Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bromocriptine 2-5 mg twice daily is effective in the treatment of both normoprolactinaemic and hyperprolactinaemic secondary amenorrhoea. This was demonstrated by the restoration of menstrual cycle and/or ovulation in 9 of 18 normoprolactinaemic and in 8 of 14 hyperprolactinaemic patients taking bromocriptine. Serum-prolactin level decreased in both groups of patients, and usually menstruation was recovered within 8 weeks'treatment. Galactorrhoea disappeared in 7 of 9 hyperprolactinaemic patients, and 2 became pregnant. After treatment had ceased spontaneous menstrual activity continued in 4 patients. 16 patients had side-effects the commonest being nausea and vertigo. These usually disappeared with the dosage was reduced, but 5 patients refused to continue. These results point to a new approach in the treatment of secondary amenorrhoea, even in those patients whose clinical findings give no indication of prolactin suppression.
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PMID:Bromocriptine treatment of secondary amenorrhoea. 5

Bromocriptine, a lysergic acid derivative with a bromine atom at position 2, has been found to have unique effects on the dopamine receptors in the pituitary and central nervous system and peripherally. It is rapidly and completely absorbed from the gut and is mainly excreted in the bile and faeces. It seems to have a particular specificity for the pituitary prolactinotrophe although it does have other effects in different diseases states. In spite of the fact that it is an ergot derivative, it is remarkably free of ergot vascular side effects in the doses needed for therapeutic benefit. The most common adverse effect are nausea, vomiting and postural symptoms. These can be overcome by starting at low doses and increasing the therapeutic levels. Its major use is in the suppression of prolactin in states where this hormone is elevated irrespective of cause. It has also been used in the treatment of acromegaly and is under investigation for use in other disease states probably linked with prolactin system or dopaminergic receptors.
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PMID:Pharmacology of bromocriptine in health and disease. 22 67

Thirty-one patients with Parkinson's disease were treated with the ergot alkaloid bromocriptine, a drug which stimulates dopamine receptors. Bromocriptine had a slight therapeutic effect in patients on no other treatment and an additional effect in patients on levodopa. The mean optimum dosage of bromocriptine, established over a 12 week period, was 26 mg daily. In 20 patients bromocriptine was compared with placebo in a double-blind controlled trial. Active treatment caused a significant (P less than 0.02) reduction in total disability and akinesia scores. The least disabled patients showed the greatest response. Side-effects of bromocriptine--nausea, vomiting, hallucinations, and abnormal involuntary movements--were similar to nature to those of levodopa. In most normal subjects, bromocriptine causes an increase in plasma growth hormone concentration. This was determined in 20 patients with Parkinson's disease after 1-15 mg bromocriptine. Only a single patient showed an obvious increase up to 120 minutes after dosage. Bromocriptine was not effective treatment in two patients who had not previously responded to levodopa and replacement of this drug by bromocriptine in patients with end-of-dose akinesia after chronic levodopa treatment did not totally abolish response swings.
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PMID:Bromocriptine treatment in Parkinson's disease. 77 75

Bromocriptine is currently and successfully used for the treatment of pituitary prolactinomas. However, bromocriptine appears unable to normalize plasma prolactin levels in about 10% and to reduce tumour size in one-third of cases. The lack of normalization of plasma prolactin levels in spite of a daily dose of bromocriptine equal to or higher than 15 mg suggests a bromocriptine resistance. We compared the long-term effects of bromocriptine and CV 205-502 (a non-ergot derivative D2 dopamine agonist) on plasma prolactin levels and tumour size in seven bromocriptine-resistant prolactinomas. Bromocriptine reduced significantly (P less than 0.001) plasma prolactin levels (from 2307 +/- 518 to 568 +/- 279 micrograms/l) (conversion to Sl units: 1 microgram/l = 20 mU/l). Visual field defects observed in five patients improved in four. However, CT scan analysis showed a decrease in tumour size in only three patients. Except for transient and minor side-effects at the beginning of the treatment, CV 205-502 was well tolerated in five of seven patients. In the remaining two patients nausea and vertigo occurred with high dosages of CV 205-502 and it was necessary to reduce the daily dose. CV 205-502 lowered plasma prolactin to levels similar to those obtained after bromocriptine therapy in four cases. In the three remaining patients, CV 205-502 was more potent than bromocriptine as demonstrated by the further 90% reduction in plasma levels obtained in one case and by the normalization of plasma prolactin levels in the two other cases. One woman became pregnant during CV 205-502 treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of the new dopaminergic agonist CV 205-502 on plasma prolactin levels and tumour size in bromocriptine-resistant prolactinomas. 167 68

The problems of long term treatment with antiparkinson drugs are numerous, involving increased involuntary movements, painful dystonic cramps, decrease or loss of therapeutic benefit, wearing-off, episodes of akinesia (on-off) and long periods of "freezing". Important side effects are also mental changes with heavy dreams, hallucinations, nocturnal confusional states and paranoid psychosis. As most of these side effects are dose-related, they are postponed and lessened by small daily doses of L-dopa and decarboxylase inhibitor. Frequent small doses may decrease the wearing-off effect but may cause unpredictable episodes of on-off. The addition of or partial replacement by bromocriptine may decrease fluctuations and dyskinesias in many patients. To reduce the side effects such as nausea, orthostatic hypotension and mental disturbances, daily doses of 15-30 mg should be built up very slowly. Painful dystonias are related to the off period and respond well to baclofen. For the treatment of severe psychic disturbances tranquilizers with little or no extrapyramidal side effects, such as clomethiazole, benzodiazepine derivatives and (if necessary) thioridazine, are recommended. Bromocriptine may also be useful in occasional cases which do not, or no longer, respond to L-dopa.
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PMID:[Parkinson therapy 1985]. 372 12

Bromocriptine (CB-154) and the 8-alpha-ergoline CU 32-085, two dopamine receptor agonists, were administered at different times to two series of 22 patients with Parkinson's disease, most of whom took levodopa (plus benserazide) at optimum dosage. The addition of bromocriptine (mean daily dose 32 mg; after 6 months 40 mg) led to a 38.5% reduction of levodopa, while CU 32-085 (mean daily dose 15.2 mg; after 6 months 17.5 mg) permitted a 33.7% reduction in levodopa. The mean dose in two patients on CU 32-085 monotherapy was 55 mg/day. A total of 15 patients tolerated adequate doses of bromocriptine (5-75 mg/day, mean duration of treatment 7.5 months) and 15 patients long-term treatment up to 14 months with CU 32-085 (dose range 1-60 mg/day; mean duration 8.8 months). Both groups showed a significant improvement of "total disability score' at 6 months by 56% and 67%, respectively, and after 6 months by 69% and 69.4%, respectively, with a significant decrease of all types of disability. All patients with fluctuations and "on-off' effects rapidly improved on both compounds. Bromocriptine and CU 32-085 were discontinued in seven patients each (32%) because of adverse effect including mental changes (for with bromocriptine, two with CU 32-085), nausea and vomiting (one and two, respectively), hypotension (one each) and increased tremor plus vomiting (one with CU 32-085). Although adverse effects were similar to those observed with levodopa, CU 32-085 in general showed less severe dyskinesia and mental changes but more frequent nausea than bromocriptine and levodopa. While the results of treatment with bromocriptine and CU 32-085 were comparable, the antitremor effect of the latter drug developed more rapidly, even at low dosage. Both compounds were useful in the management of patients with advanced Parkinson's disease, CU 32-085 having a stronger effect on tremor, bradykinesia, fluctuations and "on-off' effects than bromocriptine.
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PMID:Adjuvant treatment of Parkinson's disease with dopamine agonists: open trial with bromocriptine and CU 32-085. 618 Jan 42

Bromocriptine (0.5-6.0 mg/day) was administered to seven unmedicated chronic schizophrenic and two schizoaffective patients. Transient slight improvement was noted in four patients and marked improvement in one other. Clinical improvement was associated with nausea and drowsiness. These doses of bromocriptine stimulated serum growth hormone and inhibited serum prolactin levels in some subjects. These results suggest that bromocriptine may stimulate dopamine autoreceptors and, through this mechanism, attenuate symptoms in a small proportion of psychiatric patients.
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PMID:Effect of low-dose bromocriptine in treatment of psychosis: the dopamine autoreceptor-stimulation strategy. 641 30

Oral amantadine 100 mg and bromocriptine 2.5 + 2.5 mg, alone and in combination with ethanol (1 g/kg), were investigated in two placebo-controlled, double-blind and cross-over trials. In the first trial the psychomotor effects of amantadine and bromocriptine were compared to those of placebo, and in the second trial ethanol was added to the treatment. Bromocriptine lowered serum prolactin levels, thus confirming its absorption. Amantadine and bromocriptine alone had no psychomotor effects but unpleasant sensations, nausea and dizziness were reported after bromocriptine. Ethanol impaired performance in terms of impaired coordinative and reactive skills, lowered tapping speed, prolonged critical flicker interval and reduced gaze nystagmus angle (P less than 0.05 to 0.001; two-way ANOVA). Subjectively, ethanol induced mental slowness, clumsiness and impairment of performance (P less than 0.05 to 0.001). Amantadine and bromocriptine failed to counteract any of these ethanol-induced changes. It is concluded that in man, an acute dopaminergic activation by amantadine or bromocriptine does not significantly modify the psychomotor effects of ethanol.
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PMID:Failure of amantadine and bromocriptine to counteract alcoholic inebriation in man. 650 9

Experience with bromocriptine in 106 patients treated over nine years was reviewed. Most of the patients were already being treated with levodopa (combined with a peripheral decarboxylase inhibitor). These patients, after having initially achieved a good response to levodopa, were no longer responding satisfactorily. Most of the patients were also experiencing diurnal oscillations in performance: "wearing off" and "on-off" phenomena. In these patients previous attempts at changing the dose (increasing or decreasing) or changing the scheduling of levodopa had been unsuccessful. Bromocriptine was added to levodopa beginning at a dose of 5 mg/day, and each week was increased by another 5 mg/day. At a dose of bromocriptine of at least 25 mg/day, there was a decrease in disability in the majority of patients with a decrease in the severity of the diurnal oscillations in performance (especially "wearing off" phenomena). In most patients, the addition of bromocriptine resulted in an approximately 10% reduction in the dose of levodopa. The majority of patients sustained their improvement at least one year. In some patients improvement was sustained for up to five years. The therapeutic efficacy of bromocriptine was limited in many patients by the occurrence of adverse effects including mental changes, dyskinesias, orthostatic hypotension, and nausea. These adverse effects could often be minimized by reducing the dose of bromocriptine or levodopa. All adverse effects were reversible upon stopping the drug. We have found bromocriptine to be a valuable adjunct in the treatment of these patients.
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PMID:Should dopamine agonists be given early or late? A review of nine years experience with bromocriptine. 671 22

The diuretic therapy of patients with idiopathic edema is known to induce a secondary aldosteronism, which perpetuates edema formation and exacerbates the clinical symptoms. The observation of a decreased excretion of dopamine in these patients suggests that a treatment with the orally active dopamine agonist bromocriptine might be beneficial. Nine patients with typical symptoms of idiopathic edema, which had been present for several years, were treated with bromocriptine (Pravidel) 2 X 2.5 mg/die. The response to therapy was assessed clinically by the normalization of diurnal weight gain and general well-being. Seven patients showed a good response to bromocriptine, in one patient the response was only modest, and in one patient the medication had to be stopped because of nausea. Bromocriptine normalized diurnal weight gain without inducing weight loss. Both without therapy and during bromocriptine treatment electrolytes in serum, blood pressure, plasma renin activity and aldosterone are within the normal range. From the present pilot study it can be concluded that bromocriptine is an effective alternative to the traditional diuretic therapy in some patients with idiopathic edema. It remains unclear, whether the beneficial effect of bromocriptine reveals a dopamine deficiency, or whether bromocriptine is only a symptomatic treatment.
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PMID:[Bromocriptine in patients with idiopathic edema (author's transl)]. 732 84


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