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)

Fourteen patients with Parkinson's disease and motor fluctuations were given 125 mg of Madopar HBS or placebo twice a day in addition to their optimal standard Madopar treatment in a double-blind, cross-over study. Clinical response was evaluated by the King's College Hospital Parkinson's Disease Rating Scale, the Mobility in Bed Scale and self-scoring diaries. A significant improvement with the drug was found according to the rating scales, whereas evaluation by self-scoring diaries showed no significant changes. In three patients we observed worsening of abnormal involuntary movements. The present trial suggests that a low dose of Madopar HBS can be useful in addition to levodopa therapy in some patients on long-term treatment.
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PMID:A double-blind, cross-over trial with madopar HBS in patients with Parkinson's disease. 269 99

The most important current problem in the treatment of Parkinson disease in the so-called L-dopa long-term-treatment syndrome. We present here the results of our experience with Madopar HBS in the treatment of two groups of patients suffering from L-dopa long-term treatment syndrome. In the first study we replaced the standard Madopar with Madopar HBS. In the second study, after identifying the most disabling "off" periods, we added Madopar HBS to the previous treatment in such a way as to control these "off" phases. Our study suggests that Madopar HBS is useful in reducing typical fluctuation phenomena in the majority of patients.
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PMID:Madopar HBS and the decompensated phase of Parkinson disease. 279 13

The effect of (-)deprenyl as additive to a Madopar treatment of parkinsonian patients has been investigated in a retrospective study over the past ten years. 941 patients have been evaluated. Addition of (-)deprenyl to the standard Madopar treatment resulted in an improvement of the disability, in a prolongation of life expectancy, in a reduction of side effects caused by Madopar and a leveling down of the fluctuations in the clinical improvement. In addition the time from the onset of Parkinson's disease to significantly longer in the group of patients which were treated with Madopar and (-)deprenyl in combination.
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PMID:Effect of (-)deprenyl in long-term treatment of Parkinson's disease. A 10-years experience. 309 56

The combinations of benserazide and levodopa (1:4, Madopar) and of carbidopa and levodopa (1:10 and 1:4, Sinemet) are currently the most effective treatment of Parkinson's disease. In the present comparative study some effects of the peripheral aromatic L-amino acid decarboxylase (AADC) inhibitors benserazide and carbidopa administered alone or in combination with levodopa by the oral route were investigated in two animal species (rat and mouse) and in healthy volunteers. Benserazide is about 10 times more potent than carbidopa as inhibitor of peripheral AADC both in animals and man. Even at relatively high doses (up to 60 mumol/kg p.o.) benserazide is shown in animals to inhibit the decarboxylation of levodopa only in the extracerebral tissues, thus permitting the formation of dopamine in the striatum and in the hypothalamus. As benserazide is the most potent peripheral AADC inhibitor presently available, is well tolerated and relatively nontoxic even when used chronically, it appears to be the peripheral AADC inhibitor of choice for the development of controlled-release formulations in which Dopa is combined with a peripheral AADC inhibitor. When administered to healthy subjects the pharmacokinetics of the new drug delivery system named Madopar HBS (hydrodynamically balanced system) was characterized by lower and delayed plasma peak concentrations but a longer-lasting concentration of Dopa than after Madopar standard. Therefore, this new controlled-release system may reduce the clinical fluctuations occurring in patients with 'wearing-off' and 'on-off' phenomena.
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PMID:Inhibition of decarboxylase and levels of dopa and 3-O-methyldopa: a comparative study of benserazide versus carbidopa in rodents and of Madopar standard versus Madopar HBS in volunteers. 312 42

In a open study in 13 patients with Parkinson's disease with 'on-off' fluctuations, all (n = 3) or part (n = 10) of the usual intake of levodopa (with peripheral decarboxylase inhibitor) was replaced by Madopar HBS for 5-122 days (median 35). Time 'off' increased in 2 of the 3 monotherapy subjects. With combined therapy, time 'on' was increased in 6, unchanged in 2 and reduced in 2. However, 11 of the 13 patients complained of reduced predictability of clinical response with Madopar HBS. Only 4 of the 13 patients preferred to continue with combined standard plus HBS treatment; this continued treatment led to an increase in time 'on' in 3 and a decrease in involuntary movements in 3 patients. Two of these four patients benefited on both counts.
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PMID:Open study of Madopar HBS, a new formulation of levodopa with benserazide, in 13 patients with Parkinson's disease and 'on-off' fluctuations. 332 34

23 parkinsonian patients, 11 men and 12 women with an average age of 62 +/- 10 years, were recruited for an open substitution study of standard Madopar by Madopar HBS (hydrodynamically balanced system). All patients were presenting fluctuations in efficacy associated or not with abnormal involuntary movements. The patients in this study had been suffering from Parkinson's disease for 16 +/- 6 years and were severely disabled (Hoehn and Yahr grade III-V). The substitution was carried out dose for dose from one day to another. During the first month the dosage titration was aimed at finding the optimal therapeutic effect. After 120 days 13 patients were continuing the treatment while 10 had stopped it because of lack of therapeutic advantage. After 120 days, as compared to the initial state, end-of-dose fluctuations improved by 47%, the parkinsonian symptomatology by 54% and the abnormal involuntary movements improved by 33%. The daily dose of Levodopa had to be increased from 580 +/- 230 to 710 +/- 240 mg. The results obtained were excellent in 5 cases, good in 6 and moderate in 2 cases.
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PMID:Clinical trial of Madopar HBS in parkinsonian patients with fluctuating drug response after long-term levodopa therapy. 332 35

The clinical effects and pharmacokinetic profiles of single doses of Madopar HBS were compared with those of standard Madopar in two studies in patients with Parkinson's disease and 'on-off' fluctuations. In the first study, 10 fasting patients received equivalent doses (200 mg levodopa plus 50 mg benserazide) of each preparation. The clinical response to Madopar HBS was delayed and brief; the relative bioavailability was only 50%. In the second study in 7 non-fasted patients, the effects of 3 capsules of Madopar HBS 125 were compared with those of 2 capsules of standard Madopar 125. Delay to turn on was longer with HBS, but duration of time on, and delay to turn off, were longer with this preparation. The area under the concentration-time curve for plasma levodopa was greater with HBS, and the maximum levodopa concentration was similar to, but achieved later than standard Madopar.
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PMID:Single-dose studies of a slow-release preparation of levodopa and benserazide (Madopar HBS) in Parkinson's disease. 332 37

Eleven patients suffering from idiopathic Parkinson's disease participated in an open study of Madopar HBS. At the beginning the patients were switched from standard Madopar to Madopar HBS, initially keeping constant L-dopa dosage and the number of daily doses. In 9 of the 11 patients a marked deterioration occurred within a few days. In spite of increasing the daily dosage of L-dopa the condition remained unsatisfactory in several patients and forced us to prematurely discontinue the study in 5 cases. The Webster ratings improved in 1 patient, remained unchanged in 4 cases and a definite worsening occurred in 6 patients. Fluctuations of the symptomatology were improved in none of our patients. It is not excluded that these negative results might have been improved by a further increase of Madopar HBS, a less abrupt switch from standard Madopar to Madopar HBS and probably also a combination of the two forms.
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PMID:Open clinical study of Madopar HBS. 332 38

Results obtained in 22 patients with Parkinson's disease in whom treatment with standard Madopar was replaced by Madopar HBS, a CR formulation of the same product, are presented. All the patients presented with dyskinesia and akinesia phenomena related in part to the L-dopa treatment and in part to the disease itself. In 20 patients replacement of the standard agent by HBS led to a distinct improvement in the clinical condition and a significant reduction of the 'on-off' phenomenon. However, with the new formulation the dosage had to be increased by 86% on average as compared with standard Madopar. In 6 of the 22 patients treatment with the HBS formulation has continued for over 6 months and is still giving very good results.
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PMID:Treatment of parkinsonian conditions with a controlled-release form of levodopa--preliminary study. 332 39

In 23 patients with idiopathic Parkinson's disease presenting with severe fluctuations in motor performance and 'on-off' phenomena after long-term treatment with levodopa, the standard form of Madopar was replaced by the controlled-release form Madopar HBS. The Meerwaldt's patient card has been used to evaluate the frequency and intensity of response swings. Only 2 patients, who suffered from clear-cut 'end-of-dose' deterioration, significantly benefited by this switch from standard Madopar to Madopar HBS. Eight patients had a minimal or not essential improvement of the parkinsonian symptomatology and/or of the response fluctuations. Thirteen patients returned to their previous standard Madopar treatment after deterioration of parkinsonian symptoms or increase of dyskinesia under the HBS treatment. The overall increase in dosage of levodopa with Madopar HBS was 54% in comparison with the initial standard Madopar dosage.
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PMID:Open multicenter trial with Madopar HBS in parkinsonian patients. Preliminary assessment after short-term treatment. 332 41


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