La maladie de Parkinson au Canada (serveur d'exploration)

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Dopamine agonist monotherapy in Parkinson's disease

Identifieur interne : 000B44 ( PascalFrancis/Corpus ); précédent : 000B43; suivant : 000B45

Dopamine agonist monotherapy in Parkinson's disease

Auteurs : C. E. Clarke ; M. Guttman

Source :

RBID : Pascal:03-0040197

Descripteurs français

English descriptors

Abstract

Context Levodone is the oid standard therapy for Parkinson's disease. However, long-term treatment leads to involutary movements and response fluctuations which add to the compixities of later disease management. In addition, preclinical evidence suggests that levodopa is toxic to dopaminergic neurons. These problems have led to a move away from levodopa towards initial monotherapy with a dopamine agonist. Starting point Positron-emission tomography (PET) and single-photon emission compouted tomography (SPECT) tracers have been developed which may be considered surrogate markers for remaining dopaminergic neurons, in a randomised controlled trial in patients with early Parkinson's disease, the Parkinson Study Group used -β-CIT SPECT UAMA 2002; 287: 1653-61). Those catients given pramipexole had significantly reduced loss of striatal uptake at 46 months compared with these given levodope (16.0% vs 25.5%). In a similar trial. Aian Whose and colleagues used DOPA PET (Neurology 2002; 58 [suppl 3]: A82-83), Patients given ropinirole had significantly reduced loss of striatal uptake at 24 months compared with those given levedope (13% vs 20%). These studies suggest that agonist monotherapy may be neuroprotective and/or that levodopa is toxic. This work has been enticised as the SPECT results may have resulted from a differential effect of the agonist and levodopa on the regulation of the dopamine transporter, thereby influencing the imaging outcome measure. Other criticisms include insufficient data on the use of the potential neuroprotectant selegiline and patients on pramipexole in the SPECT study appear to have been clinically slow progressors. Single clinical trials with each of the four modern egenists compared with levodope show that as monotherapy the agonists delay the onset of invotuntary movements, although at the expense of poorer treatment of motor impairments and disability and more depaminergic adverse events. The only health-related quality of life data show no difference between pramipexole and levodopa after 4 years. No information on health-economics measures is available but agonists cost two to three times as much as levodopa. Where next? Young patients should be treated with agonist monotherapy since the trials included predominantly younger patients who have a higher incidence of motor complications. Those with significant co-morbidity, dementia, or a short life-expectancy should be treated with the lowest dose of levodopa required to maintain motor function. For the vast majority though, no clear guidance can be given. Further large-scale pragmatic trials in large numbers of patients over parolonged periods are urgently required.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A02 01      @0 LANCAO
A03   1    @0 Lancet : (Br. ed.)
A05       @2 360
A06       @2 9347
A08 01  1  ENG  @1 Dopamine agonist monotherapy in Parkinson's disease
A11 01  1    @1 CLARKE (C. E.)
A11 02  1    @1 GUTTMAN (M.)
A14 01      @1 Department of Neurology, University of Birmingham @2 Birmingham @3 GBR @Z 1 aut.
A14 02      @1 Division of Neurology, University of Toronto @2 Ontario @3 CAN @Z 2 aut.
A20       @1 1767-1769
A21       @1 2002
A23 01      @0 ENG
A43 01      @1 INIST @2 5004 @5 354000106868720140
A44       @0 0000 @1 © 2003 INIST-CNRS. All rights reserved.
A45       @0 20 ref.
A47 01  1    @0 03-0040197
A60       @1 P
A61       @0 A
A64 01  1    @0 Lancet : (British edition)
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C01 01    ENG  @0 Context Levodone is the oid standard therapy for Parkinson's disease. However, long-term treatment leads to involutary movements and response fluctuations which add to the compixities of later disease management. In addition, preclinical evidence suggests that levodopa is toxic to dopaminergic neurons. These problems have led to a move away from levodopa towards initial monotherapy with a dopamine agonist. Starting point Positron-emission tomography (PET) and single-photon emission compouted tomography (SPECT) tracers have been developed which may be considered surrogate markers for remaining dopaminergic neurons, in a randomised controlled trial in patients with early Parkinson's disease, the Parkinson Study Group used -β-CIT SPECT UAMA 2002; 287: 1653-61). Those catients given pramipexole had significantly reduced loss of striatal uptake at 46 months compared with these given levodope (16.0% vs 25.5%). In a similar trial. Aian Whose and colleagues used DOPA PET (Neurology 2002; 58 [suppl 3]: A82-83), Patients given ropinirole had significantly reduced loss of striatal uptake at 24 months compared with those given levedope (13% vs 20%). These studies suggest that agonist monotherapy may be neuroprotective and/or that levodopa is toxic. This work has been enticised as the SPECT results may have resulted from a differential effect of the agonist and levodopa on the regulation of the dopamine transporter, thereby influencing the imaging outcome measure. Other criticisms include insufficient data on the use of the potential neuroprotectant selegiline and patients on pramipexole in the SPECT study appear to have been clinically slow progressors. Single clinical trials with each of the four modern egenists compared with levodope show that as monotherapy the agonists delay the onset of invotuntary movements, although at the expense of poorer treatment of motor impairments and disability and more depaminergic adverse events. The only health-related quality of life data show no difference between pramipexole and levodopa after 4 years. No information on health-economics measures is available but agonists cost two to three times as much as levodopa. Where next? Young patients should be treated with agonist monotherapy since the trials included predominantly younger patients who have a higher incidence of motor complications. Those with significant co-morbidity, dementia, or a short life-expectancy should be treated with the lowest dose of levodopa required to maintain motor function. For the vast majority though, no clear guidance can be given. Further large-scale pragmatic trials in large numbers of patients over parolonged periods are urgently required.
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C07 03  X  SPA  @0 Encéfalo patología @5 39
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N21       @1 020
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Format Inist (serveur)

NO : PASCAL 03-0040197 INIST
ET : Dopamine agonist monotherapy in Parkinson's disease
AU : CLARKE (C. E.); GUTTMAN (M.)
AF : Department of Neurology, University of Birmingham/Birmingham/Royaume-Uni (1 aut.); Division of Neurology, University of Toronto/Ontario/Canada (2 aut.)
DT : Publication en série; Niveau analytique
SO : Lancet : (British edition); ISSN 0140-6736; Coden LANCAO; Royaume-Uni; Da. 2002; Vol. 360; No. 9347; Pp. 1767-1769; Bibl. 20 ref.
LA : Anglais
EA : Context Levodone is the oid standard therapy for Parkinson's disease. However, long-term treatment leads to involutary movements and response fluctuations which add to the compixities of later disease management. In addition, preclinical evidence suggests that levodopa is toxic to dopaminergic neurons. These problems have led to a move away from levodopa towards initial monotherapy with a dopamine agonist. Starting point Positron-emission tomography (PET) and single-photon emission compouted tomography (SPECT) tracers have been developed which may be considered surrogate markers for remaining dopaminergic neurons, in a randomised controlled trial in patients with early Parkinson's disease, the Parkinson Study Group used -β-CIT SPECT UAMA 2002; 287: 1653-61). Those catients given pramipexole had significantly reduced loss of striatal uptake at 46 months compared with these given levodope (16.0% vs 25.5%). In a similar trial. Aian Whose and colleagues used DOPA PET (Neurology 2002; 58 [suppl 3]: A82-83), Patients given ropinirole had significantly reduced loss of striatal uptake at 24 months compared with those given levedope (13% vs 20%). These studies suggest that agonist monotherapy may be neuroprotective and/or that levodopa is toxic. This work has been enticised as the SPECT results may have resulted from a differential effect of the agonist and levodopa on the regulation of the dopamine transporter, thereby influencing the imaging outcome measure. Other criticisms include insufficient data on the use of the potential neuroprotectant selegiline and patients on pramipexole in the SPECT study appear to have been clinically slow progressors. Single clinical trials with each of the four modern egenists compared with levodope show that as monotherapy the agonists delay the onset of invotuntary movements, although at the expense of poorer treatment of motor impairments and disability and more depaminergic adverse events. The only health-related quality of life data show no difference between pramipexole and levodopa after 4 years. No information on health-economics measures is available but agonists cost two to three times as much as levodopa. Where next? Young patients should be treated with agonist monotherapy since the trials included predominantly younger patients who have a higher incidence of motor complications. Those with significant co-morbidity, dementia, or a short life-expectancy should be treated with the lowest dose of levodopa required to maintain motor function. For the vast majority though, no clear guidance can be given. Further large-scale pragmatic trials in large numbers of patients over parolonged periods are urgently required.
CC : 002B02B06; 002B17G
FD : Parkinson maladie; Pramipexole; Agoniste; Récepteur dopaminergique D2; Stimulant dopaminergique; Antiparkinsonien; Neuroprotecteur; Effet biologique; Traitement; Chimiothérapie; Homme
FG : Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative
ED : Parkinson disease; Pramipexole; Agonist; D2 Dopamine receptor; Dopamine agonist; Antiparkinson agent; Neuroprotective agent; Biological effect; Treatment; Chemotherapy; Human
EG : Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease
SD : Parkinson enfermedad; Pramipexol; Agonista; Receptor dopaminérgico D2; Estimulante dopaminérgico; Antiparkinsoniano; Neuroprotector; Efecto biológico; Tratamiento; Quimioterapia; Hombre
LO : INIST-5004.354000106868720140
ID : 03-0040197

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Pascal:03-0040197

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<NO>PASCAL 03-0040197 INIST</NO>
<ET>Dopamine agonist monotherapy in Parkinson's disease</ET>
<AU>CLARKE (C. E.); GUTTMAN (M.)</AU>
<AF>Department of Neurology, University of Birmingham/Birmingham/Royaume-Uni (1 aut.); Division of Neurology, University of Toronto/Ontario/Canada (2 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Lancet : (British edition); ISSN 0140-6736; Coden LANCAO; Royaume-Uni; Da. 2002; Vol. 360; No. 9347; Pp. 1767-1769; Bibl. 20 ref.</SO>
<LA>Anglais</LA>
<EA>Context Levodone is the oid standard therapy for Parkinson's disease. However, long-term treatment leads to involutary movements and response fluctuations which add to the compixities of later disease management. In addition, preclinical evidence suggests that levodopa is toxic to dopaminergic neurons. These problems have led to a move away from levodopa towards initial monotherapy with a dopamine agonist. Starting point Positron-emission tomography (PET) and single-photon emission compouted tomography (SPECT) tracers have been developed which may be considered surrogate markers for remaining dopaminergic neurons, in a randomised controlled trial in patients with early Parkinson's disease, the Parkinson Study Group used -β-CIT SPECT UAMA 2002; 287: 1653-61). Those catients given pramipexole had significantly reduced loss of striatal uptake at 46 months compared with these given levodope (16.0% vs 25.5%). In a similar trial. Aian Whose and colleagues used DOPA PET (Neurology 2002; 58 [suppl 3]: A82-83), Patients given ropinirole had significantly reduced loss of striatal uptake at 24 months compared with those given levedope (13% vs 20%). These studies suggest that agonist monotherapy may be neuroprotective and/or that levodopa is toxic. This work has been enticised as the SPECT results may have resulted from a differential effect of the agonist and levodopa on the regulation of the dopamine transporter, thereby influencing the imaging outcome measure. Other criticisms include insufficient data on the use of the potential neuroprotectant selegiline and patients on pramipexole in the SPECT study appear to have been clinically slow progressors. Single clinical trials with each of the four modern egenists compared with levodope show that as monotherapy the agonists delay the onset of invotuntary movements, although at the expense of poorer treatment of motor impairments and disability and more depaminergic adverse events. The only health-related quality of life data show no difference between pramipexole and levodopa after 4 years. No information on health-economics measures is available but agonists cost two to three times as much as levodopa. Where next? Young patients should be treated with agonist monotherapy since the trials included predominantly younger patients who have a higher incidence of motor complications. Those with significant co-morbidity, dementia, or a short life-expectancy should be treated with the lowest dose of levodopa required to maintain motor function. For the vast majority though, no clear guidance can be given. Further large-scale pragmatic trials in large numbers of patients over parolonged periods are urgently required.</EA>
<CC>002B02B06; 002B17G</CC>
<FD>Parkinson maladie; Pramipexole; Agoniste; Récepteur dopaminergique D2; Stimulant dopaminergique; Antiparkinsonien; Neuroprotecteur; Effet biologique; Traitement; Chimiothérapie; Homme</FD>
<FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative</FG>
<ED>Parkinson disease; Pramipexole; Agonist; D2 Dopamine receptor; Dopamine agonist; Antiparkinson agent; Neuroprotective agent; Biological effect; Treatment; Chemotherapy; Human</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease</EG>
<SD>Parkinson enfermedad; Pramipexol; Agonista; Receptor dopaminérgico D2; Estimulante dopaminérgico; Antiparkinsoniano; Neuroprotector; Efecto biológico; Tratamiento; Quimioterapia; Hombre</SD>
<LO>INIST-5004.354000106868720140</LO>
<ID>03-0040197</ID>
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