levels, pituitary weight and immunoreactive prolactin cells in estradiol-treated ovariectomized rats: an experimental model of estrogen-dependent hyperprolactinemia.

The present study was designed to assess the effects of bromocriptine, a dopamine agonist, on pituitary wet weight, number of immunoreactive prolactin cells and serum prolactin concentrations in estradiol-treated rats. Ovariectomized Wistar rats were injected subcutaneously with sunflower oil vehicle or estradiol valerate (50 or 300 micrograms/rat(-1) week (-1) for 2, 4, or 10 weeks. Bromocriptine (0.2 or 0.6 mg rat (-1) day (-1)) was injected daily during the last 5 or 12 days of estrogen treatment. Data were compared with those obtained for intact control rats. Administration of both doses of estrogen increased serum prolactin levels. No difference in the number of prolactin cells in rats treated with 50 micrograms estradiol valerate was observed compared to intact adult animals. In contrast, rats treated with 300 micrograms estradiol valerate showed a significant increase in the number of prolactin cells (P < 0.05). Therefore, the increase inn serum prolactin levels observed in rats treated with 50 micrograms estradiol valerate, in the absence of morphological changes in the pituitary cells, suggests a "functional" estrogen-induced hyperprolactinemia. Bromocriptine decreased prolactin levels in all estrogen-treated rats. The administration of this drug to rats previously treated with 300 micrograms estradiol valerate also resulted in a significant decrease in pituitary weight and number of prolactin cells when compared to the group treated with estradiol alone. The general antiprolactinemic and antiproliferative pituitary effects of bromocriptine treatment reported here validate the experimental model of estrogen-induced hyperprolactinemic rats.

Animals↗
PubMed1981

Effects of bromocriptine and occlusion of nipples on prolactin receptor and lactose synthetase activity in the mammary gland of the lactating rat.

The response of prolactin receptor and lactose synthetase to suppression of plasma concentrations of prolactin was examined in normal and occluded (teat-sealed) mammary glands of Sprague-Dawley rats, Rats, with mammary glands unilaterally occluded, were given bromocriptine (2.5 mg/kg per 12 h) between 5 and 8 post partum. Bromocriptine reduced plasma prolactin concentrations from 460.4 +/- 120.8 (mean +/- s.e.m.) to 2.56 +/- 0.89 ng/ml within 12h whilst concentrations in control rats were 553.4 +/- 110.25 ng/ml. Lactose synthetase activity declined rapidly, within 24h, in occluded glands of both groups but was maintained for 24 h in normal glands of bromocriptine-treated rats and decreased thereafter. Prolactin receptors also declined significantly within 24h in occluded glands. Desaturation of the prolactin receptor by bromocriptine treatment in vivo was compared with desaturation by exposure of membranes to MgCl2 in vitro. Both treatments enhanced prolactin binding but the increase after treatment with MgCl2 may have been partly artefactual since there was a selective loss of protein from the membranes. These results indicate that the prolactin receptor in rat mammary gland may be maintained after acute suppression of prolactin secretion.

Animals↗
PubMed1982

Effects of metoclopramide and bromocriptine on prolactin secretion in the pregnant ewe.

Metoclopramide and bromocriptine, drugs which are respectively antagonistic and agonistic to dopamine receptor activity, were used to investigate the control of prolactin secretion in the ewe during pregnancy. Normal concentrations of prolactin were found during pregnancy, i.e. values were low and stable during the first 100 days but thereafter increased progressively to reach maximum values at day 140. Treatment with bromocriptine suppressed levels to undetectable values (less than 1.4 micrograms/l plasma) between days 40 and 100 of pregnancy. Later in gestation, however, bromocriptine administered between days 120 and 140 was less effective, indicating that the pituitary gland was less responsive to the same degree of inhibition. Treatment with metoclopramide alone provoked a progressively greater release of prolactin as pregnancy advanced whereas in bromocriptine-treated animals an associated release of prolactin in response to metoclopramide was seen only between days 120 and 140 of pregnancy. These results are interpreted as evidence that the raised concentrations of prolactin characteristic of late pregnancy in the ewe are due to a reduced responsiveness of the pituitary gland to inhibitory stimuli, or to a decreased secretion of endogenous dopamine into the hypophysial portal blood system or to both.

Animals↗
PubMed1983

Reduction of 5-day cycle length of female rats by treatment with bromocriptine.

Rats with 5-day ovarian cycles were injected daily with 1 mg bromocriptine. This treatment resulted in a change of cycle length from 5 to 4 days and a rapid increase in ovarian weight. The increase in ovarian weight resulted from the accumulation of large numbers of corpora lutea. Normal numbers of corpora lutea were formed during each cycle but luteal bodies did not disappear subsequently. Luteolysis affected only minor foci of luteal tissue and the majority of luteal tissue remained histologically intact throughout the further period of study. The reduction of cycle length from 5 to 4 days occurred when bromocriptine was administered from the day of ovulation only. If treatment was commenced at a later time during the cycle it was not effective. Treatment with bromocriptine appeared to affect the concentrations of progesterone in the blood during dioestrus. During treatment the rats showed the pattern characteristic for 4-day cycles: typically, the high concentrations of progesterone on the day after metoestrus remained absent. These data suggest (1) that the latter part of the production of progesterone during dioestrus by 'non-functional corpora lutea' is dependent on prolactin and (2) that prolongation of high progesterone production after metoestrus plays an important role in changing the length of the cycle from 4 to 5 days. Treatment with bromocriptine did not significantly affect the rate of maturation of follicles destined for the next ovulation. It is possible that follicular maturation is not among the critical variables which determine whether normal ovulatory cycles will last for 4 or 5 days.

Animals↗