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)

Pergolide is thought to stimulate both D1 and D2 dopaminergic receptors. Its effects on Parkinson's disease were evaluated in an open trial, using clinical assessment scales and objective tests. Nine patients had previously been treated with L-dopa, but the drug had either gradually lost its effectiveness or produced invalidating side-effects. Pergolide in doses of 2 mg per day considerably and durably improved the parkinsonian symptoms and enabled the patients to reduce L-dopa dosage by about 50%. Dyskinesia and "on-off" phenomena partially regressed. Significant improvement was also observed in 3 of 4 patients with Parkinson's disease who had not previously received L-dopa. The side-effects of pergolide were fairly frequent in both groups, but they were relatively mild and reversible.
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PMID:[Clinical study of pergolide in Parkinson's disease]. 316 Oct 45

Since the initiation of bromocriptine therapy for Parkinson's disease several newer dopamine agonists have been developed. Pergolide has reached the stage of Phase 3 clinical trials and will probably be available for general use sometime in the foreseeable future. Lisuride shows most promise in its parenteral form for infusion therapy of patients with severe fluctuations. Mesulergine, another ergot-derivative and ciladopa, a new non-ergot agonist, have been withdrawn from further clinical use due to tumorogenesis in rats. It is questionable how applicable these findings are to the use of the drugs in elderly humans with parkinsonism. Recently a small number of drugs have been found to have postsynaptic dopamine agonist properties only in the setting of denervated supersensitive dopamine receptors. These agents may be particularly effective in the early treatment of patients with Parkinson's disease. This paper will review a number of the dopamine agonists which have been developed since the introduction of bromocriptine therapy. Several of these have shown beneficial effects in early clinical trials while others show promise in preclinical studies of animal models of parkinsonism.
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PMID:Update on dopamine agonists in Parkinson's disease: "beyond bromocriptine". 331 48

Possible pergolide-induced cardiotoxicity has been reported in open trials. Over a 6-month period of observation, we prospectively analyzed ECGs and 24-hour ambulatory ECG in 23 patients with Parkinson's disease who were randomized in a double-blind fashion to pergolide or placebo treatments. Pergolide therapy was associated with a mild and transient bradycardiac effect, but no clinically significant cardiotoxicity.
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PMID:Double-blind assessment of potential pergolide-induced cardiotoxicity. 352 Mar 83

We report the clinical course of 35 patients with Parkinson's disease who experienced an initially favorable response to pergolide and who were taking the drug for at least 6 months. The duration of pergolide treatment was 6-50 (25 +/- 16 SD) months. Of the 14 patients who remained on pergolide for over 2 years, 12 remained less disabled for 26 +/- 17 SD months, seven enjoyed increased "on" time for 39 +/- 8 SD months, and nine had a lower Hoehn-Yahr stage for 25 +/- 17 SD months. Pergolide was discontinued after 5-39 months in eight patients; six patients then deteriorated. Pergolide can remain efficacious in the treatment of Parkinson's disease for up to 50 months.
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PMID:Long-term efficacy of pergolide in patients with Parkinson's disease. 370 1

Nine patients with idiopathic Parkinson's disease were treated with pergolide to a daily maintenance dose of 2.2 +/- 0.9 mg (mean +/- SD) for 17.3 +/- 8.3 months. After 1 month, there was an average 68% increase in mobile on-time, but the improvement declined to 30% by 6 months, 23% by 1 year, and virtually disappeared by 18 months of therapy. Pergolide was discontinued in seven patients because of loss of efficacy (4 patients), confusion (1 patient), or myocardial infarction or ventricular ectopy (2 patients). Partial but temporary restoration of mobility was observed in seven patients who were switched to an alternate-day dosing schedule after 9.2 +/- 2.4 months. Two patients with advanced Shy-Drager syndrome were treated with pergolide without benefit.
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PMID:Long-term experience with pergolide therapy of advanced parkinsonism. 388 13

In a 12-month open-label trial, pergolide mesylate was administered in doses with antiparkinsonian efficacy to six patients with stable heart disease. Cardiac status did not worsen in any patient. Parkinson's disease improved in all patients. Pergolide is a safe and effective therapy for Parkinson's disease, even in patients with heart disease.
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PMID:Pergolide mesylate: lack of cardiac toxicity in patients with cardiac disease. 388 7

A double-blind, placebo-controlled study was conducted of pergolide as an adjunctive treatment to levodopa in 17 patients with advanced Parkinson's disease. There was a significant improvement (p less than 0.05) in total disability score, in gait, and in "wearing off" and "on-off" phenomena. Pergolide is a useful drug in patients with advanced Parkinson's disease.
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PMID:Pergolide therapy in Parkinson's disease: a double-blind, placebo-controlled study. 389 52

The activity of pergolide, a clavine ergolene, and mesulergine, an 8-alpha amino ergoline, were compared in 18 patients with advanced Parkinson's disease. All of the patients were no longer satisfactorily responding to levodopa, and 16 patients had diurnal oscillations in performance. Pergolide, mean dose 2.7 mg, when added to levodopa resulted in a significant (27%) decrease in Parkinson disability and a significant improvement in diurnal oscillations in performance (136% increase in hours 'on'). Twelve of the 18 patients (67%) improved. However, after 2 years pergolide was discontinued in all of the patients because of decreased efficacy, adverse effects, or both. At this time, mesulergine, mean dose 9.3 mg., when added to levodopa resulted in a significant (37%) decrease in Parkinson disability and a significant improvement in diurnal oscillations (61% increase in hours 'on'). Twelve of the 18 patients (67%) improved. Adverse effects (dyskinesias) were less with mesulergine than with pergolide. A declining response to one agonist does not preclude a successful response to another agonist of a different class.
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PMID:Efficacy of pergolide and mesulergine. 394 91

Pergolide, an experimental dopamine agonist, was administered to 56 patients with advanced Parkinson disease who were no longer satisfactorily responding to levodopa, including 45 patients with diurnal oscillations in performance: "on-off" phenomena. Lisuride, an experimental dopamine agonist was administered to 63 patients with advanced Parkinson disease. Pergolide or lisuride, when added to levodopa, resulted in a significant decrease in disability in both the "on" and the "off" period, and an increase in the number of hours in which patients were "on". Forty-one of 56 patients (73%) improved on Pergolide. Thirty-seven of 63 patients (59%) improved on lisuride. Mean dose of pergolide was 2.5 mg. (range 0.2 to 10.0 mg.). Mean dose of lisuride was 2.6 mg. (range 0.2 to 5.0 mg.). Pergolide was discontinued in 18 patients because of adverse effects, including an organic confusional syndrome (six patients), dyskinesias (four patients) and cardiovascular abnormalities (three patients). Lisuride was discontinued in 26 patients because of adverse effects, including an organic confusional syndrome (15 patients), dyskinesias (five patients) and vasospasm (two patients). Pergolide was discontinued in nine patients and lisuride in 12 because of a lack of effect or a declining effect. Both drugs are equally useful in patients with advanced Parkinson disease.
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PMID:The use of pergolide and lisuride, two experimental dopamine agonists, in patients with advanced Parkinson disease. 405 Aug 44

Pergolide, a synthetic ergoline, is a potent long-acting dopaminergic drug effective in Parkinson's disease and amenorrhea-galactorrhea. After 138 micrograms 14C-pergolide orally to healthy subjects, radioactivity was present in plasma and red blood cells. Salivary radioactivity was one third to one tenth that in plasma. Radioactivity in plasma appeared after 15 to 30 min, peaked at 1 to 2 hr, and was barely detectable after 96 hr. Plasma radioactivity was not attributable to pergolide, and the levels did not correlate well with the duration of the prolactin-lowering effect induced by pergolide. Pergolide became bound to several plasma proteins and could not be displaced by other drugs that are also bound or by possible metabolites of pergolide. Radioactivity was eliminated as pergolide metabolites in urine (55%), feces (40%), and breath (5%, as 14CO2).
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PMID:Physiologic disposition of pergolide. 611 11


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