Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gas chromatographic, mass fragmentographic and liquid chromatographic techniques for the determinations of bromocriptine (2-bromo-alpha-ergocriptine; Parlodel) in human plasma are described. These methods were found to be suitable for determining concentrations of bromocriptine down to 0.5, 1.0 and 10.0 microgram/l, respectively. Accuracy, specificity and analytical capacity were satisfactory for all three methods. Gas chromatography was compared with liquid chromatography, and the two methods were demonstrated to give identical results in patients treated with bromocriptine for Parkinson's disease. Gas chromatography was also compared with mass fragmentography, and the results from these two assays were also in agreement.
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PMID:Determination of bromocriptine in plasma: comparison of gas chromatography, mass fragmentography and liquid chromatography. 54 93

The activity of DBH enzyme was measured in plasma of 7 non treated patients suffering from Parkinson's disease; a 10 mg dose of Bromocryptine was administered per os to these patients. Attained results were compared to the enzyme activity in a group of control of 7 healthy individuals. It was pointed out that in patients suffering from Parkinson's disease the decrease of DBH level in plasma after the administration of Bromocryptine was of 32.6% +/- SE 4.4% while in the group of control the decrease was only of 15% +/- SE 4.9%. This decrease in the plasmatic level of the enzyme after the administration of Bromocryptine should be due to the marked antagonistic activity of Bromocryptine on pre-synaptic dopaminergic receptors. This should mean that peripheric pre-synaptic dopaminergic receptors are involved in the physiopathology of Parkinson's disease.
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PMID:[Effect of bromocriptine on secretion of the enzyme dopamine-B-hydroxylase (DBH) in patients with Parkinson's disease]. 55 Feb 90

In this study, we compared in an intent-to-treat analysis the tolerance and efficacy of Parlodel SRO with its standard galenic formulation in 34 patients with Parkinson's disease who received optimal levodopa therapy. The results suggest that Parlodel SRO was equally efficacious as Parlodel standard, but Parlodel SRO is better tolerated.
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PMID:Parlodel SRO in Parkinson's disease: a double-blind randomized comparison of Parlodel standard and Parlodel SRO. 149 Apr 97

Patients with moderately severe Parkinson's disease complicated by the adverse effects of chronic levodopa use benefited from the addition of bromocriptine (Parlodel; Sandoz) in doses up to 26 mg daily, which allowed an approximate 30% reduction of levodopa dose. This resulted in a significant decrease in the amount of levodopa side-effects while maintaining or improving the original parkinsonian clinical stage. Increased effectiveness in these patients was not associated with increased dosage beyond 25-30 mg daily. When the doses of bromocriptine were increased slowly, the adverse reactions were minor and usually transient.
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PMID:Adjunctive therapy with bromocriptine in Parkinson's disease. 225 16

This paper presents a review of the literature on the therapeutic action and the side effects of the two main dopaminergic agents: L-DOPA/decarboxylase inhibitor (L-DOPA/DI) and bromocriptine (Parlodel used either as monotherapy or in combination in patients with Parkinson's disease. The combination of L-DOPA/DI and bromocriptine gives the best therapeutic efficacy (49% improvement) in the total score (bradykinesia, rigidity and tremor). However, treatment by monotherapy or combination gives the same pattern of activity: greatest improvement in tremor, followed by rigidity and bradykinesia. Improvement observed in the short term is not sustained over longer periods of time for monotherapy with either drug. The short-term side effects are similar for each treatment, whereas long-term complications (dyskinesia, end-of-dose deterioration and on-off phenomenon) appear only when levodopa is used, alone (high incidence) or in combination with bromocriptine (low incidence). The overall optimum treatment is obtained with a combination of L-DOPA/DI and bromocriptine.
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PMID:Optimum symptomatic control of Parkinson's disease with dopaminergic therapy. 367 21

We present an interim report of an ongoing, single-blind study of the effectiveness and safety of bromocriptine mesylate (Parlodel) in 15 patients, 14 of whom had severe idiopathic Parkinson's disease (Stages 4 and 5 on the Hoehn and Yahr Scale). The patients had never received levodopa, amantadine, or bromocriptine. Gradually increasing doses of bromocriptine were assessed: Initial daily dosage was 1.25 mg, with weekly increments of 1.25 mg/day until either the clinical response was satisfactory or a maximum of 15 mg/day was reached. The patients were on no other antiparkinsonian agents, except trihexyphenidyl HCl (Artane). Response to treatment was scored on the Columbia Scale. The patients discussed in this report had been in the study for varying times, ranging from 1 month to 3 years. Only one patient who entered this study dropped out because his response to bromocriptine was unsatisfactory; he had taken the drug for 2 weeks. No serious adverse reactions were noted with the gradually increasing dosage regimen. Response on the whole was very satisfactory; patients improved by at least two stages on the Hoehn and Yahr Scale. Improvement began within 48 h of onset of treatment with 1.25 mg daily. The preliminary results of this study indicate that low-dose bromocriptine as a first-line drug in severe Parkinson's disease is definitely warranted.
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PMID:Low-dose bromocriptine therapy in severe Parkinson's disease. 638 52

A double-blind, multicenter trial compared bromocriptine (Parlodel) with amitriptyline in 83 endogenously depressed patients. The patient sample consisted mainly of agitated endogenous depression, and most of the patients were treated within a daily dose range of 30--50 mg bromocriptine or 120--200 mg amitriptyline. In both the global assessment and the Hamilton Depression Rating Scale, amitriptyline scored higher than bromocriptine, but the differences were not statistically significant. There was little difference between the drugs with respect to tolerability. Bromocriptine's potential role in psychiatry will probably be in those patients in whom an alternative treatment to standard antidepressant therapy is required and a less sedative effect with minimal anticholinergic response is indicated. Bromocriptine's use in Parkinson's disease, where the incidence of depression has been reported to be as high as 37%, has been well documented. Bromocriptine's antidepressant properties add to its therapeutic value in this disease.
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PMID:A comparative, multicenter trial between bromocriptine and amitriptyline in the treatment of endogenous depression. 675 39

Forty patients with severe Parkinson's disease (23 men, 17 women) who had been treated for six years with L-dopa-decarboxylase inhibitor, were part of a placebo-controlled double-blind trial to test the effectiveness of bromocriptin. In all patients the effectiveness of L-dopa had been decreasing, 34 patients had L-dopa-induced dyskinesias, 35 "on-off" symptoms. Bromocriptin dosage was gradually increased to a total dose of 30 - 40 mg daily. This led to a 25% reduction in L-dopa requirements. The symptoms of Parkinson's disease were favourably influenced, with rigor, tremor and also walking disturbances responding better than bradykinesia of the hands. At the same time, there was a marked prolongation of the periods of good mobility ("on" time) from 7 to 10.8 hours without influence on other "on-off" symptoms such as paradoxical akinesia. Two patients had to be excluded from the trial because the treatment caused side effects (orthostatic hypotension, exogenous psychotic symptoms). Other side effects, such as nausea and mild forms of collapse, could be controlled by drugs.
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PMID:[Bromocriptin in the treatment of progressive stages of Parkinson's disease (author's transl)]. 679 66

In order to compare two titrations of Parlodel in early combination with levodopa in the treatment of Parkinson's disease a multicentre randomized open study was performed with a fast titration in group A (15 mg/day for 3 weeks) and slow in group B (15 mg/day for 5 weeks). 153 patients were included: 77 in group A and 76 in group B. The recommended titration was observed in 76% in group A and 88% in group B, the difference was not significant. The efficacy assessed by the Webster Scale was remarkable and similar in the two groups. This study confirms the additive benefit of bromocriptine on the symptoms and long term complications of levodopa therapy, but no absolute conclusion can be drawn regarding the best titration.
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PMID:[Parlodel in early combination with levodopa in the treatment of Parkinson disease. Comparison of 2 dosage forms]. 790 47

Advances in our understanding of the cause and pathogenesis of Parkinson's disease (PD) have permitted the rational selection of putative neuroprotective agents for study in PD. However, the list of agents that might provide neuroprotective effects derived from laboratory studies is daunting, and we face the challenge of determining which agents to bring to the clinic and how to find the resources (patients and funds) to properly study so many promising therapeutic opportunities.1 Appropriate outcome variables that are not confounded by any symptomatic effect of the drug and are acceptable to clinicians and regulatory authorities also remain to be defined. The first clinical trials designed to test the capacity of putative neuroprotective agents to alter the natural history of PD have now been performed and illustrate some of these problems. The DATATOP (Deprenyl and Tocopherol Antioxidant Therapy of PD) study used the time to reach a disease milestone in untreated PD patients (ie, need for levodopa) as the primary end point. However, interpretation of results was confounded by the drug's symptomatic effect. The SINDEPAR (Sinemet-Deprenyl-Parlodel) study used the change in motor score between initial visit and final visit after washout of all study medications as the primary end point. However, here too there were concerns about confounding symptomatic effects, because antiparkinsonian medications have now been shown to have a long duration response that can persist for weeks and perhaps even months after withdrawal. More recent studies have used surrogate markers of the integrity of nigrostriatal function such as striatal uptake of fluorodopa on positron emission tomography (PET) or beta-CIT-on single-photon emission computerized tomography (SPECT) as primary outcome measures. However, it has not yet been confirmed that striatal uptake of these isotopes does in fact correlate with the remaining number of dopamine neurons or terminals, and the possibility of a confounding pharmacological effect has not yet been completely excluded. To date, no drug has been established to have a neuroprotective effect in PD, and none has been approved for a neuroprotective indication. Furthermore, regulatory agencies have not yet agreed that any of the outcome measures currently used will be acceptable for approval of a new drug. Resolution of these issues is of critical importance to convince pharmaceutical companies to expend the hundreds of millions of dollars necessary to bring a new drug to market. Drugs that already have been approved in PD for their symptomatic effects, such as dopamine agonists or propargylamines (eg, selegiline), offer the best opportunity for establishing that a drug is neuroprotective in PD in the immediate future, but herein also lies the difficulty of establishing that any benefits observed are not solely because of the drug's symptomatic properties. Currently, this will most likely entail demonstrating that the drug provides benefit for PD patients for both imaging and clinical markers of disease progression.
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PMID:Neuroprotection in Parkinson's disease: clinical trials. 1266 1


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