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PubMed1996

Suggestive evidence for bromocriptine-induced pleurisy.

Pleurisy of initially unknown origin was found in a patient who was treated with bromocriptine for Parkinson's disease for 6 years. At presentation, bilateral pleural thickening existed that caused severe restriction of pulmonary function. There were an elevated erythrocyte sedimentation rate, polyclonal hypergammaglobulinaemia, increased levels of acute phase proteins and anaemia. After withdrawal of the bromocriptine the patient's complaints as well as the laboratory parameters markedly improved. Further loss of pulmonary function did not occur. However, the pleural thickening did not resolve, not even upon subsequent corticosteroid treatment, probably due to fibrosis. Together, these findings strongly suggest a causative role of bromocriptine. The results of the laboratory studies suggested an immunopathogenetic mechanism, but in vitro lymphocyte-proliferation studies and skin patch tests with bromocriptine were negative. Bromocriptine should be considered as a cause of pleurisy. The drug must be stopped immediately upon the occurrence of pleural thickening in order to prevent impairment of pulmonary function. In addition, periodic laboratory and X-ray studies in patients on long-term bromocriptine treatment should be considered.

Aged↗
PubMed1996

Bromocriptine prevents spinal motor neuron death following sciatic nerve transection in neonatal rats.

Bromocriptine, a potent dopamine D2 receptor agonist, appears to have neuroprotective actions. In order to investigate the effect of bromocriptine on axotomy-induced cell death, we have examined the survival of spinal motor neurons after sciatic nerve transection in the neonatal rats. Newborn rats were anesthetized with hypothermia. Sciatic nerve was transected near the obturator tendon in the left thigh. Animals were then treated daily with bromocriptine for 14 days with intraperitoneal injections. Control animals received PBS in the same fashion. After the treatment, the number of spinal motor neurons in the L4-6 was counted. There is approximately a 50% loss of spinal motor neurons in the PBS treated group. By contrast, bromocriptine prevents spinal motor neuron death after axotomy. The motor neuron diameter on the lesioned side is significantly larger in the bromocriptine-treated group. These results are consistent with the possible role of bromocriptine as a survival factor for developing spinal motor neurons.

Animals↗
PubMed2005

Bromocriptine treatment for cocaine addiction: association with plasma prolactin levels.

Bromocriptine is a dopamine receptor agonist used with mixed success in the treatment of cocaine addiction. Variations in dopamine receptor sensitivity may help account for these differences. We evaluated this question in a 24-week outpatient controlled clinical trial in 70 cocaine-abusing (DSM-III) men (86% African-American, mean age 34 years, mean 39 months of regular cocaine use [predominantly smoked]). Subjects received 4 weeks of inpatient treatment. During the last 2 weeks they were inducted onto bromocriptine (maximum dose 2.5mg po tid) (n=35) or placebo (n=35). Plasma prolactin concentrations were assayed before and after the first bromocriptine dose (1.25mg po) as a measure of dopamine receptor sensitivity. After discharge, subjects continued on medication with weekly group counseling. Bromocriptine significantly suppressed prolactin concentrations (4.4 ng/ml decrease), while placebo did not (0.1 ng/ml decrease). Both groups decreased their cocaine use, with no significant group differences in retention in treatment or proportion of cocaine-positive urine samples. There was no significant association between basal plasma prolactin concentrations or prolactin response to first bromocriptine dose and either outcome measure. These data do not support the efficacy of bromocriptine treatment nor a role for prolactin concentration in predicting treatment response.

Bromocriptine↗
PubMed1984

The effect of bromocriptine on the mammary glands of hyperprolactinemic rats. A histologic, ultrastructural and morphometric study.

Old female Long-Evans rats with elevated serum prolactin levels were used to study the effect of bromocriptine on the stimulated mammary glands by histology, electron microscopy, and morphometry. Untreated rats were divided into normoprolactinemic (below 30 ng prolactin/ml serum) and hyperprolactinemic control groups (above 30 ng/ml). Treated groups were injected subcutaneously with 1 mg/kg of bromocriptine once daily for 1 day, 30 days and 44 days. One group was treated with bromocriptine for 30 days, and then the drug was withdrawn for an additional 14 days. The light and electron microscopic features of breasts of hyperprolactinemic control, 1 day treatment and withdrawal groups resembled those of postpartum lactating breasts. A unique feature was the presence of large membrane-bound bodies, possibly lysosomes. The breasts of normoprolactinemic control, 30 and 44-day treatment groups were similar by histology and ultrastructure to involuted breasts after cessation of lactation. However, many large lysosome-like bodies and microvilli were found in the alveolar cells which remained tightly apposed. Hyperprolactinemic control rats showed breast stimulation which could be correlated with serum prolactin levels. Serum prolactin concentrations fell within 1 day of bromocriptine treatment, whereas breast tissue responded only after a longer interval. Pituitary weights could be correlated with serum prolactin levels. Withdrawal of bromocriptine resulted in an elevation of serum prolactin levels and breasts returned to the stimulated stage. It can be concluded that bromocriptine reversibly suppresses the stimulation of mammary glands in hyperprolactinemic rats.

Animals↗
PubMed1993

Bromocriptine treatment of periparturient goats: long-term suppression of prolactin and lack of effect on lactation.

British Saanen dairy goats (n = 10) were treated with bromocriptine or vehicle from day 147 of pregnancy to day 4 post partum, a treatment duration of 8.8 +/- 1.7 d (mean +/- SEM). The periparturient prolactin surge was abolished by this treatment, but there were no significant effects on plasma growth hormone or insulin concentrations. Lactogenesis was delayed in the bromocriptine-treated goats, milk yields being significantly depressed (P < 0.01) for the first week of lactation. Yields had recovered to control values by day 10 when prolactin concentrations were still significantly depressed. Mammary gland biopsies were taken on day 4 post partum from five animals in each group. Using this tissue, no significant differences could be shown in mammary morphology or DNA synthesis, but the RNA:DNA ratio was significantly reduced (P < 0.05). After week 1, there were no significant differences between bromocriptine-treated and control goats in milk yield, milk composition, udder volume, time of peak yield or persistence. The goats given short-term bromocriptine treatment at parturition showed prolonged effects on prolactin secretion, their seasonal prolactin rise being severely blunted (P < 0.001). A normal lactation is therefore not prevented in goats by a delay in lactogenesis, suppression of prolactin at parturition or the resulting prolonged depression of circulating prolactin. Goats in established lactation given bromocriptine for 8 d showed, by contrast, a rapid recovery of plasma prolactin concentrations within 5 d post treatment. Milk yield declined significantly (P < 0.03) compared with pretreatment values during and for 1 week after bromocriptine but then began to recover, with no significant change in vehicle-treated goats.

Animals↗
PubMed1983

Bromocriptine in the long-term management of advanced Parkinson's disease.

Thirty-seven patients with advanced Parkinson's disease who initially tolerated, and responded to bromocriptine therapy were followed for 12 to 50 (mean 28) months. Using a method of gradual increase of bromocriptine, with concomitant levodopa reduction, the peak effect of the drug was apparent by three months, at which time the mean daily dose of bromocriptine was 23.9 mg and Sinemet (levodopa + carbidopa) had been reduced by 34 percent. Eight patients had sustained improvement without further drug changes for an average of 29 (range 14-50) months. After periods of improvement varying between 3 and 30 months, 29 patients had a fall-off from peak effect. Peak effect was regained in 21 of these 29 patients for an average of 16 additional months by initially increasing bromocriptine or Sinemet, or by eventually increasing both drugs. The main adverse effect was a confusional state which necessitated late withdrawal of bromocriptine in four patients. The best results were in younger patients with end-of-dose deterioration and levodopa induced dyskinesias. With cautious introduction, and intermittent dosage adjustment, bromocriptine can be of long-term benefit to patients with advance Parkinson's disease. The majority of patients have a gradual late fall-off in effect which can frequently be reversed with dosage adjustment.

Aged↗
PubMed1998

Growth hormone secretion elicited by GHRH, GHRP-6 or GHRH plus GHRP-6 in patients with microprolactinoma and macroprolactinoma before and after bromocriptine therapy.

OBJECTIVE: Growth hormone-releasing peptides (GHRPs) are potent GH releasers which act at both pituitary and hypothalamic levels through specific G-protein coupled receptors, recently cloned. A synergistic effect from the simultaneous administration of GHRH + GHRP-6 on GH release is observed in normal subjects, while it is absent in patients with hypothalamo-pituitary disconnection. We studied the effects of GHRH, GHRP-6 and both secretagogues on GH release in patients harbouring pituitary tumours that may be reduced in size by medical treatment. DESIGN: Analysis of peak GH response to GHRH, GHRP-6 and GHRH plus GHRP-6 in patients with micro- and macroprolactinomas. Integrated GH response over 2 hours calculated as AUG-GH mU/l x 120 min. Analysis of delta PRL above the basal level in response to the same GH releasers. PATIENTS: Eleven patients with macroprolactinomas aged 41.2 +/- 4.8 years (range 24-75), nine patients with microprolactinomas aged 31.5 +/- 3.4 (range 22-53) and 13 healthy subjects aged 42.1 +/- 4.7 years (range 22-64) were studied. Prolactinoma patients were then treated with bromocriptine (15-20 mg orally) for 6-24 months. Tests were repeated when there was evidence of tumour shrinkage and normalized plasma prolactin concentrations. RESULTS: Peak GH response before treatment in macroprolactinoma patients was 4.9 +/- 0.9 mu/l after GHRH, 8 +/- 4 mU/l after GHRP-6 and 18 +/- 5 mU/l after GHRH + GHRP-6. Synergism was absent. AUC were 390 +/- 90; 500 +/- 100 and 1100 +/- 300 mU/l x 120 min respectively. These values were all significantly different (P < 0.05) from normal subjects and patients with microprolactinomas with peak GH 16.8 +/- 0.9 mU/l after GHRH; 43 +/- 6 mU/l after GHRP-6 and 130 +/- 10 mU/l after GHRH + GHRP-6. AUC-GH was 1200 +/- 400 after GHRH, 2200 +/- 400 after GHRP-6 and 9000 +/- 1000 mU/l x 120 min after GHRH + GHRP-6. As in normal subjects, synergism was preserved in patients with microprolactinoma (P > 0.05). After treatment with bromocriptine peak GH in patients with macroprolactinoma was 8 +/- 4 mU/l after GHRH, 22 +/- 5 mU/l after GHRP-6 and 70 +/- 20 mU/l after GHRH + GHRP-6. AUC-GH was 800 +/- 300, 1100 +/- 300 and 3500 +/- 800 mU/l x 120 min, respectively. The response of GH after GHRP-6 and GHRH + GHRP-6 improved significantly (P < 0.05) in treated patients with macroprolactinoma. There was no significant change in GH response in microprolactinoma patients after treatment with bromocriptine. Peak GH after GHRH was 30 +/- 20 mU/l, after GHRP-6 it was 75 +/- 8 mU/l and after GHRH + GHRP-6 it was 200 +/- 30 mU/l. AUC-GH was 1500 +/- 700 after GHRH, 4500 +/- 500 after GHRP-6 and 15,100 +/- 600 mU/l x 120 min. Delta prolactin after GHRP-6 did not change before and after bromocriptine treatment in patients with macroprolactinoma or microprolactinoma. CONCLUSION: GH release after GHRP-6 or GHRH + GHRP-6 is fully preserved in patients with microprolactinomas and does not differ before and after treatment with bromocriptine. Patients with macroprolactinoma have blunted responses of GH after GHRH and GHRP-6 and synergism is severely compromised. GH responsiveness to and synergistic interaction between GHRH and GHRP-6 recovers after shrinkage of macroprolactinoma with bromocriptine. Prolactin release stimulated by intravenous administration of GHRP-6 in healthy subjects was not seen in patients with micro- or macroprolactinomas.

Adult↗
PubMed1994

Antioxidant properties of bromocriptine, a dopamine agonist.

It has been suggested that free radicals may adversely influence the pathogenesis of Parkinson's disease. We conducted this study to determine whether bromocriptine, an agent widely used for treating parkinsonism, possesses antioxidant effects. Bromocriptine scavenged superoxide produced from a superoxide generating system (hypoxanthine-xanthine oxidase) by the spin-trapping method using electron spin resonance. Bromocriptine had a strong scavenging effect on the 5,5-dimethyl-1-pyrroline-N-oxide hydroxide signal produced from Fenton's reaction. Bromocriptine also attenuated the stable free radical diphenyl-p-picrylhydrazyl signal. This drug inhibited the autooxidation of rat brain homogenates in a dose-dependent manner in vitro. Autooxidation of brain homogenates collected from rats treated with bromocriptine (2.5 mg/kg, i.p., daily for 3 days) was significantly reduced as compared with values in untreated rat homogenates. These observations suggest that bromocriptine is a free radical scavenger and a potent antioxidant.

Animals↗
PubMed1990

Effect of bromocriptine administration on maintenance of late pregnancy in the pig.

Plasma concentrations of prolactin, luteinizing hormone (LH) and progesterone were determined in pregnant gilts (n = 6) administered bromocriptine from 67-72 days of pregnancy. Blood samples were taken daily at 2 h intervals from 60 to 80 days of pregnancy. Bromocriptine treatment reduced prolactin from 9.7 +/- 1.4 before to 1.9 +/- 0.6 ng/ml during the treatment (p less than or equal to 0.05) and then returned to the pre-treatment concentrations (10.5 +/- 2.0) following cessation of bromocriptine. Bromocriptine increased LH from 1.4 +/- 0.2 before treatment to 2.9 +/- 0.5 ng/ml (p less than or equal to 0.01) during administration and maintained elevated (3.0 +/- 0.7) in the post-treatment period (p less than or equal to 0.05). Administration of bromocriptine did not alter progesterone concentration in plasma (7.5 +/- 1.2; 7.2 +/- 1.6 and 6.6 +/- 1.6 ng/ml in pretreatment, treatment and post-treatment periods, respectively). This study shows that decrease of prolactin level by bromocriptine treatment does not cause depletion of progesterone secretion in late pregnant pigs.

Animals↗
PubMed1996

Enzyme immunoassays for bromocriptine and its metabolites.

We have developed two bromocriptine enzyme immunoassays with different specificities for applications in human and animal pharmacokinetic studies. The first assay uses antibodies directed against the cyclopeptide structure of bromocriptine, and is specific for untransformed bromocriptine. The second assay uses antibodies directed against the bromolysergic part of the molecule and allows the measurement of both bromocriptine and its metabolites. Enzymatic tracers were obtained by covalent coupling of bromocriptine analogs to acetylcholinesterase from the electric eel Electrophorus electricus. Both assays have a limit of detection of 10 pg/ml and a limit of quantification of 50 pg/ml. The specificity of the assays was determined following fractionation by high-performance liquid chromatography of rat samples obtained after administration of bromocriptine.

Administration, Oral↗
PubMed1993

Central dopaminergic origin of bromocriptine induced tachycardia in normotensive rats.

OBJECTIVES: This study was undertaken to investigate the mechanism of the tachycardic effect of bromocriptine, a specific dopamine D-2 receptor agonist, which is not abolished, as previously reported, by intravenous domperidone, a selective dopamine D-2 antagonist unable to cross the blood brain barrier. Two hypotheses were tested: (1) that the increase in heart rate after intravenous treatment with bromocriptine could be related to central dopamine receptor stimulation and (2) that it could be induced by a release of adrenaline from the adrenal medulla. METHODS: Changes in mean aortic pressure and heart rate, induced by treatment with 150 micrograms.kg-1 bromocriptine intravenously, were measured in conscious or anaesthetised normal or adrenalectomised rats submitted to various pretreatments. RESULTS: In conscious intact rats, intravenous bromocriptine decreased mean aortic pressure (-11 (SEM1) mm Hg) and increased heart rate (62(12)) beats.min-1). Both effects were prevented by intravenous pretreatment (0.3 mg.kg-1) with dopamine D-2 receptor antagonists able to cross the blood brain barrier, such as haloperidol, sulpiride, and metoclopramide. In anaesthetised rats, domperidone (50 and 20 micrograms.kg-1) given via a lateral cerebral ventricle abolished the bromocriptine induced tachycardia without affecting the hypotensive response. Both effects were unchanged after bilateral adrenalectomy but were completely abolished by intravenous haloperidol pretreatment (0.3 mg.kg-1) in conscious adrenalectomised rats. CONCLUSIONS: These results suggest that in anaesthetised and conscious normotensive rats, the bromocriptine induced tachycardia is not related to a release of adrenaline from the adrenal medulla but could be elicited by central dopamine D-2 receptor stimulation through a possible increase in cardiac sympathetic tone.

Adrenalectomy↗
PubMed1997

The long-acting dopamine agonist bromocriptine mesylate as additive immunosuppressive drug after kidney transplantation.

BACKGROUND: Acute rejection is an important risk factor for kidney graft loss. As evidence suggests that prolactin has important immunostimulatory properties, we conducted a randomized, prospective open trial in which bromocriptine, a drug suppressing prolactin secretion, was administered as an additive immunosuppressive drug after first cadaver kidney transplantation. METHODS: In the treatment group bromocriptine was given intramuscularly to 22 patients after their first kidney transplantation along with conventional immunosuppression (cyclosporin A, glucocorticoids). Twenty-three patients receiving only conventional immunosuppression served as control subjects. The incidence of acute graft rejections, graft losses, and infections was evaluated. RESULTS: Serum prolactin concentrations were slightly elevated above normal values before transplantation (32 +/- 5.3 ng/ml) and decreased to values between 13 and 16 ng/ml in the control group and were totally suppressed in the bromocriptine group. After 6 months of follow-up overall patient and allograft survival was 97.7% and 91% respectively. Acute rejection episodes occurred in 31 patients (77.5%): 15 in the bromocriptine group vs 20 in the control group (n.s.). In each group eight patients experienced a cytomegalovirus infection. The incidence of severe bacterial infections (i.e. pneumonia and sepsis) was five and six respectively. The necessity of haemodialysis after transplantation was 3.1% in the patients on bromocriptine and 23% in those without. CONCLUSIONS: Suppression of circulating prolactin concentration by bromocriptine did not improve the clinical outcome of patients after kidney transplantation receiving cyclosporin and prednisolone.

Acute Disease↗
PubMed1994

Discontinuation of prolonged bromocriptine therapy in Parkinson's disease patients with uncontrolled motor oscillations.

The beneficial effect of bromocriptine in fluctuating Parkinson's disease (PD) under chronic levodopa therapy has been reported to be lost in the long term in most patients. We attempted slow bromocriptine discontinuation in nine PD patients to whom this drug have been added to levodopa because of fluctuating motor responses but who appeared to cease benefitting from this association after an average of 4.6 years (range, 1.3-8 years) of sustained bromocriptine therapy. Bromocriptine was discontinued by gradually tapering off the dosage (mean, 8.5 mg/week) while leaving levodopa medication unchanged. The percentage time spent "off" during waking hours increased in all patients (average, 30.2 +/- 18.5% versus 65.6 +/- 82.6%, p < 0.001) and in three patients the "on-off" pattern shifted from random fluctuations to disabling "off" periods 23-26 times longer than before discontinuation. Sustained bromocriptine therapy does not prevent the continuous deterioration of motor fluctuations. However, we believe that this drug remains partially effective over the long term and should not be discontinued in PD patients with uncontrolled fluctuations, even though their condition may actually appear to worsen as compared to when bromocriptine therapy was first started.

Aged↗
PubMed1991

Long-term effects of radiotherapy and bromocriptine treatment in patients with previous surgery for macroprolactinomas.

The long-term effect of radiotherapy and bromocriptine treatment was retrospectively evaluated in 25 patients who had previously undergone transsphenoidal surgery for treatment of macroprolactinomas. Surgery had reduced the median serum prolactin (PRL) value from 613 micrograms/l, a reduction of 53%. Postoperative bromocriptine was administered to 21 of the 25 patients. In 14 of these patients, serum PRL values became normal or almost normal with medication. There were no radiological or ophthalmological signs of progressive tumor growth during bromocriptine treatment. Fourteen patients received postoperative radiotherapy. After withdrawal of bromocriptine in 13 of these patients an average of 7 years after radiotherapy, the median serum PRL value had further decreased by 95%. The PRL reduction was similar for all doses applied, 38 to 52 Gy. After withdrawal of bromocriptine in 8 patients not receiving radiotherapy an average of 7 years after operation, the median serum PRL level had further decreased by 75%. At follow-up, 18 additional instances of pituitary insufficiency had developed in the group receiving radiotherapy, compared with 8 cases of insufficiency in the group not receiving radiotherapy. Thus, because bromocriptine has a long-standing effect on prolactin secretion, and radiotherapy is associated with a notably high incidence of pituitary insufficiency, we propose that photon irradiation should be considered mainly for patients who are not candidates for surgical or medical treatment.

Adult↗
PubMed1983

Bromocriptine and premenstrual symptoms: a survey of double blind trials.

This is a survey of 14 placebo-controlled studies regarding the treatment of premenstrual symptoms with bromocriptine. There is no substantial support that bromocriptine is an effective drug in the premenstrual syndrome as an entity. Symptoms such as irritability, depression, and anxiety were not significantly improved during treatment with bromocriptine compared to placebo treatment. Bromocriptine appears to be the treatment of choice in premenstrual mastodynia if the dosage of bromocriptine is at least 5 mg daily. Bromocriptine may therefore have a place in selected cases of the premenstrual syndrome with associated mastodynia.

Adult↗
PubMed1980

The effects of bromocriptine in methyldopa treated hypertension.

1. The effects of treatment with the dopaminergic agonist bromocriptine were studied in nine patients with essential hypertension receiving methyldopa as sole therapy. 2. In Phase 1 of the study, the addition of bromocriptine on a single-blind basis caused a significant fall in lying and standing blood pressures. Plasma prolactin fell significantly but there was no significant change in the other biochemical parameters measured. All patients volunteered that they felt a sense of well-being after starting bromocriptine treatment. 3. In Phase 2 of the study the substitution of placebo for bromocriptine in a randomized double-blind trial significantly increased lying and standing blood pressures and plasma prolactin. No consistent or significant changes were observed in methyldopa-induced side-effects following the substitution of placebo for bromocriptine. 4. In Phase 3 of the study, a gradual increase in blood pressure was observed in all patients over a few months after stopping bromocriptine therapy. 5. The significance of these findings in relation to the role played by plasma prolactin and central dopaminergic activity in blood pressure regulation is discussed.

Adult↗
PubMed1978

Bromocriptine: lack of effect on the angiotensin II and aldosterone responses to sodium deprivation.

Five normal subjects took a low sodium diet for four days on two occasions, one with and one without added bromocriptine 2.5 mg three times a day by mouth. Daily measurements of urinary electrolytes and the concentrations of plasma renin (PRC), angiotensin II (AII), aldosterone, 18-hydroxycorticosterone, cortisol, electrolytes and prolactin were made in both phases of the study. Deprivation of sodium without bromocriptine resulted in progressive and highly significant increases in the plasma concentration of aldosterone from 230 +/- 50 to 418 +/- 44 (SEM) pmol/l, 18-hydroxycorticosterone from 627 +/- 138 to 1420 +/- 478 pmol/l, PRC from 108 +/- 38 to 166 +/- 14 muU/ml and AII from 16 +/- 3 to 29 +/- 4 pmol/l. Similar changes were found during bromocriptine administration despite suppression of prolactin secretion. Sodium deprivation together with bromocriptine resulted in increases in the plasma concentrations of aldosterone from 230 +/- 47 to 416 +/- 72 pmol/l, 18-hydroxycorticosterone from 630 +/- 99 to 1629 +/- 552 pmol/l, PRC from 105 +/- 12 muU/ml and AII from 14 +/- 3 to 26 +/- 5 pmol/l. Plasma cortisol did not change either in response to sodium deprivation or bromocriptine. Mean cumulative negative sodium balance was 101 +/- 14 mmol on bromocriptine and 118 +/- 14 mmol in the control period. We conclude that prolactin is not necessary for the steroidogenic response to sodium deprivation in man.

18-Hydroxycorticosterone↗
PubMed1983

Effect of bromocriptine in pituitary-dependent Cushing's syndrome.

To assess the therapeutic value of a dopaminergic drug on abnormal ACTH secretion, we studied the effect of bromocriptine during short and long-term treatment in nine patients with active pituitary-dependent Cushing's syndrome. The single oral dose effect of bromocriptine (2.5 mg at 0800 h) on ACTH samples obtained every half hour for 3 h, was studied in six patients with Cushing's disease; in no case was suppression of ACTH observed. In five patients, the effect of bromocriptine was also investigated after its administration for two consecutive days (5 mg/d) with plasma samples taken every half hour for 12 h; in three cases no suppression of plasma ACTH was observed, while the other two showed a significant decrease. Three of our patients (a nonresponder to the single dose, a responder to the two-day treatment, and an untested patient) were subjected to prolonged bromocriptine administration (2-45 months). In the first two patients only, biochemical data and clinical symptoms showed improvement, while the other patient showed only initial benefit. These data show that bromocriptine may occasionally reduce ACTH secretion in pituitary-dependent Cushing's syndrome, and that a single oral dose bromocriptine test fails to identify the patients who will benefit from this treatment.

Adrenocorticotropic Hormone↗