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We used pergolide to treat 10 patients with idiopathic Parkinson's disease who had first responded to, and then failed, bromocriptine therapy. At the end of 5 years, patients had improved when compared with study entry. Peak efficacy, equal with both drugs, was seen at 12 months. After a mean treatment of 29 months, bromocriptine was no longer effective, but pergolide was still beneficial.
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.
An open follow-up of a controlled study in patients with restless legs syndrome (RLS) shows that the beneficial effect of pergolide on RLS symptoms persists throughout at least 1 year. Twenty-two patients of 28 (78.6%) continued to take pergolide. Polysomnographic measurements showed a persistent improvement of PLM index, PLMS arousal index, total sleep time, and sleep efficiency (p = 0.0001). Side effects, in particular nausea, were common but were well controlled by domperidone in most patients.
Pergolide is an ergot-derived dopamine agonist used in Parkinson's disease and, increasingly, in restless legs syndrome. We report a patient with a 2.5-year history of weight loss, pleuropulmonary fibrosis, and exudative pleural effusion that developed insidiously while taking this medication. The extensive and invasive workup that preceded the diagnosis highlights the difficulty in attributing such a process to a drug reaction. This is the second report of such a reaction to pergolide, which is one of the increasing number of ergot-derived compounds in common clinical use.
The duration of the inhibition of Prl secretion by pergolide, a new dopaminergic ergoline, was investigated in 5 hyperprolactinaemic women after a single oral 50 micrograms dose. In each subject, blood samples were collected every 2 h for 18-24 h to establish baseline Prl level and then every 3 h for 48-51 h after pergolide administration. In each subject, levels were potently suppressed by at least 80% of baseline and brought down to the normal range. Prolactin suppression was quite sustained throughout the study period in 4 patients and to a lesser degree in the remaining subject. This potent long-lasting inhibition of Prl secretion should enhance the efficacy and acceptability of the chronic treatment of hyperprolactinaemia with this new dopamine agonist and, for example, allow drug intake only once every other day.
Pergolide is a dopaminergic agonist used to treat Parkinson's disease but is associated with the development of retroperitoneal fibrosis (RPF). Newer nonergot agents (pramipexole, ropinirole) may not carry this same risk. A patient with a history of pergolide-induced RPF was treated successfully with ropinirole for 1 year without complications.
Plasma ACTH levels have been variable in horses with a positive clinical response for therapy for equine Cushing's Disease (ECD). Therefore, our purpose was to determine the value of monitoring plasma adrenocorticotropin (ACTH) levels during treatment of equine Cushing's disease (ECD) with either cyproheptadine (n = 32) or pergolide (n = 10). First, we validated the chemiluminescent ACTH assay (specificity, precision, accuracy, intra-assay and interassay variations) and tested methods of handling the whole blood from the time of collection to when the ACTH was assayed. The sensitivity and specificity of high plasma ACTH levels for detecting ECD was determined in a retrospective study on hospitalised horses (n = 68). Surveys were sent to veterinarians who submitted equine ACTH levels that were high initially and had at least 2 ACTH samples to determine the value of monitoring ACTH levels during therapy of ECD. The ACTH chemiluminescent assay was valid. The ACTH was stable when whole blood was collected and held in plastic tubes for 8 h before separating the plasma. The sensitivity and specificity of plasma ACTH levels for detecting ECD were 84% (n = 19,95% CI 60,97) and 78% (n = 49,95% CI 63,88), respectively. Treated horses generally showed a decrease in plasma ACTH. Plasma ACTH levels may be helpful when monitoring therapy of ECD, although improvement in clinical signs should be considered most important. There were no differences between cyproheptadine and pergolide in terms of improvements in any of the clinical signs.
In this preliminary report from a placebo-controlled, double-blind, dose-response study on the use of pergolide mesylate for cocaine dependence in outpatients 8 out of 235 subjects noted adverse events requiring breaking of the blind. Events occurred at or within 7 days of receiving the first dose of medication and included side effects (four cardiovascular, one psychiatric); drug-drug interactions (one): and clinical exclusions (two pregnancies). Two anecdotes of illicit abuse are reported. Although efficacy is unestablished, pergolide appears to be safe in the early treatment of cocaine dependence except where there are relative contraindications.
The efficiency of pergolide has been confirmed by the study of a group 29 parkinsonian patients. They were relatively young, and the duration of evolution of their Parkinson's disease was more then ten years, with levodopa-induced dyskinesia and fluctuations. In this group of patients with most serious motor disability, it has been possible to improve dyskinesia and fluctuations with a relatively important dosage of pergolide and without increase of levodopa dosage.
For the purpose of determining the optimal dose, pergolide was administered to patients with Parkinson's disease using a dose-escalation protocol up to the maximum dosage permissible in Japan. The study was completed in 16 subjects with Parkinson's disease. Prior to the start of the dose-escalation study, the daily dose of pergolide was 500 microg in 6 patients and 750 microg in 10 patients. The daily dose was raised by 250 microg at 4-week intervals up to the approved maximum dose of 1,250 microg/day, which was used as the final level. Just before the start of study and after administration for 4 weeks at each dose level, UPDRS-III and PDQ-39 assessments were performed. The mean UPDRS-III score was 28.6 +/- 7.9 before the start of the study and 17.3 +/- 8.3 after the end, indicating an improvement (improvement rate, 39.3%; p < 0.01). The mean PDQ-39 score was 45.2 +/- 21.8 before the start and 37.3 +/- 17.8 after the end, indicating an improvement (improvement rate, 17.5%; p < 0.05). Clinical conditions including their QOL improved significantly after dose-escalation up to the 1,250 microg.
Sixteen parkinsonian patients, mean age 57 (range 41-71), with a mean 9 year duration of Parkinson's disease, with "on-off" motor fluctuations were treated with pergolide mesylate 1.6 mg/die (range 1-5) for three months. The treatment resulted in an improvement of akinesia, tremor and rigidity, of the severity of phase "off" and of the duration of time "on". No significant improvements were obtained in the severity of dyskinesia. Three patients considered the treatment excellent and capable of restoring their working abilities. The drug was generally well tolerated. Pergolide was discontinued because of orthostatic hypotension in two patients and because of hallucinations in one patient. We consider these results a favorable progress in the treatment of Parkinson's disease.
Side effects occasionally limit the use of bromocriptine for cocaine withdrawal. The recently released medication pergolide shares some pharmacologic properties with bromocriptine but differs in potency and dopamine receptor subtype specificity. The authors tested pergolide in the treatment of 21 patients experiencing cocaine withdrawal. Sixteen patients reported rapid improvement in sleep and decreased cocaine craving. Side effects were limited primarily to gastrointestinal complaints.
6,7-Dihydroxy-2-dimethylaminotetralin (TL-99), N-n-propyl-3-(3-hydroxyphenylpiperidine [(+/-)-3-PPP], N-n-propylnorapomorphine and pergolide were evaluated for activity on a number of biochemical parameters that are presumed to indicate an agonist effect at dopamine (DA) autoreceptors (antagonism of the gamma-hydroxybutyrate-induced increase in dopa formation), at postsynaptic DA receptors (elevation of acetylcholine levels) or at both types of DA receptors (diminution of DA synthesis and homovanillic acid levels) in rat striatum. All four agents decreased striatal dopa accumulation (in the presence and in the absence of gamma-hydroxybutyrate). N-propylnorapomorphine, pergolide and TL-99 also reduced homovanillic acid levels and increased acetylcholine concentrations in striatum whereas (+/-)-3-PPP was inactive. The compounds were all more potent in diminishing dopa accumulation caused by gamma-hydroxybutyrate treatment than in increasing acetylcholine levels [(+/-)-3-PPP showing the highest dissociation] indicating a preferential agonist activity at DA autoreceptors. The relative selectivity of the compounds for DA autoreceptors and postsynaptic DA receptors was evaluated further by studying the antagonism by these drugs of the activation of striatal dopa formation (index of both DA autoreceptor and postsynaptic DA receptor stimulation) and tyrosine hydroxylase (index of postsynaptic DA receptor stimulation only) induced by haloperidol or reserpine. The DA agonists were all more potent in antagonizing the neuroleptic-induced increase in DA synthesis than in counteracting the drug-induced activation of tyrosine hydroxylase, with (+/-)-3PPP exhibiting the highest dissociation. The present results indicate that the DA agonists studied possess some selectivity for striatal DA autoreceptors, (+/-)-3-PPP being the most selective in this respect.
Pergolide, LY141865 and SKF-38393 were compared to clonidine for their effects on urine output in normally hydrated rats. SKF-38393 and LY141865 have been considered to be specific D-1 and D-2 dopamine receptor agonists, respectively. Clonidine had a marked effect to increase urine output (17-18 ml at doses as low as 0.08 mg/kg s.c.), whereas the specific dopamine agonists SKF-38393 (0.32-5 mg/kg s.c.) and LY141865 (0.16-1.25 mg/kg s.c.) did not affect urine output. Pergolide, a nonspecific dopamine agonist, slightly increased urine output at the highest dose (0.64 mg/kg s.c.). Specific dopamine agonists do not increase urine output in normally hydrated rats.
Tardive dyskinesia may result from neuroleptic-induced supersensitivity of striatal dopamine receptors. Alteration of receptor site sensitivity may be a therapeutic goal. Pergolide, a direct acting dopamine agonist, decreased in guinea pigs haloperidol-induced increases in striatal dopamine receptor density both when coadministered and when given following haloperidol. Pergolide down-regulates supersensitive dopamine receptors and should be tested in the treatment of tardive dyskinesia.
We report the case of a parkinsonian patient treated by pergolide who developed aortic and mitral regurgitations and pulmonary hypertension. When she stopped the medication, the cardiac symptoms disappeared. Retroperitoneal and pleural fibrosis have been described with pergolide but never valvulopathy until 3 cases reported in December 2002.
In reserpinized (5 mg/kg, s.c.) mice treated with alpha-methyl-p-tyrosine (200 + 100 mg/kg, i.p.), increasing doses of the D-2 antagonist sulpiride had varying effects on locomotor activity induced by the mixed D-1/D-2 agonist pergolide (2 mg/kg, s.c.). Low doses of sulpiride (1 mg/kg, i.p.) significantly enhanced this activity whereas at higher doses (50 mg/kg) an inhibitory effect was observed. Amphetamine (3 mg/kg, i.p.) failed to reverse akinesia in this animal model, precluding the possibility of a presynaptically mediated phenomenon; in contrast, mice receiving reserpine alone showed a high degree of locomotor activity when challenged with amphetamine. The bimodal effect of sulpiride is thought to be mediated either by two different D-2 receptors located on the same cell or by the same receptor with different topographical localization on postsynaptic neurons mediating opposite functions.
The antagonistic effect of dopamine (DA) D-1 and D-2 antagonists against circling behaviour induced by various DA agonists in 6-OHDA-lesioned rats has been investigated. DA D-1/D-2 selectivity of agonists in vitro was measured by the stimulatory effect on DA-sensitive adenylate cyclase in rat striatal homogenates (D-1), the inhibitory effect on electrically-induced release of 3H-DA in rabbit striatal slices (D-2) and the affinity to 3H-piflutixol (D-1) and 3H-spiroperidol (D-2) binding sites in rat striatal membranes. The contralateral circling behaviour induced by the DA D-1 agonist SK & F 38393 was blocked by the DA D-1 antagonist, SCH 23390, and by the mixed DA D-1/D-2 antagonist cis(Z)-flupentixol, but was not influenced by the DA D-2 antagonists spiroperidol and clebopride. In contrast, circling behaviour induced by the preferential DA D-2 agonists pergolide and LY 171555 was blocked by clebopride, spiroperidol, and cis(Z)-flupentixol, but weakly or not influenced by SCH 23390. Apomorphine-induced circling behaviour was blocked by cis(Z)-flupentixol, partially antagonized by SCH 23390 and clebopride but not inhibited by spiroperidol, although the time-course of circling was changed. Combinations of SCH 23390 with spiroperidol or clebopride in low doses completely blocked the effect of apomorphine. These results indicate that DA D-1 and D-2 receptors mediate circling behaviour through separate mechanisms which can be independently manipulated with respective agonists and antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)