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)

The efficacy of a novel oral sustained-release preparation of L-dopa (Madopar HBS) was compared to that of previous standard L-dopa treatment in 10 patients with idiopathic Parkinson's disease and severe fluctuations in motor performance in an open inpatient trial. Clinical assessment included evaluation of self-scoring 'on-off' diaries kept by the patients throughout the study. It revealed a reduction of end-of-dose deterioration and, to a lesser degree, of random 'on-off' swings in 6 cases. Doses of Madopar HBS required for an optimal response averaged the 1.6-fold of previous conventional L-dopa. Plasma levels of L-dopa were more stable with Madopar HBS compared to standard L-dopa treatment in 4 of 5 patients.
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PMID:Clinical and pharmacokinetic observations with Madopar HBS in hospitalized patients with Parkinson's disease and motor fluctuations. 332 42

During a long-term double-blind study, which began February 1985, we have treated 16 patients with Morbus Parkinson or Parkinson's syndrome with deprenyl or identically appearing placebo tablets. The aim of the study is to ascertain whether a reduction of other antiparkinsonian medication, especially Madopar, can be achieved with deprenyl, in order to minimize the known late undesirable collateral effects ("on-off"-phenomena, dyskinesias). The criteria used in evaluation of the course of disease are the clinical-neurological findings as well as a series of motor performance tests. The results to date indicate that the dose of Madopar could be reduced in 7 of the 16 patients. Two of these patients were receiving Madopar alone, while 5 had been given anti-cholinergics in addition. In one female patient the dose of Madopar had to be reduced due to the development of dyskinesias. It is noteworthy that the psychological condition of the patients remained constant. There was no increase in side-effects, e.g. headaches, dizziness, nausea, etc. with administration of the study substance. In 3 patients with longstanding Parkinson's disease treated with Madopar or Nacom, who were not included in the study, the doses of the above drugs could be maintained or reduced by addition of deprenyl.
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PMID:Levodopa and monoamine oxidase inhibitor combination therapy. A controlled clinical trial. 332 20

Madopar Hydrodynamically Balanced System (HBS), a new sustained-release levodopa preparation, was used to control severe nightly disabilities in 15 outpatients suffering from Parkinson's disease in an advanced state and with long-term levodopa therapy. This medication was given ante noctem in addition to an otherwise unchanged daily regimen of levodopa administration. In 13 patients a considerable diminution in nocturnal akinesia and in the frequency of waking up was reached with a mean dosage of 308 mg of Madopar HBS. Early morning akinesia was only slightly alleviated in four patients. The nocturnal off-period pain disappeared in one patient. Adverse effects consisted of nocturnal dyskinesia in two patients and early morning dystonia in another two patients. The regular use of sleeping pills was clearly reduced after Madopar HBS therapy.
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PMID:Madopar HBS in Parkinson patients with nocturnal akinesia. 335 32

In an open pilot study, 10 patients with Parkinson's disease and nocturnal and/or early-morning disabilities were given Madopar HBS (hydrodynamically balanced system; mean dose 250 mg) shortly before retiring in addition to their usual daytime antiparkinsonian treatment. Eight patients derived worthwhile improvement; the most gratifying responses were seen in the relief of nocturnal bradykinesia, rigidity and tremor. Early-morning symptoms were also improved in 3 out of 5 patients, possibly as a secondary response to an improved nights sleep. Cramps, early-morning dystonia and pain, however, responded poorly. Overall results are sufficiently encouraging to warrant further controlled studies with Madopar HBS in what has been a relatively neglected area of distress for many patients with Parkinson's disease.
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PMID:A sustained-release formulation of L-dopa (Madopar HBS) in the treatment of nocturnal and early-morning disabilities in Parkinson's disease. 342 6

In this open study patients with advanced Parkinson's disease, who experienced pronounced fluctuations in symptoms while on standard L-dopa, were switched from Madopar/Sinemet to Madopar HBS. The dosage was adjusted until optimal response was obtained. The effect was unsatisfactory in 4 cases and side effects intervened in another 2. The remaining 16 patients exhibited substantial and frequently significant improvements with regard to both akinetic and dyskinetic phenomena. L-Dopa dosage was increased in all cases, and addition of standard L-dopa was required in one third of the cases. These benefits continued in the majority of patients.
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PMID:Madopar HBS: slow-release levodopa and benserazide in parkinsonian patients presenting marked fluctuations in symptoms on standard L-dopa treatment. 342 10

In a general practice population of 57 000, 32 patients suffering from Parkinson's disease were identified from repeat prescription indexes and direct questioning of all members of the primary health care team. Of these patients 26 were receiving an L-dopa preparation and 10 an anticholinergic drug. The only newer drug found to be in use was bromocriptine and three patients were receiving this treatment.Of the 26 patients receiving an L-dopa preparation one received L-dopa alone, six L-dopa with benserazide (Madopar, Roche) and 19 L-dopa with carbidopa (Sinemet, Merck, Sharp and Dohme). The patients treated with Sinemet were receiving inadequate doses of carbidopa - three quarters received less than 75 mg per day which was in part a reflection of the low doses of L-dopa the patients received, the average dose being 468 mg per day. The L-dopa preparations were given in adequately spaced doses.The general practitioner made the diagnosis in 20 of the 32 cases and was in control of the drug therapy in 15 cases, however 25 cases were referred for specialist advice.
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PMID:Audit of the drug treatment of Parkinson's disease in general practice. 403 54

The thyrotrophin (TSH) and prolactin (Prl)-releasing effects of TSH-releasing hormone (TRH) were investigated in 20 subjects with Parkinson's disease (PD), unmedicated, on chronic treatment with a combination levodopa-benserazide (Madopar) or levodopa-carbidopa (Sinemet) or withdrawn from therapy. Administration of TRH (200 micrograms iv) induced in unmedicated patients TSH and Prl responses significantly lower than those of sex-and age-matched controls. In patients on Madopar therapy the TSH and Prl responses to TRH were greater than in unmedicated patients and comparable to those of controls, while in patients on Sinemet therapy the pituitary responses were undistinguishable from those of unmedicated subjects. Withdrawal of Madopar therapy resulted in a marked diminution of the TSH response but did not affect the Prl response to TRH. Withdrawal of Sinemet therapy did not alter the TSH and Prl responses to TRH. Concomitant evaluation of growth hormone (GH) levels, in none of the subjects evidenced non-specific changes in plasma GH following TRH. Since TSH and Prl responses to TRH are inhibited by an enhancement of the dopaminergic tone, it would appear that the latter is preserved in the tuberoinfundibular system of unmedicated subjects and subjects on chronic Sinemet therapy, but is defective in subjects on chronic Madopar therapy.
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PMID:Thyrotrophin and prolactin responses to thyrotrophin-releasing hormone in patients with Parkinson's disease. 680 85

The authors report the results of treatment of hereditary extrapyramidal diseases with new preparations acting upon neurotransmitter systems. Patients with torsion dystonia, Huntington's chorea, Parkinson's disease, hereditary tremor, myoclonic epilepsy were followed-up for several years.. The best results in akinetic-rigidity syndromes (Parkinson's disease, rigid froms of torsion dystonia, Hallevorden-Spatz disease) were obtained with L-DOPA (including Sinemet, Nacom, Madopar) and in many patients these preparations were given in combination with other drugs (cholinolytic agents, Midantan) which contributed to compensation of the disturbed equilibrium of neurotransmitter systems and reduction of side effects. For decreasing the side effects of L-DOPA (hyperkineses of dystonic type, chorea and myoclonia) preparations from the group of phenothiazine and diazepine were given. In many cases improvement was achieved by slover increase of L-DOPA doses. In the hyperkinetic syndromes (Huntington's chorea, idiopathic tremor, myoclonic epilepsy, hyperkinetic torsion dystonia) preparations of phenothiazine, butyrophenone and new drugs active on the GABAergic system (Baclophen, Lyoresal, Pantogam) and diazepine (Clonazepam) were used. The analysis of the results shows that disturbed equilibrium of central neurotransmitters plays and important role in the pathogenesis of hereditary extrapyramidal system diseases.
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PMID:[Pathogenetic treatment of various hereditary extrapyramidal disorders with new drugs]. 732 7

Madopar, a combination of levodopa with benserazide, induced an inconsistent rise in plasma growth hormone in unmedicated patients with Parkinson's disease and in controls, and a greater growth hormone rise in Parkinsonian subjects on chronic Madopar therapy. In subjects on chronic therapy with levodopa and carbidopa (Sinemet), the growth hormone releasing effect of Madopar was blunted. Madopar increased plasma prolactin (PRL) in controls, unmedicated patients and patients on Madopar therapy while in patients on Sinemet therapy the PRL-releasing effect of Madopar was strikingly reduced. Since these data were interpreted as due to a defective dopamine tone in the hypothalamus of Parkinsonian subjects on Madopar but not Sinemet therapy, a direct dopamine receptor agonist, lisuride was administered. Lisuride, however, elicited a blunted growth hormone response both in patients on Madopar and Sinemet therapy, without revealing a state of supersensitivity of dopamine receptors for growth hormone control in Parkinsonian subjects on Madopar therapy. No difference was present in the PRL-lowering effect of lisuride in the different experimental groups. These findings suggest that: (1) hypothalamic dopamine function is impaired in Parkinsonian subjects on Madopar therapy, preserved in unmedicated patients and enhanced in patients on Sinemet therapy; (2) the endocrine effects observed in Parkinsonian subjects on chronic Madopar therapy may be due to some penetration of benserazide across the blood brain barrier in the region of the hypothalamus; (3) since Madopar and Sinemet are in essence equally effective antiparkinsonian remedies, penetration of benserazide does not occur across the blood brain barrier surrounding the nigrostriatal system.
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PMID:Growth hormone and prolactin stimulation by Madopar in Parkinson's disease. 733 6

The peripheral decarboxylase inhibitors benserazide and carbidopa, often administered in combination with L-dopa in the treatment of Parkinson's disease, are also very good inhibitors of semicarbazide-sensitive amine oxidase (SSAO). In untreated patients and in patients treated with L-dopa alone, plasma SSAO activity is normal. In patients treated with L-dopa plus benserazide or carbidopa (Madopar or Sinemnet), however, plasma SSAO activity is strongly inhibited, contrary to the paradoxical 3-fold increase in plasma aromatic-L-amino acid decarboxylase activity we reported previously. Single-dose and longitudinal studies show that the SSAO inhibition proceeds rapidly and increases even further to nearly complete inhibition after continued treatment, while aromatic-L-amino acid decarboxylase activity only transiently decreases after a single dose and increases slowly with continued treatment above pretreatment levels. Dialysis experiments confirm that the binding of benserazide to SSAO is irreversible, especially after chronic treatment. The lack of knowledge about the exact function of SSAO precludes definite conclusions about the effect of this chronic SSAO inhibition on patients. Careful follow-up studies of patients treated with Madopar or Sinemet might provide further information about the possible physiological role of SSAO.
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PMID:Contrasting effects of peripheral decarboxylase inhibitors on plasma activity of aromatic-L-amino acid decarboxylase and semicarbazide-sensitive amine oxidase in Parkinson's disease. 747 17


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