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PubMedDate not supplied

Effects of bromocriptine on responses to stress in spontaneously hypertensive rats.

Treatment of 2-month-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) normotensive controls with the dopamine agonist, bromocriptine, for 7 days significantly affected hormonal responses to immobilization stress in both groups. However, basal blood pressures and pressor responses to immobilization stress were significantly reduced only in SHR. Basal levels of catecholamines were similar in the two groups of rats, but catecholamine responses to immobilization stress following saline (vehicle) treatment were marked greater in SHR; following bromocriptine treatment for 7 days, catecholamine responses were similar in the two groups. Basal serum prolactin levels and prolactin responses to immobilization were greater in SHR after saline treatment; after bromocriptine, they were similar in the two groups. Basal plasma renin activity (PRA)and PRA responses to immobilization were significantly less in SHR following saline treatment; after bromocriptine treatment these responses were paradoxically greater in SHR without being significantly changed in WKY. Basal levels of plasma aldosterone and corticosterone following saline were significantly greater, but responses to immobilization less, in SHR. Bromocriptine treatment decreased aldosterone and corticosterone responses to stress in WKY but paradoxically increased these responses in SHR. These results suggest that increased pressor responses to stress are dependent on heightened sympathetic nerve activity, perhaps secondary to decreased central dopaminergic activity. Increased basal prolactin levels and stress-mediated prolactin responses may be related to decreased central dopaminergic activity. Paradoxical PRA, plasma aldosterone, and corticosterone responses to stress following bromocriptine suggest altered dopaminergic modulation of these hormones in the SHR.

Animals↗
PubMed1997

Effects of the D2 receptor agonist bromocriptine on sleep bruxism: report of two single-patient clinical trials.

An altered dopamine receptor status has been associated with sleep bruxism. Evidence from a functional neuro-imaging study has implicated an abnormal side imbalance in striatal D2 receptor expression in its pathophysiology. To assess the significance of this finding, we studied the effects of short-term administration of the preferential dopamine D2 receptor agonist bromocriptine on sleep bruxism in a double-blind, placebo-controlled polysomnographic and neuro-imaging study with a single crossover design. Six otherwise healthy and drug-free patients with sleep bruxism were entered into the trial. One of the patients dropped out due to an intercurrent illness, while three others were discontinued from the study due to severe adverse reactions to bromocriptine. Because of the high frequency and intensity of the side-effects, the trial was interrupted. Two patients, however, completed the trial without any adverse reactions. Their outcome measures are presented as single-patient clinical trials. Following a two-week administration of bromocriptine, both patients showed a decrease in the number of bruxism episodes per hour of sleep of about 20% to 30% with respect to the placebo. WHile no significant differences between both conditions (i.e., placebo and bromocriptine) were found for the number of bruxism bursts per episode, significantly lower root-mean-squared EMG levels per bruxism burst occurred during bromocriptine use. In association with this polysomnographically established attenuation of sleep bruxism, bromocriptine afforded a decreased normal side distribution of striatal D2 receptor binding, as was evidenced by single-photon-emission computed tomography using the radioactive D2 receptor antagonist iodine-123-iodobenzamide. This study supports previous suggestions that the central dopaminergic system may be involved in the modulation of sleep bruxism. To see if the present findings apply across a population, investigators should use a peripheral D-2 antagonist to prevent side-effects.

Adult↗
PubMed1998

Effects of bromocriptine and haloperidol on prepulse inhibition of the acoustic startle response in man.

Experiments with animals have shown that D2 dopamine (DA) receptors are involved in prepulse inhibition of the acoustic startle reflex (suppression of the reflex response evoked by a loud sound by prior presentation of a low-intensity stimulus). The present experiment attempted to extend this observation to man. Twelve healthy males (18-30 years), screened for normal hearing thresholds, participated in four sessions in which they received oral doses of placebo, bromocriptine 1.25 mg (a D2 receptor agonist), haloperidol 3 mg (a D2 receptor antagonist) and combined treatment with bromocriptine 1.25 mg+haloperidol 3 mg, according to a balanced double-blind protocol. Thirty-minute electromyographic recordings from the orbicularis oculi muscle of the right eye were carried out 120 min after ingestion of haloperidol and/or 90 min after ingestion of bromocriptine. Subjects received 36 40-msec sound pulses (115 dB), separated by variable intervals (mean 25 sec); in 24 of the trials the pulse was preceded by a 40-msec prepulse (75 dB in 12 trials and 85 dB in 12 trials; prepulse-pulse interval, 120 msec). The amplitude of the startle response was not significantly altered by any of the active treatments. Under the placebo condition, both 75- and 85-dB prepulses inhibited the startle response. Bromocriptine significantly attenuated this prepulse inhibition; haloperidol also produced a small but statistically significant attenuation of prepulse inhibition. Haloperidol significantly antagonized the attenuation of prepulse inhibition produced by bromocriptine. Neither drug altered self-rated alertness, physiological finger tremor, systolic or diastolic blood pressure or salivation. Bromocriptine significantly suppressed and haloperidol significantly elevated serum prolactin levels, these changes being absent when the two drugs were given in combination. The results provide evidence for the involvement of D2 DA receptors in prepulse inhibition of the startle reflex in man.

Acoustic Stimulation↗
PubMed1981

Bromocriptine enhances guanylate cyclase activity.

Bromocriptine and its parent compound alpha-ergocryptine were investigated with respect to their ability to interact with the guanylate cyclase (E.C.4.6.1.2)-cyclic GMP system in vitro in the rat pituitary and ovary. Both bromocriptine and alpha-ergocryptine enhanced guanylate cyclase two- to threefold in both of these tissues over a concentration range of 1 nM to 1 microM. Since bromocriptine is thought to be a dopamine agonist in the pituitary, dopamine's effects on guanylate cyclase were also tested. Dopamine caused a twofold enhancement of guanylate cyclase activity in the pituitary and ovary. When bromocriptine and dopamine were used in combination, bromocriptine had to be in equal or a greater concentration with respect to dopamine in vitro to enhance guanylate cyclase activity. These findings suggest that bromocriptine's effect at the level of the pituitary and ovary may be mediated through enhancement of guanylate cyclase activity.

Animals↗
PubMed1985

Pure alpha-subunit-secreting mouse pituitary tumor: inhibition of growth and secretion by combined treatment with thyroxine and bromocriptine.

We have recently documented the spontaneous development of a mouse pituitary tumor line (MGH 101A) secreting only the alpha-subunit of the glycoprotein hormones. Secretion of alpha-subunit by MGH 101A was not inhibited by either physiological or pharmacological levels of thyroid hormones. The present study demonstrates that combined treatment with bromocriptine and pharmacological doses of T4 for 1 month significantly decreased both tumor growth and alpha-subunit secretion of MGH 101A in thyroidectomized host mice. Either treatment alone was ineffective. The fall in plasma alpha-subunit concentrations after the combined treatment was probably due to the inhibition of tumor growth, since the decreases in plasma alpha-subunit levels and tumor weights were quantitatively similar, and there was no significant change in tumor steady state concentrations of alpha-subunit mRNA. In two of three experiments, the combined treatment resulted in a significant fall in tumor total DNA concentrations; this suggests that decreased tumor growth was at least in part due to inhibition of tumor cell replication. To compare the effects of the various treatments on the pure alpha-subunit-producing pituitary tumor with their effects on non-tumorous pituitary, we also measured secretion of TSH and PRL into plasma by the host pituitary. Treatment with T4 alone profoundly suppressed plasma concentrations of TSH and significantly reduced plasma PRL levels compared to levels in the thyroidectomized controls. Surprisingly, both thyroidectomized and euthyroid tumor hosts treated with bromocriptine alone showed no suppression of plasma PRL levels. However, combined treatment with bromocriptine and pharmacological doses of T4 resulted in plasma PRL concentrations significantly lower than those after treatment with T4 alone. Thus, the tumor and nontumorous host pituitaries differed in their responses to T4 alone. However, the two tissues were similar in their responses to bromocriptine alone and to combined treatment with bromocriptine and T4. We conclude that combined treatment with T4 and bromocriptine inhibited the growth and secretion of the pure alpha-subunit-secreting tumor MGH 101A. The data on PRL secretion by the host pituitary suggest that T4 may have acted by enhancing the function of dopamine receptors.

Animals↗
PubMed1990

Prolactin (PRL) regulation of maternal behavior in rats: bromocriptine treatment delays and PRL promotes the rapid onset of behavior.

Recent findings indicate that PRL helps stimulate the onset of maternal behavior in inexperienced hypophysectomized steroid-treated female rats. In a series of five experiments we have further examined the involvement of PRL in maternal behavior using nonhypophysectomized ovariectomized rats treated concurrently (type I) or sequentially (type II) with progesterone (P) and estradiol (E2) and administered either bromocriptine (to suppress endogenous PRL secretion) or bromocriptine plus ovine PRL. In Exp 1 plasma PRL concentrations were measured in ovariectomized rats treated for 2 weeks with a combination of E2 and P Silastic implants. Type I steroid-treated (2mm E2, days 1-24; three 30 mm P, days 3-13) rats exhibited elevated plasma PRL levels throughout the sampling period compared with nonsteroid-treated controls. In contrast, PRL concentrations in type II steroid-treated (P, days 3-13; E2, days 13-24) females were low (similar to controls) from days 3-13 when the type II steroid-treated females were exposed to P only. Like type I treated rats, PRL levels in type II steroid-treated rats were elevated from day 13 onward after E2 capsule insertion. In Exp 2, treatment of both type I and type II steroid-treated rats with bromocriptine (2 mg/kg, sc) twice daily beginning on treatment day 13 suppressed basal PRL concentrations and prevented the estrogen-induced diurnal PRL surge. Whereas PRL was effectively suppressed by bromocriptine in both steroid-treated groups, the absolute levels of PRL were lower in rats treated with the type II steroid regimen. Behavioral analyses in Exp 3, 4, and 5 revealed that bromocriptine administration, while failing to interfere with the onset of maternal behavior in rats treated with the type I concurrent steroid regimen, disrupted the onset of maternal care in rats treated with the type II sequential steroid regimen. When a separate set of type II steroid-treated rats was given both bromocriptine (2 mg/kg) plus ovine PRL (0.5 mg, sc) twice daily, maternal behavior rapidly appeared. Thus, suppression of endogenous PRL secretion delays the onset of maternal behavior in nonhypophysectomized steroid-primed rats, an effect prevented by concurrent administration of ovine PRL. In addition to providing further experimental support for PRL's role in maternal behavior, the development of this endocrine regimen provides researchers with a potentially fruitful model to examine neural sites and mechanisms of PRL regulation of maternal behavior in mammals.

Animals↗
PubMed1980

Does bromocriptine block thyrotropin-releasing hormone-induced prolactin release during pregnancy?

PRL responses to 200 microgram of iv TRH were measured in 16 healthy women with normal early pregnancy before and at the endo of bromocriptine treatment of 5.0--7.5 mg daily for 1--2 weeks. Before the start of bromocriptine, TRH caused a PRL elevation from 19.1 +/- 2.2 to 95.2 +/- 12.6 ng/ml (mean +/- SE) after 20 min, with a mean maximal PRL increment of 71.7 +/- 11.6 ng/ml. Bromocriptine suppressed basal plasma PRL level to 3.6 +/- 0.8 ng/ml (P less than 0.001). TRH then caused a PRL rise to 18.8 +/- 1.8 ng/ml at 20 min, with a mean maximal PRL increment of 15.7 +/- 1.8 ng/ml. The absolute PRL response was significantly smaller (P less than 0.001) during bromocriptine intake than before, whereas the mean percent increments in PRL levels after TRH administration were similar in the presence and absence of bromocriptine. Fifteen of these women were restudied with TRH stimulation 4--6 weeks after legal abortion, and the PRL responses to TRH were normal. When 7 of these women were once again treated with bromocriptine and retested with TRH, no absolute or relative PRL response to TRH emerged. These results release differs between the pregnant and nonpregnant states.

Abortion, Induced↗
PubMed1981

Dopaminergic mechanisms and luteinizing hormone (LH) secretion. II. Differential effects of dopamine and bromocriptine on LH release in normal women.

After our observation of the failure of bromocriptine to inhibit LH secretion in hyperprolactinemic women, we have investigated the effects of bromocriptine and dopamine (DA) on LH secretion in normal ovulatory women within 5 days of the midcycle LH peak. Both bromocriptine (2.5 mg, orally) and DA (4 micrograms/kg . min, iv) for 4 h lowered serum PRL levels by more than 80%. Bromocriptine was ineffective in suppressing LH secretion and, in fact, resulted in a slight but significant stimulation, while, in contrast, DA was effective in lowering circulating LH levels by approximately 30% and reducing spontaneous LH fluctuations. The dissociation of the effects of these two dopaminergic agents on LH secretion may be explained by the existence of multiple DA receptors. The slight stimulatory effect of bromocriptine might be due to a preferential presynaptic action of bromocriptine inhibiting endogenous DA secretion in the hypothalamus and thus reducing this catecholamine's tonic inhibitory influence on LH secretion.

Adult↗
PubMed1981

Bromocriptine therapy in acromegaly: use in patients resistant to conventional therapy and effect on serum levels of somatomedin C.

Seven patients with clinically active acromegaly who had not responded completely to previous surgical or radiation therapy were treated with bromocriptine. Bromocriptine was well tolerated; only one of the seven patients discontinued treatment secondary to side effects. Six of the seven patients improved during bromocriptine therapy, although GH levels were normalized in only two patients. All patients had elevated levels of somatomedin C (Sm-C) before therapy even when basal levels of GH were less than 10 ng/ml. One patient normalized both GH and Sm-C during bromocriptine therapy and had an excellent clinical response. Five patients had moderately good clinical responses; four of these patients had substantial falls in GH levels, but Sm-C levels fell minimally if at all in four and actually increased in one patient. In one patient, there was no change in clinical status, GH levels, or Sm-C levels. Thus, the clinical response did not correlate well with changes in Sm-C in most patients. The patterns of response to provocative stimuli of GH secretion in acromegaly were maintained during bromocriptine therapy, as has been previously been reported. Based on our experience, bromocriptine appears to be a useful adjunct in the therapy of acromegaly, even in patients who have had prior ablative therapy.

Acromegaly↗
PubMed1982

Bromocriptine does not inhibit the aldosterone response to sodium depletion.

This study was designed to investigate the influence of the dopamine agonist, bromocriptine, on the renin-angiotensin-aldosterone system during dietary sodium restriction. Five normal white male volunteer subjects were studied in metabolic balance at constant 150 meq sodium, 60 meq potassium intake, and then daily for 7 days on an isocaloric constant diet of 10 meq sodium and 60 meq potassium/day. The subjects were studied once during administration of bromocriptine and again in the presence of bromocriptine placebo. After a stepwise daily decrease in urinary sodium excretion, sodium balance was achieved on the sixth day of low sodium intake. Renal sodium conservation in response to dietary sodium restriction was associated with parallel increases in PRA, plasma aldosterone concentration, and urinary aldosterone excretion. These changes were not significantly different during placebo and bromocriptine administration. Bromocriptine was active at the pituitary dopamine receptor, as serum PRL concentrations were suppressed to undetectable levels. The results indicate that bromocriptine does not alter the response of the renin-angiotensin-aldosterone system to sodium restriction.

Adult↗
PubMed1984

Gonadotropin and prolactin pulsations in hyperprolactinemic women before and during bromocriptine therapy.

Pulsatile gonadotropin secretion and its relationship to PRL and estradiol (E2) secretion were investigated in 20 hyperprolactinemic amenorrheic women by obtaining serial blood samples for 6- to 24-h periods. Thirteen patients were restudied in the early follicular phase of the menstrual cycle (days 3-5) after ovulatory periods were established during bromocriptine therapy. In the hyperprolactinemic women, the number of LH peaks ranged from 0-12/24 h, and LH peak amplitude ranged from 0-1.7 mIU/ml. Serum E2 correlated with mean LH concentrations (P less than 0.001) and LH pulse frequency (P less than 0.05), but not with LH pulse amplitude. FSH pulsations were identified in 3 of the 20 women. There was no correlation between mean FSH concentrations and either serum E2 or PRL. There was a significant correlation between LH and FSH concentrations (P less than 0.001). During bromocriptine therapy, with comparable E2 concentrations, 5 of the 6 patients studied with blood sampling every 20 min for 24 h had a significant decrease (P less than 0.01) in the number of LH peaks per 24 h, with no change in LH peak amplitude. Mean FSH concentrations were unchanged in bromocriptine-treated patients; however, there was a significant (P less than 0.02) decrease in FSH levels during sleep. Serum PRL was normal in all bromocriptine-treated patients, but normal PRL secretory patterns were not reestablished, and there was no correlation between LH pulsations and serum PRL concentrations. We conclude that 1) hyperprolactinemic women have a heterogeneous pattern of pulsatile gonadotropin secretion; 2) serum E2 correlates with LH pulse frequency but not pulse amplitude; 3) LH pulsations and PRL pulsations are asynchronous in hyperprolactinemic women before and during bromocriptine therapy; and 4) normal PRL secretory patterns are not required for ovulatory function in hyperprolactinemic women treated with bromocriptine.

Adenoma↗
PubMed1986

A comparison among the growth hormone-lowering effects in acromegaly of the somatostatin analog SMS 201-995, bromocriptine, and the combination of both drugs.

The acute GH inhibitory effects of 50 micrograms SMS 201-995, a somatostatin analog, and 2.5 mg bromocriptine were compared in 17 acromegalic patients. SMS 201-995 suppressed plasma GH levels after 2-6 h to 5 micrograms/liter or less in 10 of these 17 patients, while bromocriptine did the same in only 5 of them. There was much variation in the responsiveness to both drugs in these patients, but the GH-lowering effect of 50 micrograms SMS 201-995 was significantly greater than that of 2.5 mg bromocriptine. SMS 201-995 and bromocriptine together significantly suppressed plasma GH levels in 2 of 3 acromegalic patients who were insensitive to both compounds when tested separately. We conclude that most acromegalic patients respond better to SMS 201-995, while a few patients are more sensitive to the GH-lowering effect of bromocriptine. In addition, the combination of SMS 201-995 and bromocriptine can be of value in a few acromegalic patients who do not respond to either drug alone.

Acromegaly↗
PubMed1990

A randomized study of SMS 201-995 versus bromocriptine treatment in acromegaly: clinical and biochemical effects.

Twenty-six acromegalic patients were randomized to treatment with either SMS 201-995 or bromocriptine in increasing doses and were investigated before treatment, after 2, 4, and 8 weeks of treatment, and 2 weeks after discontinuation of treatment. There were two dropouts from the bromocriptine group and one from the SMS 201-995 group. Amelioration of clinical signs and symptoms was seen in both groups during treatment. After 8 weeks mean 12-h GH concentrations had declined from 13.8 +/- 5.2 to 2.9 +/- 4.4 (mean +/- SEM) in SMS 201-995-treated and from 18.8 +/- 7.5 to 5.4 +/- 1.2 micrograms/L in bromocriptine-treated patients. Somatomedin-C concentrations fell from 3.04 +/- 0.36 to 1.43 +/- 0.36 in SMS 201-995-treated and from 2.93 +/- 0.40 to 2.13 +/- 0.27 U/mL in bromocriptine-treated patients. Size reduction of the pituitary tumor was seen in one patient receiving bromocriptine. Gastrointestinal glucose absorption was delayed, and insulin secretion suppressed during treatment with SMS 201-995. Hemoglobin-A1 concentrations remained unchanged in SMS 201-995-treated patients, but declined in the bromocriptine group. Side-effects were common, but usually tolerable, with both treatments. It is concluded that both drugs are of benefit in the treatment of acromegaly.

Acromegaly↗
PubMed1997

Acute effects of bromocriptine, cyproheptadine, and valproic acid on plasma adrenocorticotropin secretion in Nelson's syndrome.

Previous studies have found that bromocriptine, cyproheptadine, and valproic acid can reduce ACTH secretion in Nelson's syndrome, but none of these agents has achieved widespread use due to their failure to normalize ACTH in most patients. The current study was undertaken to determine whether these three agents, which act through different mechanisms, decrease plasma ACTH synergistically when administered together. Six adult female patients (mean age, 41 yr) with Nelson's syndrome were studied. ACTH was measured every 20 min for 8 h, 2 h before and 6 h after each of the following six treatments: placebo, bromocriptine (2.5 mg), cyproheptadine (8 mg), valproic acid (1 g), cyproheptadine plus valproic acid, and the combination of all three drugs. The sequence of treatments was determined randomly, and there was an interval of at least 2 days between each treatment. The hourly ACTH values were averaged, and the percent maximal suppression of plasma ACTH, relative to the baseline values before drug administration, was compared among the six treatments. Basal plasma ACTH levels in the six patients ranged from 40-3324 pmol/L (normal range, 1-8). The percent maximal suppression of ACTH after administration of placebo (6 +/- 11%), cyproheptadine (17 +/- 15%), valproic acid (37 +/- 10%) or the combination of cyproheptadine and valproic acid (19 +/- 14%) did not achieve statistical significance. Bromocriptine, on the other hand, caused a significant decrease in plasma ACTH (52 +/- 8%; P < 0.05), as did the combination of bromocriptine, cyproheptadine, and valproic acid (58 +/- 12%; P < 0.05). However, the combined effect of the three drugs did not significantly exceed the effect of bromocriptine alone. We conclude that at the doses studied, bromocriptine had the greatest acute effect in suppressing ACTH secretion in Nelson's syndrome, and that combined administration with valproic acid and cyproheptadine did not further increase this acute ACTH-suppressive effect.

Adrenocorticotropic Hormone↗
PubMed1999

Chronic constrictive pericarditis induced by long-term bromocriptine therapy: report of two cases.

OBJECTIVE: To report two cases of chronic constrictive pericarditis that appear to be related to the intake of bromocriptine for Parkinson's disease. CASE SUMMARY: Two white men (aged 63 and 69 y) were treated with bromocriptine for four (40 mg/d) and two years (30 mg/d), respectively, with a cumulative dose intake of 58.4 and 21.9 g, respectively. The patients experienced dyspnea with bilateral lower-limb edema and pleural effusion, suggesting right cardiac dysfunction. Echocardiography, computed tomography, and cardiac catheterization results were compatible with a diagnosis of constrictive pericarditis, so pericardectomy was performed on both patients. The anatomic pathology examination showed a fibrous pericardium; cultures were sterile. In the first case, pleural effusion recurred seven months after the pericarditis; bromocriptine was suspected and treatment was discontinued. In the second case, just prior to the pericardectomy, an episode of mental confusion occurred and prompted the cessation of bromocriptine therapy. DISCUSSION: To the best of our knowledge, only one case of constrictive pericarditis induced by bromocriptine therapy has previously been described in the literature. CONCLUSIONS: Our cases call attention to a possible association between bromocriptine use in patients who have Parkinson's disease and constrictive pericarditis.

Aged↗
PubMed1988

Pleuropulmonary involvement during bromocriptine treatment.

The use of bromocriptine in the treatment of Parkinson's disease is increasing. More than 20 cases of suggested drug-induced pleuropulmonary disorders during bromocriptine therapy have been reported. We describe four male parkinsonian patients taking bromocriptine in whom pleuropulmonary abnormalities were discovered in a pulmonary hospital during a one-year period. In only one case were the roentgenographic changes reversible after withdrawal of the drug. Pleural fluid from two patients was analyzed and showed lymphocyte-predominant chronic inflammatory changes. Raised erythrocyte sedimentation rate (ESR) and C-reactive protein values decreased after cessation of bromocriptine. Lung function studies demonstrated volume restriction with normal or high CO transfer coefficient. The frequency of pleuropulmonary changes during bromocriptine therapy may be greater than assumed, and such patients may initially present with nonrespiratory symptoms. Follow-up of patients during bromocriptine treatment by ESR, C-reactive protein, and chest roentgenogram is recommended.

Aged↗
PubMed1994

[Unique type of Cushing's disease in clinical profile: cyclic Cushing's syndrome and Cushing's disease with favorable outcome to a high daily dose of bromocriptine].

A rare case of cortisol-responsive, dexamethasone-non-responsive cyclic Cushing's disease for whom a high daily dose of bromocriptine was effective was presented, and 58 cases of cushing's syndrome with variable hormonogenesis from the literature were reviewed with our own case (a total of 59 cases). In addition, the results of the high daily dose of bromocriptine treatment in our 7 cases of Cushing's disease were described. The presented case, a 57-year-old female, had a clinically and biochemically proven 3-8 day cycle length. With 40mg daily of bromocriptine, periodic hypercortisolemia disappeared and the patient was in remission with normal suppression of plasma cortisol by dexamethasone. Out of 59 cases of cyclic Cushing's syndrome, 39 were pituitary Cushing's disease or Cushing's syndrome with bilateral adrenal hyperplasia. 15 cases (25%) were adrenal adenoma and ectopic ACTH syndrome. In 22 out of 34 cases (62%), paradoxical response of plasma cortisol to dexamethasone was observed. Only 4 out of 16 cases (25%) on whom Hardy's operation was performed remitted completely. Our own presented case alone showed long-term remission with medical treatment. Seven Cushing's disease patients were treated with a high daily dose of bromocriptine (17.5-55mg/day). Three cases, in whom the highest dose of bromocriptine was 40, 55, and 35mg/day, showed clinical and biochemical long-term remission. In these 3 cases, an escape phenomenon was observed during the early treatment period with a decreased dose of bromocriptine. Thereafter the dose was increased, resulting in a beneficial outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1980

Bromocriptine treatment during early human pregnancy: effect on the levels of prolactin, sex steroids and placental lactogen.

To elucidate the role of prolactin (Prl) in the endocrinology of early human pregnancy, 28 healthy women were given 5.0-7.5 mg of bromocriptine daily for two weeks between weeks 6-9 of normal gestation. Plasma Prl, oestradiol-17 beta (Oe2), progesterone (P), testosterone (T) and human placental lactogen (hPL) were measured before, and one and two weeks after the start of bromocriptine, and they were compared with those in 22 control women who were followed similarly but without bromocriptine treatment. Bromocriptine treatment induced a significant Prl depression at one week (7.3 +/- 4.3 ng/ml vs 23.7 +/- 11.4 ng/ml) and two weeks (5.3 +/- 2.5 ng/ml vs 31.9 +/- 16.4 ng/ml). Oe2, P, T and hPL levels, however, showed no significant differences between the groups. Two women undergoing bromocriptine treatment (7.1%) and one control women (4.5%) experienced spontaneous incomplete abortion during the study period, but these three already had a low Oe2 level and a low/or undetectable hPL level at the beginning of the study. It is obvious that neither maternal 'hypoprolactinaemia' nor bromocriptine during early human pregnancy interfere with the normal progress of pregnancy or with the normal synthesis of sex steroids and hPL at this time.

Bromocriptine↗