Slower progression of Parkinson's disease with ropinirole versus levodopa: The REAL‐PET study
Identifieur interne : 001225 ( Istex/Curation ); précédent : 001224; suivant : 001226Slower progression of Parkinson's disease with ropinirole versus levodopa: The REAL‐PET study
Auteurs : Alan L. Whone [Royaume-Uni] ; Ray L. Watts [États-Unis] ; A. Jon Stoessl [Canada] ; Margaret Davis [États-Unis] ; Sven Reske [Allemagne] ; Claude Nahmias ; Anthony E. Lang [Canada] ; Olivier Rascol [France] ; Maria J. Ribeiro [France] ; Philippe Remy [France] ; Werner H. Poewe [Autriche] ; Robert A. Hauser [États-Unis] ; David J. Brooks [Royaume-Uni]Source :
- Annals of Neurology [ 0364-5134 ] ; 2003-07.
Abstract
Preclinical studies suggest ropinirole (a D2/D3 dopamine agonist) may be neuroprotective in Parkinson's disease (PD), and a pilot clinical study using 18F‐dopa positron emission tomography (PET) suggested a slower loss of striatal dopamine storage with ropinirole compared with levodopa. This prospective, 2‐year, randomized, double‐blind, multinational study compared the rates of loss of dopamine‐terminal function in de novo patients with clinical and 18F‐dopa PET evidence of early PD, randomized 1 to 1 to receive either ropinirole or levodopa. The primary outcome measure was reduction in putamen 18F‐dopa uptake (Ki) between baseline and 2‐year PET. Of 186, 162 randomized patients were eligible for analysis. A blinded, central, region‐of‐interest analysis showed a significantly lower reduction (p = 0.022) in putamen Ki over 2 years with ropinirole (−13.4%; n = 68) compared with levodopa (−20.3%; n = 59; 95% confidence interval [CI], 0.65–13.06). Statistical parametric mapping localized lesser reductions in 18F‐dopa uptake in the putamen and substantia nigra with ropinirole. The greatest Ki decrease in each group was in the putamen (ropinirole, −14.1%; levodopa, −22.9%; 95% CI, 4.24–13.3), but the decrease was significantly lower with ropinirole compared with levodopa (p < 0.001). Ropinirole is associated with slower progression of PD than levodopa as assessed by 18F‐dopa PET. Ann Neurol 2003
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DOI: 10.1002/ana.10609
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Lang</name><affiliation wicri:level="1"><mods:affiliation>Division of Neurology, Department of Medicine, University of Toronto, Ontario, Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Department of Medicine, University of Toronto, Ontario</wicri:regionArea></affiliation></author><author><name sortKey="Rascol, Olivier" sort="Rascol, Olivier" uniqKey="Rascol O" first="Olivier" last="Rascol">Olivier Rascol</name><affiliation wicri:level="3"><mods:affiliation>Department of Clinical Pharmacology, Clinical Investigation Centre, INSERM U455, Toulouse University Hospital, Toulouse</mods:affiliation><country>France</country><placeName><settlement type="city">Toulouse</settlement><region type="region" nuts="2">Occitanie (région administrative)</region><region type="old region" nuts="2">Midi-Pyrénées</region></placeName><wicri:orgArea>Department of Clinical Pharmacology, Clinical Investigation Centre, INSERM U455, Toulouse University Hospital</wicri:orgArea></affiliation></author><author><name sortKey="Ribeiro, Maria J" sort="Ribeiro, Maria J" uniqKey="Ribeiro M" first="Maria J." last="Ribeiro">Maria J. Ribeiro</name><affiliation wicri:level="1"><mods:affiliation>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay, France</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay</wicri:regionArea></affiliation></author><author><name sortKey="Remy, Philippe" sort="Remy, Philippe" uniqKey="Remy P" first="Philippe" last="Remy">Philippe Remy</name><affiliation wicri:level="1"><mods:affiliation>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay, France</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay</wicri:regionArea></affiliation></author><author><name sortKey="Poewe, Werner H" sort="Poewe, Werner H" uniqKey="Poewe W" first="Werner H." last="Poewe">Werner H. Poewe</name><affiliation wicri:level="1"><mods:affiliation>Department of Clinical Neurology, University of Innsbruck, Innsbruck, Austria</mods:affiliation><country xml:lang="fr">Autriche</country><wicri:regionArea>Department of Clinical Neurology, University of Innsbruck, Innsbruck</wicri:regionArea></affiliation></author><author><name sortKey="Hauser, Robert A" sort="Hauser, Robert A" uniqKey="Hauser R" first="Robert A." last="Hauser">Robert A. Hauser</name><affiliation wicri:level="2"><mods:affiliation>University of South Florida and Tampa General Healthcare, Tampa, FL</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Floride</region></placeName><wicri:cityArea>University of South Florida and Tampa General Healthcare, Tampa</wicri:cityArea></affiliation></author><author><name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. Brooks</name><affiliation wicri:level="1"><mods:affiliation>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</mods:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Faculty of Medicine, Imperial College, Hammersmith Hospital, London</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, UK</mods:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Faculty of Medicine, Imperial College, Hammersmith Hospital, London</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2003-07">2003-07</date><biblScope unit="volume">54</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="93">93</biblScope><biblScope unit="page" to="101">101</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">0787EB91885A5AF7606EBCBF69CF2E45C0539042</idno><idno type="DOI">10.1002/ana.10609</idno><idno type="ArticleID">ANA10609</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Preclinical studies suggest ropinirole (a D2/D3 dopamine agonist) may be neuroprotective in Parkinson's disease (PD), and a pilot clinical study using 18F‐dopa positron emission tomography (PET) suggested a slower loss of striatal dopamine storage with ropinirole compared with levodopa. This prospective, 2‐year, randomized, double‐blind, multinational study compared the rates of loss of dopamine‐terminal function in de novo patients with clinical and 18F‐dopa PET evidence of early PD, randomized 1 to 1 to receive either ropinirole or levodopa. The primary outcome measure was reduction in putamen 18F‐dopa uptake (Ki) between baseline and 2‐year PET. Of 186, 162 randomized patients were eligible for analysis. A blinded, central, region‐of‐interest analysis showed a significantly lower reduction (p = 0.022) in putamen Ki over 2 years with ropinirole (−13.4%; n = 68) compared with levodopa (−20.3%; n = 59; 95% confidence interval [CI], 0.65–13.06). Statistical parametric mapping localized lesser reductions in 18F‐dopa uptake in the putamen and substantia nigra with ropinirole. The greatest Ki decrease in each group was in the putamen (ropinirole, −14.1%; levodopa, −22.9%; 95% CI, 4.24–13.3), but the decrease was significantly lower with ropinirole compared with levodopa (p < 0.001). Ropinirole is associated with slower progression of PD than levodopa as assessed by 18F‐dopa PET. Ann Neurol 2003</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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