Dopamine agonist monotherapy in Parkinson's disease
Identifieur interne : 000B44 ( PascalFrancis/Corpus ); précédent : 000B43; suivant : 000B45Dopamine agonist monotherapy in Parkinson's disease
Auteurs : C. E. Clarke ; M. GuttmanSource :
- Lancet : (British edition) [ 0140-6736 ] ; 2002.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
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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 |
Links to Exploration step
Pascal:03-0040197Le document en format XML
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<front><div type="abstract" xml:lang="en">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.</div>
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<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>
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<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>
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