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PubMedDate not supplied

Bromocriptine for infertile males with mild hyperprolactinemia: hormonal and spermatogenic effects.

To clarify the influence of hyperprolactinemia on spermatogenesis and steroidogenesis in infertile male patients, the serum prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol concentrations were and the effect of bromocriptine treatment on spermatogenesis was examined. A total of 1234 patients were evaluated and 147 men had hyperprolactinemia. Of these, only 30 had PRL concentrations more than twice the upper limit of normal and most of them had a little excess over the upper limit. For 10 of these 30, serum hormone concentrations were measured and semen was analyzed before and after bromocriptine administration. No relationship between the PRL and other hormone concentrations was found. No changes were noted in the LH, FSH, testosterone, or estradiol concentrations, or in the sperm density and motility after treatment. The mean PRL decreased from 26.5 +/- 4.5 to 1.4 +/- 1.8 ng/mL. In infertile men who are mildly hyperprolactinemic, bromocriptine administration does not improve semen analysis, although it does normalize the PRL.

Bromocriptine↗
PubMed1997

Bromocriptine prevents neuron damage following inhibition of superoxide dismutase in cultured ventral spinal cord neurons.

Rosen et al. have reported point mutations in the cytosolic Cu/Zn superoxide dismutase (SOD 1) gene in some families with familial amyotrophic lateral sclerosis (ALS). To determine whether decreased SOD activity could contribute to neuronal damage, rat embryo ventral spinal cord neurons were incubated with diethyldithiocarbamate (DDC), an inhibitor of SOD. There was a marked increase in neuronal damage in cultures exposed to DDC and this phenomenon was dose-related. In this paradigm, these deteriorative changes were prevented by bromocriptine. DDC-treated ventral spinal cord neurons provide an in vitro model of free radical neurotoxicity secondary to decreased SOD activity. Simultaneous treatment with bromocriptine and DDC reduced neurotoxicity, indicating that bromocriptine has a neuroprotective effect against free radicals.

Animals↗
PubMedDate not supplied

The use of bromocriptine for the treatment of attention deficit disorder in two chemically dependent patients.

The dually diagnosed patient with attention deficit disorder, residual type (ADD-RT) may be especially prone to cocaine abuse, because ADD includes dopamine deficiencies and cocaine is a dopamine agonist. It is hypothesized that bromocriptine, a dopamine agonist, will reduce a patient's craving for cocaine and simultaneously address the patient's ADD-RT symptoms. A single-organism, double-blind research design is used to evaluate the efficacy of bromocriptine, as measured by scale 9 of the MMPI, the digit span and digit symbol tests of the Wechsler Intelligence Scale-Revised, and the signaling to numbers test. Statistical analysis of the results revealed an equivocal response to bromocriptine.

Adolescent↗
PubMed2002

Bromocriptine use is associated with decreased smoking rates.

Dopaminergic transmission in the central nervous system is thought to underlie addictive behaviours, including smoking. One effective smoking cessation drug, bupropion, enhances dopaminergic transmission; conversely, antipsychotic drugs, which are dopamine antagonists, are associated with increased smoking. Thus we hypothesized that subfertile women treated with the potent dopamine agonist bromocriptine might smoke less as a consequence of their treatment. Among 4,608 subfertile women those conceiving on bromocriptine were half as likely to smoke as those taking other drugs or those conceiving without medication (p < 0.0001). This observation supports the role of dopamine in nicotine addiction, and suggests that bromocriptine-like drugs could be used effectively by pregnant women to aid cessation.

Bromocriptine↗
PubMed1990

Retroperitoneal fibrosis in two patients with Parkinson's disease treated with bromocriptine.

Retroperitoneal fibrosis has been observed in two patients with Parkinson's disease treated with bromocriptine. The patients complained of abdominal or lower back pain and presented with various degrees of renal insufficiency, with anuria in one. Laboratory evaluation furthermore showed an increased sedimentation rate and inflammatory anemia. Computerized tomography disclosed marked retroperitoneal thickening, and biopsy was performed in one patient. The symptoms appeared eighteen months and five years after treatment was started, at doses of 20 and 22.5 mg of bromocriptine daily. The medication was discontinued in both patients and steroid therapy was initiated, with resolution of all clinical, biological and radiological evidence of disease. This potential but rare complication of a widely prescribed drug warrants monitoring of renal function and sedimentation rate in patients undergoing bromocriptine treatment.

Aged↗
PubMed2001

Cyclophosphamide plus somatostatin, bromocriptin, retinoids, melatonin and ACTH in the treatment of low-grade non-Hodgkin's lymphomas at advanced stage: results of a phase II trial.

PURPOSE: Somatostatin, prolactin, retinoids, melatonin and ACTH have been shown to influence the lymphatic growth, and the action of the cyclophosphamide in lymphoproliferative disorders is well known. This provided the rationale to conduct, in patients with low-grade non-Hodgkin's lymphomas (NHL), a phase II trial of a combined association of cyclophosphamide, somatostatin, bromocriptin, retinoids, melatonin and ACTH. PATIENTS AND METHODS: Twenty patients with a diagnosis of low-grade NHL, stage III or IV, were included in this study. Patients received for one month the following treatment: cyclophosphamide, somatostatin, bromocriptin, retinoids, melatonin, and ACTH. The therapy was continued for two additional months in patients with stable or responding disease. After three months, the responding patients continued the therapy for three months and more. RESULTS: Twenty patients were assessable for toxicity and response; 70% (14 of 20 patients; 95% confidence interval [CI], 50% to 90%) had a partial response; 20% (4 of 20) had stable disease, and 10% (2 of 20) progressed on therapy. Going on with the treatment, none of the 14 patients with partial response had a disease progression (average follow-up time of 21 months, range, 7 to 25), and 50% of these patients had a complete response; among 4 patients with stable disease, 25% (1 of 4) had a partial response and 75% (3 of 4) progressed on therapy (mean time to progression [TTP] 14.3 months, range, 7 to 21). The toxicity was very mild, the most common side effects being drowsiness, diarrhea and hyperglycemia. CONCLUSIONS: The association of cyclophosphamide, somatostatin, bromocriptin, retinoids, melatonin, and ACTH is well tolerated and effective in treatment of low-grade NHL at advanced stage.

Adrenocorticotropic Hormone↗
PubMed1991

Simplification of the initiation of bromocriptine in elderly patients with advanced Parkinson's disease.

One hundred and seventy-three parkinsonian patients treated with levodopa entered a randomized multicentre comparison between two introductory schedules for adjuvant bromocriptine. A 2-week placebo run-in was followed by a double-blind 8-week titration phase of bromocriptine up to 15 mg daily, according to the standard seven-step, or a simpler three-step, regimen. They were maintained on this dose for a further 8 weeks and then followed for a further 12 weeks. One hundred and fifty-nine patients completed the placebo run-in period, and 132 completed 16 weeks. No significant differences were found between the standard and simplified regimens for efficacy, side-effects, withdrawals or deaths, nor for any of the clinical or functional assessments. The Webster score improved by 29% and the Cape ADL by 32%. The simpler schedule offers advantages to those elderly parkinsonian patients in whom bromocriptine is added to optimal levodopa dosage.

Aged↗
PubMed1982

Atresia of preovulatory follicles in rats treated with sodium pentobarbital: effects of bromocriptine.

Preovulatory rat follicles matured during normal cycles go gradually into atresia if ovulation is inhibited by injections of sodium pentobarbital from proestrus for 2 or more days. The gradual process of atresia is characterized by a rapid decrease of follicular estrogen secretion within 1 day after the start of pentobarbital injections. Furthermore, structural signs of atresia appear in predictable order during the ensuing 3 days. In the present study experiments are described demonstrating clear and reproducible effects of daily treatment with bromocriptine on the above processes. Bromocriptine delayed the decrease of follicular estrogen production by about 1 day and also delayed the occurrence of structural signs of atresia. Further study revealed that the effect on estrogen secretion was likely through the action of bromocriptine to suppress prolactin secretion. It thus seems that prolactin is involved in the mechanisms whereby preovulatory follicles lose their capacity to secrete estrogen. This effect of prolactin may occur at the ovarian level and, thus, be involved in reduced secretion of estrogen by the ovaries during physiological or pathological hyperprolactinemic states.

Animals↗
PubMed1991

Effects of levodopa and bromocriptine on blood pressure and plasma catecholamines in parkinsonians.

Blood pressure (BP), heart rate (HR), plasma noradrenaline (NA), and adrenaline (A) levels in the lying and standing position were compared in patients with Parkinson's disease (PD) and control subjects. Three groups of PD patients (stage 2 and 3) were investigated: six patients deprived of antiparkinsonian drugs from 48 h, seven levodopa + benserazide-treated patients, and seven bromocriptine-treated patients. BP, HR, NA, and A were similar at rest and in the standing position in controls and in PD patients deprived of antiparkinsonian drugs from 48 h. Chronic treatment with levodopa (+ benserazide) failed to modify BP, HR, NA, and A. Bromocriptine decreased BP, HR, and NA (but not A) at rest. In PD patients treated with levodopa (+ benserazide) or bromocriptine alone, the rise in NA (but not A) elicited by standing up was reduced. These results indicate that (a) stages 2 to 3 of Parkinson's disease are not accompanied by major changes in autonomic cardiovascular function and (b) dopaminergic drugs blunted the sympathetic response to standing up.

Aged↗
PubMed1992

No effect of chronic bromocriptine therapy on levodopa pharmacokinetics in patients with Parkinson's disease.

We studied the effect of chronic bromocriptine cotherapy on levodopa kinetics in seven patients with Parkinson's disease who were receiving levodopa therapy. Plasma levodopa concentrations were measured after a standard oral levodopa fasting dose over a 5-hour period, on two different sessions, without and with bromocriptine at a fixed daily dose of 15 mg. We found no statistically significant difference in the rate and extent of levodopa absorption between the two treatments, with minimal intrasubject variability. Our observations suggest that chronic bromocriptine cotherapy is unlikely to affect the plasma levodopa pharmacokinetics under standardized intake conditions or to contribute to a less predictable pattern of drug plasma concentrations.

Aged↗
PubMed1993

Effects of bromocriptine in human narcolepsy.

Bromocriptine, a preferential D2 receptor agonist, was administered to six human narcoleptic patients during a double-blind, cross-over study. Laboratory sessions consisted of two all-night polysomnographic recordings and three daytime tests of vigilance: the Analogue Vigilance Scale (AVS), the Maintenance of Wakefulness Test (MWT), and the Four-Choice Reaction Time Test (FCRTT). No change in nocturnal sleep organization, daytime somnolence, or psychomotor performance was observed during bromocriptine administration. Periodic limb movements in sleep (PLMS) were significantly reduced during bromocriptine condition. These results suggest that D2 receptors are unlikely to play a major role in the physiopathology of human narcolepsy, and support the hypothesis that dopaminergic mechanisms are involved in PLMS.

Adult↗
PubMed1994

Bromocriptine therapy in multiple sclerosis: an open label pilot study.

Bromocriptine suppresses the duration and severity of clinical signs of experimental allergic encephalitis, which is considered as an animal model for multiple sclerosis (MS). We conducted an open pilot study with 2.5 mg of bromocriptine two times a day on 18 patients with clinically or laboratory-supported definite MS (10 with the relapsing-remitting form and eight with the chronic progressive form). After 1 year of treatment, 14 of the 15 patients who completed the study showed disease progression as evidenced by one or more of the following parameters: worsening of the EDSS score, clinical relapses, appearance of new lesions on MRI of the brain and brainstem, or increased latencies of visual or auditory evoked responses. These findings indicate that bromocriptine does not completely suppresses ongoing disease activity in patients with multiple sclerosis.

Adult↗
PubMedDate not supplied

The dopamine agonist bromocriptine induces hypotension by venous and arteriolar dilation.

Acute bromocriptine administration reduced sitting and standing blood pressure and produced severe orthostatic hypotension in 12 normal subjects. Concomitantly, there was an increase in venous distensibility and basal blood flow, and a decrease in peripheral vascular resistance, as determined by forearm plethysmography. After administration of bromocriptine, plasma norepinephrine concentration decreased. Bromocriptine lowers blood pressure by dilating arterioles and veins, at least in part by means of dopaminergic inhibition of sympathetic nervous system activity.

Adult↗
PubMed1984

Pregnancy after bromocriptine-induced reduction of an extrasellar prolactin-secreting pituitary macroadenoma.

In patients with a large prolactin-secreting pituitary adenoma, a marked reduction in tumor size may be achieved with bromocriptine therapy. However, before consideration of pregnancy, surgical removal of the lesion usually is advised. A 36-year-old woman with a large extrasellar pituitary macroadenoma was treated with bromocriptine, 10 mg/day, which resulted in dramatic reduction of the tumor mass. Subsequently, she became pregnant and drug therapy was maintained throughout gestation. This case illustrates the use of bromocriptine in the management of large prolactin-secreting pituitary tumors and the necessity for adequate radiologic follow-up.

Adenoma↗
PubMed1984

Efficacy of bromocriptine versus breast binders as inhibitors of postpartum lactation.

Fifty postpartum patients were randomly given either bromocriptine (2.5 mg by mouth b.i.d. X 30 doses) or breast binders for inhibiting lactation. The breast binder group had a high incidence of symptoms (breast pain, engorgement, secretion) for the first week postpartum; these symptoms rapidly decreased by the second week. Bromocriptine successfully suppressed the breast problems in virtually all of the patients who took the drug correctly. Because of the high rate of side effects and a significant incidence of "rebound," the dosage of bromocriptine should probably be changed, and we recommend a revised dosage.

Adolescent↗
PubMed1987

Postpartum psychosis induced by bromocriptine.

Two multigravida patients with no prior psychiatric history were seen with postpartum psychosis, having received bromocriptine for inhibition of lactation. Bromocriptine given in high doses has been associated with psychosis in patients receiving the drug for Parkinson's disease. These cases demonstrate that bromocriptine may cause psychosis even when given in low doses.

Adult↗
PubMed1982

Effects of long-term bromocriptine treatment on catecholamine excretion and on circulatory adaptation to orthostasis and to exercise in patients with hyperprolactinemia.

Sympatho-adrenally regulated mechanisms of the circulatory system have been studied in seven patients with hyperprolactinemia in order to evaluate the effects of long-term (1-3 months) treatment with bromocriptine. Before treatment catecholamine excretion was within the normal range. Blood volume was low and there was a marked heart rate reaction to orthostasis. ECG showed no abnormalities. Blood pressure and ECG reaction during exercise were normal. The blood pressure heart rate response to handgrip was less marked than in healthy young men. During bromocriptine treatment, serum prolactin levels normalized in all but one patient. Total catecholamine excretion was lowered. Body weight diminished. Resting heart rate and blood pressure fell significantly. Blood volume per kg body weight remained unchanged as did the orthostatic heart rate increase. The circulatory response to handgrip was less marked than before therapy. It seems that long-term bromocriptine therapy provokes a cardiovascular pattern reflecting an inhibition of sympatho-adrenal activity.

Adenoma↗
PubMed1977

Bromocriptine suppression of plasma growth hormone in acromegaly.

Twelve acromegalic patients were studied in one or more of three protocols to establish the response of plasma growth hormone (hGH) concentraions to (a) a single oral test dose of bromocriptine, (b) incremental dose therapy from 10 mg/day to 40 mg/day over 4 weeks, and (c) sustained therapy with 20 mg/day over a 3 month period. Ten of the patients studied had previously been treated by yttrium implantation, external pituitary irradiation or surgical hypophysectomy. A high incidence of side effects including postural hypotension, hallucinations and peripheral vasospasm was noted reducing the numbers of patients completing the three protocols. Suppression of hGH concentrations was disappointing; significant reductions in hGH concentraions occurred in five of eleven patients in response to a single test dose of bromocriptine, and in only one of seven patients treated with the drug over a sustained period. An impression of clinical improvement was gained in one patient, but there was no associated reduction in plasma hGH concentrations. It seems likely that acromegalic patients who have failed to respond to conventional treatment may be more resistant to bromocriptine therapy.

Acromegaly↗