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At least 775 records · Page 43Linked to original sources
PubMed1998

Does combined levodopa and bromocriptine therapy in Parkinson's disease prevent late motor complications?

Levodopa-carbidopa (LD) in low dosages adequately controls symptoms in most patients with Parkinson's disease and delays the appearance of fluctuations and dyskinesias. It has been suggested that early combination therapy with bromocriptine and levodopa delays or prevents the onset of late treatment complication associated with LD monotherapy in Parkinson's disease. We have conducted this study to assess the possible benefit of combined therapy compared with levodopa monotherapy. Seventy-eight previously untreated patients with Parkinson's disease were recruited over a period of 54 months and randomly allocated to either a levodopa-carbidopa (LD) Group or a levodopa-carbidopa in combination with low-dose bromocriptine (LD-Br) Group. The appearance of motor complications determined the end point of the study. We gradually increased the doses of bromocriptine (2.5-15 mg/d) or levodopa (125-500 mg/d) until the maximum "on" time was reached. In six patients, the doses of levodopa had to be increased up to the optimal dose (625-1000 mg/day). In the last evaluation the on-time and parkinsonian disability were similar in both treatment groups. We did not find statistically significant differences in the frequency of motor complications when comparing the two groups of treatment. Our study suggests that early combination of levodopa and bromocriptine does not confer any clinical benefit over levodopa alone in treating early Parkinson's disease, nor will it influence the evolution of the disease.Copyright Lippincott-Raven Publishers

Journal Article↗
PubMed1976

The antiparkinsonian efficacy of bromocriptine.

The antiparkinsonian activity of bromocriptine, a presumed dopaminergic receptor agonist, was investigated in monkeys with surgically induced tremor and in a group of parkinsonian patients. A single administration of bromocriptine resulted in a dose-dependent relief of tremor in monkeys. Repeated administration enhanced this effect. Only mild abnormal involuntary movements were observed and only after repeated administration. Eleven patients with Parkinson's disease were treated with bromocriptine (mean dose, 26.4 mg a day). Clinically obvious improvement was noted in one or more of the cardinal signs of the disease in six patients (responders). No obvious improvement in any of the cardinal signs was noted in the remaining five patients (nonresponders). Clinically, the responders were older and more severely affected and had been on a higher dose of levodopa. However, they had had the disease for a shorter period. It is suggested that failure to respond to bromocriptine may be related to a decrease in the sensitivity of postsynaptic dopaminergic receptors.

Age Factors↗
PubMedDate not supplied

Thyrotropin-secreting pituitary adenoma responsive to bromocriptine therapy.

OBJECTIVE: To describe a case of a thyrotropin-secreting pituitary adenoma that responded to bromocriptine therapy by suppression of thyrotropin and tumor shrinkage. METHODS: We present the clinical course, laboratory data, and radiographic findings in a 32-year-old woman with a thyrotropin-secreting pituitary adenoma before and after treatment with bromocriptine. RESULTS: The patient's pituitary tumor was detected after she had been treated with radioactive iodine for thyrotoxicosis presumed to be due to Graves' disease. After thyroid ablation, the thyrotropin levels could not be brought into the normal range, even while the patient was receiving supraphysiologic doses of orally administered levothyroxine. Magnetic resonance imaging of the pituitary, along with hormonal workup, confirmed the diagnosis of a thyrotropin-secreting pituitary adenoma. Because the tumor was not threatening vital structures and was considered incurable by operation, medical therapy was elected. A trial of bromocriptine was initiated at 15 mg/day and increased to 30 mg/day in three divided doses. Follow-up hormonal studies showed that thyrotropin levels declined into the suppressed range, and repeated magnetic resonance imaging scans showed substantial shrinkage of the pituitary lesion. CONCLUSION: Thyrotropin-secreting tumors may respond hormonally and structurally to bromocriptine therapy. In patients with such tumors, a trial of dopamine agonists at high dose may be considered before initiation of more invasive medical treatment.

Journal Article↗
PubMed1993

[Effects of bromocriptine microinjection into VTA on the DOPAC level in nucleus accumbens].

The experiment was performed in sodium pentobarbital anesthetized male SD rats. In vivo differential pulse voltammetry (DPV) was used to monitor a metabolite of dopamine-3,4-dihydroxyphenylacetic acid (DOPAC) level in the ipsilateral nucleus accumbens following microinjection of bromocriptine (2.5 micrograms/0.5 microliters, n = 5) into left ventral tegmental area (VTA). The results indicated that after microinjection the amplitude of DOPAC peak increased gradually and reached to 128% and 143% compared to the control at the 50th and 80th min respectively (P < 0.01). The duration of the effect was about two hours. One hundred and eighty min after injection, the amplitude of DOPAC decreased to 111% of control (P > 0.05). SCH23390 (2 nmol/0.5 microliters, n = 4), a selective D1 antagonist was given into left VTA 40 min prior to microinjection of bromocriptine. In this group, the above-mentioned effect of bromocriptine was blocked, the amplitude of DOPAC peak showed no increase. The results suggest that the microinjection of bromocriptine into VTA induces an increase of activity of mesolimbic dopaminergic neurons probably mediated by D1 receptor.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Bromocriptine treatment of spasmodic torticollis. A double-blind crossover study.

A double-blind crossover study (12 weeks and 12 weeks) was performed to evaluate the effects of bromocriptine on the symptoms and serum prolactin levels of 14 women with spasmodic torticollis. While the serum prolactin level decreased in response to bromocriptine, no difference was found between the effects of placebo and bromocriptine on the symptoms of spasmodic torticollis. Our findings suggest that dopaminergic neurotransmission is not involved in the pathogenesis of this syndrome.

Adult↗
PubMed1980

Bromocriptine for an acromegalic patient. Improvement in cardiac function and carpal tunnel syndrome.

A 64-year-old woman with active acromegaly of 33 years' duration, severe carpal tunnel syndrome, and subclinical heart disease was treated with bromocriptine mesylate. Within eight months of therapy, basal growth hormone (GH) levels decreased from 90.0 to 7.0 ng/mL, and hand volume was reduced from 375 to 295 mL. Concomitantly, echocardiographic studies showed normal left ventricular size and function. Electromyographic studies demonstrated normal function in both median nerves. Bromocriptine may correct cardiac dysfunction and carpal tunnel syndrome in acromegaly either by reduction of GH oversecretion or by a direct effect of bromocriptine on dopamine receptors in the heart and peripheral nerve endings.

Acromegaly↗
PubMed1985

Effects of bromocriptine on prolactin-secreting pituitary adenomas. Mechanism of reduction in tumor size evaluated by light and electron microscopic, immunohistochemical, and morphometric analysis.

Prolactin-secreting pituitary adenomas were studied to clarify the mechanism by which bromocriptine reduces tumor size. Patients examined consisted of three groups: Group I (four cases) received no medication, Group II (six cases) continued bromocriptine treatment (10 mg/day for 2 weeks) until the operation, and Group III (five cases) discontinued the treatment 1 week before the operation. Adenomas in Group II showed a variety of degenerative and necrotic changes of tumor cells in addition to marked decrease in volume of individual cell. Adenomas in Group III showed divergent structural changes. Irreversible changes seen in Group II became more pronounced with a marked increase in stromal tissue. Proliferative areas consisting of intermediate-sized cells were found in the scarce stromal tissue. The findings seem to indicate that the reduction in size of prolactinomas by bromocriptine treatment results from the reduction in size of individual tumor cell as well as from cell loss secondary to necrosis.

Adenoma↗
PubMed2001

Cortical effects of bromocriptine, a D-2 dopamine receptor agonist, in human subjects, revealed by fMRI.

Studies of human subjects performing cognitive tasks on and off dopaminergic drugs have suggested a specific role of dopamine in cognitive processes, particularly in working memory and prefrontal "executive" functions. However, the cortical effects of these drugs have been poorly understood. We used functional magnetic resonance imaging (fMRI) to examine both task-specific and general changes in cortical activity associated with bromocriptine, a selective agonist for D-2 dopamine receptors. Bromocriptine resulted in task-specific modulations of task-related activity in three cognitive tasks. Across tasks, the overall effect of the drug was to reduce task-related activity. We also observed drug effects on behavior that correlated with individual differences in memory span. We argue that bromocriptine may show both task-specific modulation and task-general inhibition of neural activity due to dopaminergic neurotransmission.

Adult↗
PubMed1987

Bromocriptine-desipramine protocol in treatment of cocaine addiction.

Thirty-six male cocaine abusers, in withdrawal, were studied for 99 days in a double-blind design. Treatment with bromocriptine was significantly more effective than placebo in alleviating withdrawal symptoms. Adding desipramine to the bromocriptine regimen was significantly more effective than either placebo or bromocriptine alone. The authors hypothesize that these results support a model of dopamine depletion and receptor supersensitivity in cocaine withdrawal.

Adult↗
PubMedDate not supplied

Bromocriptine in the management of infertile men after surgery of prolactin secreting adenomas.

This study evaluated bromocriptine treatment in nine patients with prolactin secreting adenomas who continued to have elevated circulating levels of prolactin after surgery, and who were interested in improving their sperm counts. These patients were brought into the study 3.2 +/- 1.8 years (mean +/- SD) after surgery. All of them presented with high circulating levels of prolactin, and eight of the patients had oligozoospermia (range 0-10 X 10(6) spermatozoa/ml). LH and testosterone levels were low in seven patients, and eight patients had low FSH values. All patients were treated for 90 days with 7.5 mg/day of bromocriptine. After treatment, prolactin levels decreased significantly in all patients, while sperm counts increased significantly in five of them. Testosterone levels increased in four subjects. Bromocriptine therefore seems useful in the management of this type of patient because of the observed decline in prolactin levels and the increase in sperm counts. Possible mechanisms involved in this action are discussed.

Adenoma↗
PubMed1991

Relevance of pH dependency on in vitro release of bromocriptine from a modified-release formulation.

Since pH profiles of the dissolution rate are thought to be predictive for the in vivo performance of oral modified-release formulations with respect to bioavailability and dose dumping with food, these pH profiles were established for a new modified-release (MR) formulation for bromocriptine (Parlodel SRO). The results show a marked decrease of bromocriptine dissolution with increasing pH of the dissolution medium. However, when measured in native human duodenal juice (pH 8.1), dissolution was significantly higher than when measured in buffer of comparable pH. In a human pharmacokinetic study, this MR formulation showed good bioavailability and no food effect on the pharmacokinetic profile. Therefore, pH profiles alone seem to have only a limited predictive power for the in vivo performance of this MR formulation for bromocriptine.

Bromocriptine↗
PubMed1993

Effect of adding the D1 agonist CY 208-243 to chronic bromocriptine treatment. I: Evaluation of motor parameters in relation to striatal catecholamine content and dopamine receptors.

A group of four cynomolgus monkeys previously rendered parkinsonian by the toxin 1-methyl-4-phenyl,1,2,3,6-tetrahydropyridine (MPTP) were observed in locomotion cages equipped with photocells during four periods of 7 days during which they received saline or two doses of the D1 agonist CY 208-243. The larger dose of 0.5 mg/kg produced a significant increase in locomotion in three of four animals. A second group of eight monkeys also previously rendered parkinsonian by MPTP and having received no other treatment were given a daily treatment of bromocriptine 1.66 mg/kg orally daily during 4 weeks. In four of the animals, after a week on bromocriptine alone, the D1 agonist CY 208-243 was added in increasing doses of 0.05, 0.1, and 0.5 mg/kg. The motor response as measured by locomotion, hand dexterity, and a disability score improved progressively at least in some of the animals on bromocriptine alone. The addition of CY 208-243 produced a more striking improvement of all three parameters, which appeared to be dose dependent. Biochemical analysis of the brain of these animals plus one control and one MPTP untreated monkey showed a > 90% loss of dopamine in the striatum in six of the eight treated monkeys. Both D2 and D1 dopamine receptors were increased in density by denervation, but both treatments abolished this increase for the D2 receptors while increasing the affinity of the D1 receptors.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1981

Circadian aspects of serum prolactin and TSH lowering by bromocriptine in patients with prostatic hypertrophy.

Bromocriptine mesylate lowers the serum concentration of prolactin and TSH in patients with prostatic hypertrophy as a function of drug administration time. The effect of a 2.5-mg dose in lowering these two hormones in presumably similar patients is statistically highly significant and relatively large at unusual test times (in the evening); at other, conventional test or administration times (early morning or midday), it is smaller, questionable, or not demonstrable with the dose and conditions used. Dosing without timing may lead to reduced effect or lack of effect, ambiguity and controversy, and lack of timing may account for the circumstance that an effect of bromocriptine upon TSH in human serum was not previously established. Rigorous assessment of the effect of bromocriptine mesylate upon circulating TSH and prolactin requires consideration of the entire spectrum of rhythms, ultradian and infradian as well as circannual. The circadian approach here analyzed represents a step toward that goal and indicates that the circadian frequency is a critical determinant of this response. Manipulation of TSH concentration in serum, in turn, is of interest in view of the demonstrated alteration of the circannual TSH rhythm in patients with prostatic cancer.

Aged↗
PubMed1995

Bromocriptine immunomodulation of experimental SLE and primary antiphospholipid syndrome via induction of nonspecific T suppressor cells.

Bromocriptine (BRC) is a dopamine agonist that suppresses the secretion of prolactin by the pituitary gland and is known to have immunomodulating properties. In the present study, we investigated the effect of BRC on the development of two autoimmune experimental models: (i) systemic lupus erythematosus (SLE), induced by injection of a human anti-dsDNA monoclonal antibody (MIV-7); (ii) primary anti-phospholipid syndrome (PAPS), induced by injection of a mouse anticardiolipin monoclonal antibody (CAM). BRC had a suppressive effect on in vivo autoantibody production, as well as on the appearance of other manifestations of the respective disease. The BRC activity seems to be nonspecific, since the same effect was demonstrated in mice with lupus and with PAPS. These data were supported by the in vitro nonspecific effect of CD8 cells induced in vivo by bromocriptine, on specific lymph node cell proliferation in the presence of the pathogenic monoclonal antibodies (MIV-7 or CAM, respectively), and on the response to an irrelevant autoantigen, myelin basic protein. These data were complemented by the nonspecific suppressive effect by the T-suppressor factor, produced by the CD8 cells, on specific thymidine uptake by lymph node cells from experimental SLE or PAPS in the presence of the immunizing mAb. Injection of CD8 cells from BRC-treated mice with SLE or PAPS abolished the disease development in the lupus and PAPS experimental models. The data suggest a possible novel role of bromocriptine in downregulating autoimmune phenomena through induction of natural nonspecific CD8+ suppressor cells.

Animals↗
PubMed1986

Bromocriptine induces marked locomotor stimulation in dopamine-depleted mice when D-1 dopamine receptors are stimulated with SKF38393.

In mice pretreated with reserpine plus alpha-methyl-p-tyrosine, neither the D-2 selective agonist bromocriptine, nor the D-1 selective agonist SKF38393, produced any measurable increase in locomotion in mice. However, the combination of the two agonists produced a marked and dose-dependent increase in co-ordinated locomotor activity. In mice with their dopamine stores and dopamine synthesis intact, SKF38393 was inactive by itself, but significantly enhanced the stimulant effect produced by bromocriptine. The data suggest that bromocriptine requires concomitant stimulation of D-1 receptors for the full expression of its behavioural stimulant effects.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1984

Primary tissue culture of human adrenocortical Conn's adenomata. Bromocriptine as a possible agonist-antagonist of angiotensin at the cellular level.

Angiotensin II-induced the hypertrophy of the cytoplasmic compartment and significantly increased (5-3H)uridine incorporation into RNA species by Conn's human adult adenomatous cells in primary tissue culture. On its own, bromocriptine, while enlarging only the nucleolar compartment, also intensely stimulated the incorporation of (5-3H)uridine into RNA species by the cultured adrenocortical adenomatous cells. However, an equimolar mixture of angiotensin II and bromocriptine was totally ineffective, eliciting no change in cellular morphometry or isotope incorporation with respect to the control specimens run in parallel. The present findings support the view that bromocriptine can influence the metabolism of Conn's cells directly at the cellular level by acting as an agonist-antagonist of angiotensin.

Adenoma↗
PubMed1976

Effect of prolactin and the anit-prolactin bromocriptin on the testosterone uptake and metabolism in androgen-sensitive and insensitive canine organs.

Prolactin promotes the growth and function of the prostate in low doses, whereas high doses or previous castration reduce this effect. The antiprolactin bromocriptin should reverse the prolactin action. In the castrated dog the highest accumulation of H3-testosterone given i.v. occurred in the prostate as compared with muscle, urethra, penis, liver and kidney. Prolactin pretreatment increased the radiosteroid uptake only in the liver. Converseley, bromocriptin suppressed the tracer incorporation into the liver, but increased prostatic accumulation. The highest testerone reduction occurred in the prostate of the untreated castrated dogs as compared with other organs. Prolactin suppressed 5 alpha -dihydrotestosterone formation but otherwise did not significantly influence testosterone turnover. Bromocriptin, however, stimulated dihydrotestosterone formation in the prostate and caused complete inhibition of hepatic testosterone reduction.

Animals↗
PubMed1981

Treatment of psoriasis with bromocriptin.

Sixty patients suffering from psoriasis of all clinical forms have been treated with an increased dosage of Bromocriptin. The age of the patients ranged from 20 to 72 years. Patients with contraindications for Bromocriptin were excluded from the test. In 80% a remission or reduction of psoriasis lesions was noticed. Side effects in the form of nausea, dizziness and vomiting occurred in 15%, but decreased in the course of Bromocriptin therapy.

Adult↗