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PubMed2001

Long-term mortality results of the randomized controlled study comparing bromocriptine to which levodopa was later added with levodopa alone in previously untreated patients with Parkinson's disease.

The present paper compares, in terms of mortality, two treatment regimens for Parkinson's disease (PD), i.e., bromocriptine later combined with levodopa versus levodopa only. Between 1982 and 1989, 60 PD patients (29 treated with levodopa alone [group D] and 31 receiving first bromocriptine followed by an association of bromocriptine + levodopa [group B/D]) were recruited. Data were updated in January 2000. Survival functions were estimated using Kaplan Meier product-limit method and comparison between the two groups with the log-rank test. Mortality was also compared with that of the general French population using standardized mortality ratios (SMRs). The mean duration of follow-up was 10.3 +/- 3.0 years. Seventeen patients died during the follow-up: nine in the group B/D and eight in the group D. The probability of survival at 10 years was 79.0% [95% confidence interval [CI]: 71.4-86.6] in group B/D and 72.9% [95% CI: 63.3-82.6] in group D. In comparison with the general French population, SMRs were not statistically different from 1, in the whole sample of PD patients (1.21, 95 % CI [0.71-1.95]), in group D (0.98 [0.42-1.93]), or in group B/D (1.53 [0.70-2.92]). In this population, we were unable to find any favourable effect of an early use of bromocriptine on mortality in PD in comparison with levodopa alone.

Aged↗
PubMed1995

A "combined" levodopa test as a useful method for evaluating the efficacy of dopamine agonists: application to pergolide and bromocriptine.

The efficacy of pergolide as adjunct to levodopa therapy was compared to that of bromocriptine in 12 parkinsonian patients with fluctuating motor disability and levodopa-induced dyskinesias (mean age of onset, 50.6 +/- 8 years; Hoehn and Yahr stage between II and IV; mean basal UPDRS motor score, 30.6 +/- 8.6), in a double-blind crossover study. After an 8-day habituation to each agonist, an acute challenge of a supraliminal dose of levodopa ("levodopa test") was performed in association with either 1 mg pergolide or 10 mg bromocriptine. The delay to onset and the duration of therapeutic benefit, the percentage improvement in motor disability, and the severity of onset and peak-dose dyskinesias were evaluated. Both agonists significantly increased the duration of therapeutic benefit, but pergolide more so than bromocriptine (p = 0.02). Pergolide also tended to reduce the severity of dyskinesias and was globally perceived by the patients to be more efficacious than bromocriptine on parkinsonian symptoms and fluctuations. This study illustrated the usefulness of the "levodopa test" in evaluating, objectively, the effects of dopamine agonists.

Aged↗
PubMed1999

Effect of repeated L-DOPA, bromocriptine, or lisuride administration on preproenkephalin-A and preproenkephalin-B mRNA levels in the striatum of the 6-hydroxydopamine-lesioned rat.

Abnormal involuntary movements, or dyskinesias, plague current symptomatic approaches to the treatment of Parkinson's disease. The neural mechanisms underlying the generation of dyskinesia following repeated l-3,4-dihydroxyphenylalanine (L-DOPA) or dopamine agonist administration in Parkinson's disease remain unknown. However, de novo administration of bromocriptine or lisuride to either l-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned primates or patients can alleviate parkinsonian symptoms without the development of dyskinesia. In this study, we have investigated behavioral responses and alterations in the expression of opioid neuropeptide precursors preproenkephalin-A (PPE-A, encoding methionine- and leucine-enkephalin) and preproenkephalin-B (PPE-B), the precursor encoding dynorphins (dynorphin A1-17 and B1-13, leucine-enkephalin, and alpha-neoendorphin) in striatal output pathways of the 6-hydroxydopamine (6-OHDA)-lesioned rat model of Parkinson's disease. Expression was assessed following repeated L-DOPA, bromocriptine, or lisuride administration. Given the functional organization of basal ganglia circuitry into anatomically discrete parallel circuits, we investigated alterations in peptide expression with reference to the detailed topography of the striatum. Following repeated L-DOPA administration (6.5 mg/kg, b.d., 21 days) in the 6-OHDA-lesioned rat a rotational response was observed. This became markedly enhanced with repeated treatment. We have previously characterized the pharmacology of this enhanced response and have suggested that it is a useful model for the elucidation of the cellular and molecular mechanisms underlying L-DOPA- and dopamine agonist-induced dyskinesia. In contrast to l-DOPA, de novo administration of bromocriptine (1 or 5 mg/kg, b.d., 21 days) or lisuride (0.01 or 0.1 mg/kg, b.d., 21 days) did not lead to an enhanced behavioral response. In vehicle-treated, 6-OHDA-lesioned animals, PPE-A expression was elevated rostrally and dorsally, while PPE-B expression was reduced in the striatum at all rostrocaudal levels. Repeated l-DOPA administration was accompanied by elevations in striatal PPE-B mRNA levels and a further elevation, above lesion-induced levels, in PPE-A expression. This further elevation was restricted to the dorsolateral striatum. However, following repeated bromocriptine or lisuride administration no increase in PPE-B expression was observed and the lesion-induced increase in PPE-A expression was normalized to prelesion levels. Increased PPE-A and PPE-B levels may, through decreasing GABA and glutamate release, respectively, in output nuclei of the basal ganglia, play a role in the development of L-DOPA- and dopamine-agonist induced dyskinesia in Parkinson's disease. These studies suggest that anti-parkinsonian treatments which are not associated with an elevation in PPE-B and/or normalize elevated PPE-A precursor expression, such as NMDA-receptor antagonists or long-acting dopamine D2 receptor agonists, e.g., cabergoline or ropinirole, may reduce dyskinesia in Parkinson's disease.

Animals↗
PubMed1999

Bromocriptine protects dopaminergic neurons from levodopa-induced toxicity by stimulating D(2)receptors.

Neuroprotective properties of bromocriptine, a D(2) receptor agonist, were investigated using the in vitro neurotoxicity of levodopa for dopaminergic neurons from rat embryonic ventral mesencephalon. Levodopa, when added to the culture medium, showed toxicity which was specific for dopaminergic neurons. Bromocriptine was found to protect dopaminergic neurons from levodopa toxicity. Another D(2) agonist, 2-(N-phenethyl-N-propyl-amino-5-hydroxytetralin, showed similar protective effects. The neuroprotective effect of bromocriptine was inhibited by supplementation of the culture medium with sulpiride, a D(2) antagonist, or by D(2) receptor knockdown with an antisense oligonucleotide. Dopaminergic neurons treated with levodopa showed an increase in free radicals. These data suggest that neuroprotective properties of bromocriptine seen in this cellular model of neurotoxicity are dependent on dopamine D(2) autoreceptor binding and that levodopa toxicity may be related to increased free radical generation in dopaminergic neurons.

1-Methyl-4-phenylpyridinium↗
PubMed1982

Long-term experience with bromocriptine in advanced parkinsonism. Results after one year's treatment.

The long-term effects of bromocriptine as an adjuvant were investigated in 32 patients (20 male, 12 female), aged 43-76 years (mean 65.4), suffering from parkinsonism for 3-20 years (mean 9.3). Patients were pretreated with levodopa/decarboxylase inhibitor for 24-116 months (mean 74.9). Bromocriptine was given because of a decline in the response to levodopa, various kinds of "on-off" phenomena, and disabling dyskinesias. Levodopa was reduced by 18%, while bromocriptine was added with a mean dose of 29 mg. The results showed a marked tremor and rigidity response, clearly greater than that of bradykinesia of the hands. The improvement after 4 weeks of bromocriptine treatment was maintained over 12 months. Only gait disturbances tended to increase. At the same time the self-ratings of the patients showed an increase in disability as far as daily activities were concerned. Likewise, the "on-off" symptoms with regard to the wearing-off effects worsened in comparison with the condition during the 4-week period. Akinesia paradoxica was never definitely influenced. An increase in dyskinesias was avoided and serious side-effects could be kept under control.

Adult↗
PubMed1983

CT follow-up of microprolactinomas during bromocriptine-induced pregnancy.

In the last few years complete or partial regression of prolactinomas has been demonstrated in nonpregnant women treated by bromocriptine. Thus bromocriptine therapy appears as an attractive alternative to surgery for management of infertility related to hyperprolactinemia. However, numerous reports emphasized the possibility of an excessive growth of the pituitary adenoma with visual field defects during the last 3 months of pregnancy. To avoid these complications, the authors followed with serial CT scans the growth of microprolactinoma at the 5th or 6th month of pregnancy. Among six pregnant women, one patient presented a marked upward extension of the adenoma. Bromocriptine was then reintroduced and the effectiveness in reducing tumor growth was proved by CT scan at the 7th month. Regarding low risk of using intravenous iodinated contrast medium in pregnant women and of fetal radiation damage, the authors emphasize the value of CT in the follow-up of bromocriptine-induced pregnancies.

Adult↗
PubMed1977

Evidence for selective and long-lasting stimulation of "regulatory" dopamine-receptors by bromocriptine (CB 154).

Bromocriptine, an ergot-derivate with DA-receptor stimulating properties in vivo, produces long-lasting hypomotility in mice not accustomed to the motility cage and decreases brain DOPAC and HVA without affecting brain DA. These effects are obtained with doses 25 times lower than those which produce hypermotility. The decrease of brain DOPAC is correlated to the hypomotility both on a dose- and on a time-basis. Potent neuroleptics as pimozide, benzperidol and droperidol, which are considered to be fairly specific DA-receptor blockers, antagonize the hypomotility and the decrease of brain DOPAC produced by bromocriptine. These effects are obtained with very low doses (0.05--0.3 mg/kg) of neuroleptics which per se do not affect motility or brain DOPAC. The maximal decrease of brain DOPAC and HVA produced by bromocriptine is similar to that produced by apomorphine and the combination of these drugs does not result in a further decrease of brain DOPAC or HVA. On the basis of these results it is postulated that bromocriptine decreases brain DA-turnover and produces hypomotility by acting on "regulatory" DA-receptors different from the post-synaptic ones of the "terminal" dopaminergic areas.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1977

[Changes in carbohydrate tolerance in the puerperium by inhibition of lactation with bromocriptine and quinestrol (author's transl)].

In the present study the influence of bromocriptine on carbohydrate tolerance was examined and its effects compared with those of an estrogenic compound (Quinestrol). Sixteen patients were studied in each group. The controls consisted of 16 women who breastfed their children. No significant difference was found in the oGTT in patients who had Quinestrol compared with the controls. However blood sugar values in women receiving bromocriptine were significantly lowered when compared with values of individuals who had Quinestrol. The reduction of blood sugar values depends on the dosage of bromocriptine. Inhibition of lactation with bromocriptine may lead to false negative results in patients who are at risk to have a prediabetic condition.

Blood Glucose↗
PubMed1996

Early institution of bromocriptine in Parkinson's disease inhibits the emergence of levodopa-associated motor side effects. Long-term results of the PRADO study.

Long-term levodopa treatment in Parkinson's disease is typically associated with "motor side effects" consisting in dyskinesias and/or fluctuations in motility referred to as the on-off phenomena. The main objective of this prospective, randomized, multi-centre study was to determine to what extent the development of such complications could be prevented by partial substitution of levodopa monotherapy (L-DOPA/benserazide) by bromocriptine in patients with early symptoms of the disease. The basic trial population included 674 newly diagnosed Parkinsonian patients that were randomly allocated to monotherapy with levodopa or a combination therapy based upon a nearly 40% replacement of levodopa by bromocriptine. The two target regimens had to be consistently maintained for 42 months. Parkinsonian symptoms were assessed by means of the Webster rating scale, the Hoehn and Yahr scale, and the Zung Self-Rating Depression scale. Motor side effects and adverse events were recorded at each regular clinic visit. Neurological symptoms improved and stabilized in a similar manner during treatment with both regimens throughout the study period. Motor side effects were observed in more patients on levodopa alone than on combination therapy (28.8 vs 20%; p = 0.008). According to Kaplan-Meier estimates the cumulative probability of experiencing motor side effects was 0.43 on monotherapy, compared to 0.28 on combination therapy, which was equal to a one third reduction of risk (p = 0.025). In regard to motor side effects, the degree of substitution of levodopa proved relevant: patients with > 50% substitution by bromocriptine exhibited half the risk observed in those with < 30% (p = 0.045). The overall burden of motor side effects, as reflected by a sum score based upon the relevance, the severity and the extent of motor dysfunction, was also significantly less on combination therapy (p = 0.046). In conclusion, partial substitution of levodopa by bromocriptine (> 30%) as first-line treatment of Parkinson's disease proves active in the prophylaxis of levodopa associated motor side effects. Early combination therapy therefore extends the period of optimal disease control.

Aged↗
PubMed1987

Bromocriptine in pregnancy: safety aspects.

Since Bromocriptine is used to restore fertility in hyperprolactinemic women, its safety in pregnancy and the offspring was investigated in a stepwise approach: (i) the first survey in pregnancy was based on spontaneous reporting, (ii) the second investigation was conducted at 33 clinics as an intensive monitoring project and, (iii) the third study consisted in a full examination of children up to the age of 9 years who had been exposed to Bromocriptine in utero. The data collated in this program includes information on 2587 pregnancies in 2437 women treated with Bromocriptine during some stage of gestation, and follow-up examinations for 988 infants. The results show that the use of Bromocriptine in the treatment of infertility in women is not associated with an increased risk of spontaneous abortion, multiple pregnancy or the occurrence of congenital malformation in their progeny. Moreover, exposure to this drug in utero has no adverse influence on the postnatal development.

Abnormalities, Drug-Induced↗
PubMed1992

Timed bromocriptine administration reduces body fat stores in obese subjects and hyperglycemia in type II diabetics.

Obese postmenopausal female volunteers were given timed daily oral dosages of bromocriptine, and tested for reduction of body fat stores. This dopamine agonist has been shown to reset circadian rhythms that are altered in obese animals and to reduce body fat levels in several animal models. The participants were instructed not to alter their existing exercise and eating behavior during treatment. Skinfold measurements were taken on 33 subjects as indices of body fat. The measurements (e.g., suprailiac) were reduced after six weeks by about 25%, which represents a reduction of 11.7% of the total body fat. These dramatic decreases in body fat, which are equivalent to that produced by severe caloric restriction, were accompanied by more modest reductions of body weight (2.5%), indicating a possible conservation of protein that is usually lost as a consequence of such caloric restriction. The effects of bromocriptine treatment on body fat and hyperglycemia were also examined in non-insulin dependent diabetics being treated with oral hypoglycemics (7 subjects) or insulin (7 subjects). Total body fat was reduced by 10.7% and 5.1% in diabetics on oral hypoglycemics and insulin, respectively, without any significant reductions in body weight. Hyperglycemia was reduced in most of the 15 diabetic subjects treated leading to euglycemia and even cessation of hypoglycemic drugs in 3 of the 7 subjects during 4-8 weeks of bromocriptine treatment. These findings support the hypothesis that obesity and type II diabetes may be treated effectively with bromocriptine when administered at the proper times and dosages.

Body Composition↗
PubMed1992

Bromocriptine lessens the incidence of mortality in L-dopa-treated parkinsonian patients: prado-study discontinued.

L-Dopa supplemented by a peripheral decarboxylase inhibitor is considered the most potent therapeutic regimen prolonging active life in Parkinsonian patients. The long-term benefit of therapy is limited by adverse effects, such as dyskinesia and on-off phenomena, which can be mitigated by the concomitant administration of dopamine agonists, such as bromocriptine. In order to quantify the beneficial impact of early combination therapy, a controlled clinical trial (PRADO: PRA videl1 + DO pa) in patients with early Parkinson's disease was carried out, whereby L-Dopa monotherapy (in a fixed combination with benserazide (DoBe) was being compared with the same combination plus bromocriptine (DoBeBro). Patients were recruited and treated by 101 practising neurologists in the Federal Republic of Germany and in Hungary. Twenty seven clinical university centers cross-checked the patients at regular intervals. The trial started with 3 months of DoBe monotherapy (median dose of 375 mg L-Dopa for both randomized groups) followed by gradual substitution of DoBe by bromocriptine over 3 months in one of the groups (250 mg L-Dopa/10 mg bromocriptine). The target medication was maintained from study months 6 to 54. Parkinsonian symptoms were classified according to the Webster rating scale, the Hoehn and Yahr scale and the Zung Self-Rating Depression Scale. Adverse events and life status were checked at regular intervals. Special emphasis was given to motor performance tests. 587 patients (302 in the DoBe group and 285 in the DoBeBro group) were available for intention-to-treat analysis. Both groups were homogeneous at baseline in all observed parameters.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Bromocriptine enhancement of responding for conditioned reward depends on intact D1 receptor function.

It has been suggested that reward-related learning may require intact functioning at the dopamine D1 receptor. The present experiment tested this hypothesis by challenging the reward-enhancing effects of the D2 agonist, bromocriptine, with a D1 antagonist, SCH 23390. For comparison, the effects of the D2 antagonist, pimozide, were also evaluated. Male rats (n = 240) were pre-exposed to a chamber with two levers, one producing a 3-s lights-off stimulus and the other a 3-s tone stimulus. Four conditioning sessions followed, during which levers were absent and presentations of the lights-off stimulus were paired with food. Testing consisted of comparing presses on each lever after conditioning to before conditioning for each rat. Control groups showed a significantly greater increase in responding for lights-off than tone, indicating that the lights-off stimulus had become a conditioned reward. Results showed that bromocriptine (0.25-10.0 mg/kg, IP, 60 min before test session) enhanced responding at doses of 2.5 and 5.0 mg/kg significantly more on the conditioned reward lever than on the other lever. The lowest dose of SCH 23390 (1.0 microgram/kg, SC, 2 h before testing) eliminated the bromocriptine-produced enhancement at 2.5 mg/kg and a significant enhancement was seen at 10.0 mg/kg. The higher doses of SCH 23390 (5.0 and 10.0 micrograms/kg) eliminated the bromocriptine effect and the conditioned reward effect itself, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

Usefulness of thyrotropin-releasing hormone test, SMS 201-995, and bromocriptine in the diagnosis and treatment of gonadotropin-secreting pituitary adenomas.

Five patients with gonadotropin-secreting pituitary adenomas were studied. The utility of gonadotropin response to TRH stimulation in the diagnosis and follow-up of these tumors was evaluated, as well as the effects of somatostatin analogue SMS 201-995 and bromocriptine on gonadotropin release. Three patients had FSH and LH secreting adenomas while the other two tumors secreted FSH and alpha-subunit. Transsphenoidal resection of the pituitary adenomas were performed in all patients. Following preoperative TRH administration (400 micrograms i.v.), marked increases were observed in FSH levels in two cases, in LH levels in three and in alpha-subunit in one. The FSH and LH responses to t.his stimulus persisted in the same patients after surgery. Following acute bromocriptine administration (5 mg orally), FSH was reduced in all cases by 19% to 46%, LH in three cases by 50-67% and alpha-subunit in one by 33%. In patient no. 5, with persistent high FSH levels in the immediate postoperative period, long-term bromocriptine treatment was administered (15 mg/d orally), resulting in normalization of FSH levels 6 months later, although the size of the tumor was not reduced. After acute SMS 201-995 administration (100 micrograms sc) FSH decreased in two cases by 38% and 76%, LH in three by 30-56% and alpha-subunit in one by 20%. We conclude that gonadotropin response to TRH stimulation is useful in the diagnosis and follow-up of patients with gonadotroph adenoma. Bromocriptine and SMS 201-995 may be effective as coadjuvant treatment following surgery and radiotherapy in these patients, although long-term studies will be necessary to confirm these proposals.

Adenoma↗
PubMed1987

Long-acting bromocriptine for the acute treatment of large macroprolactinomas.

Six patients with hyperprolactinemia, visual impairment and large macroprolactinoma were treated with a long-acting bromocriptine, in dosage of 50 mg as a single im injection. All patients underwent a full assessment of pituitary prolactin (PRL) secretion before treatment and the studies were repeated about every week during 40 days. Following bromocriptine injection a rapid amelioration of the clinical and visual defects occurred in all patients. Likewise, a significant reduction of the hyperprolactinemia was documented in all six patients and in three of them serum PRL levels reached values as low as 20 ng/ml, and a tumor size reduction was demonstrated by cranial computerized tomography in three of the six cases. No side effects were associated with the administration of bromocriptine. From this study we conclude that the long-acting bromocriptine represents an additional option for the initial management of large prolactinomas in particular when they are associated with severe visual impairment.

Bromocriptine↗
PubMedDate not supplied

Effects of bromocriptine on CSF proteins and amines in patients with empty sella syndrome, acromegaly and prolactin producing pituitary adenomas.

The effect of the dopamine agonist bromocriptine (5-40 mg/day) on cerebrospinal fluid proteins and amines was studied in 7 hyperprolactinemic patients, 4 with empty sella syndrome and 3 patients with pituitary adenoma. Small as well as high doses of bromocriptine depressed the endogenously formed dopamine, noradrenalin and adrenalin. Five patients initially exhibited changes consistent with slight to marked blood-cerebrospinal-fluid (CSF) barrier disturbances and 5 abnormal CSF-protein fractions. One CSF-protein fraction (isolelectric points (pI) approximately 5.3 pH-units) became more prominent during bromocriptine treatment. Analyses of his fraction indicated that it represented a transferrin component. It is stated that bromocriptine treatment besides affecting amine and trace metal metabolism also affects protein metabolism.

Acromegaly↗
PubMed1983

Reenlargement of macroprolactinomas during bromocriptine treatment: report of two cases.

We report two cases with macroprolactinoma who during medical treatment with bromocriptine showed a normalization of PRL levels and a reduction of tumor size as documented by computed tomography. After a few months of therapy both patients suddenly complained of worsening of their visual fields and a computed tomography demonstrated a reenlargement of the tumor mass; whereas in one patient PRL levels remained always within normal range, in the other patient, who was taking spiramycin for an intercurrent illness, there was also an escape of the hormonal secretion from the inhibitory effect of bromocriptine. The first patient underwent surgery, whereas in the second patient continuation of bromocriptine and interruption of antibiotic treatment resulted in progressive improvement in visual fields and a reduction of tumor size again. We want to stress that in patients with macroprolactinomas responsive to the medical treatment both in terms of PRL secretion and of tumor size reduction, an escape from the effects of bromocriptine, although infrequently, may occur.

Adult↗
PubMed2001

The role of hypertension in bromocriptine-related puerperal intracranial hemorrhage.

The spate of medicolegal inquiries following the disqualification of Parlodel (bromocriptine mesylate) by the Food and Drug Administration for postpartum ablactation, uncovered previously unreported side effects associated with its postpartum administration. In 1994, bromocriptine mesylate was withdrawn from the market as a milk suppressant. Since this time, over a dozen cases of postpartum intracranial hemorrhages associated with its use have been reported. We describe three additional cases of postpartum intracranial hemorrhage related to bromocriptine usage. One patient, previously normotensive, developed hypertension and a headache; initial CT was normal, but CT 24 h later demonstrated intracranial hemorrhage. This suggests that the blood-pressure elevation was drug-induced and was the cause, rather than the consequence, of bromocriptine-related intracranial hemorrhage.

Adult↗