Slower progression of Parkinson's disease with ropinirole versus levodopa: The REAL‐PET study
Identifieur interne : 001414 ( Main/Corpus ); précédent : 001413; suivant : 001415Slower progression of Parkinson's disease with ropinirole versus levodopa: The REAL‐PET study
Auteurs : Alan L. Whone ; Ray L. Watts ; A. Jon Stoessl ; Margaret Davis ; Sven Reske ; Claude Nahmias ; Anthony E. Lang ; Olivier Rascol ; Maria J. Ribeiro ; Philippe Remy ; Werner H. Poewe ; Robert A. Hauser ; David J. BrooksSource :
- 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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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Slower progression of Parkinson's disease with ropinirole versus levodopa: The REAL‐PET study</title><author><name sortKey="Whone, Alan L" sort="Whone, Alan L" uniqKey="Whone A" first="Alan L." last="Whone">Alan L. Whone</name><affiliation><mods:affiliation>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Watts, Ray L" sort="Watts, Ray L" uniqKey="Watts R" first="Ray L." last="Watts">Ray L. Watts</name><affiliation><mods:affiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</mods:affiliation></affiliation></author><author><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A. Jon" last="Stoessl">A. Jon Stoessl</name><affiliation><mods:affiliation>University of British Columbia, Vancouver, British Columbia, Canada</mods:affiliation></affiliation></author><author><name sortKey="Davis, Margaret" sort="Davis, Margaret" uniqKey="Davis M" first="Margaret" last="Davis">Margaret Davis</name><affiliation><mods:affiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</mods:affiliation></affiliation></author><author><name sortKey="Reske, Sven" sort="Reske, Sven" uniqKey="Reske S" first="Sven" last="Reske">Sven Reske</name><affiliation><mods:affiliation>Universität Ulm, Ulm, Germany</mods:affiliation></affiliation></author><author><name sortKey="Nahmias, Claude" sort="Nahmias, Claude" uniqKey="Nahmias C" first="Claude" last="Nahmias">Claude Nahmias</name><affiliation><mods:affiliation>McMaster University, Hamilton</mods:affiliation></affiliation></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E." last="Lang">Anthony E. 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Whone</name><affiliation><mods:affiliation>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Watts, Ray L" sort="Watts, Ray L" uniqKey="Watts R" first="Ray L." last="Watts">Ray L. Watts</name><affiliation><mods:affiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</mods:affiliation></affiliation></author><author><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A. Jon" last="Stoessl">A. Jon Stoessl</name><affiliation><mods:affiliation>University of British Columbia, Vancouver, British Columbia, Canada</mods:affiliation></affiliation></author><author><name sortKey="Davis, Margaret" sort="Davis, Margaret" uniqKey="Davis M" first="Margaret" last="Davis">Margaret Davis</name><affiliation><mods:affiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</mods:affiliation></affiliation></author><author><name sortKey="Reske, Sven" sort="Reske, Sven" uniqKey="Reske S" first="Sven" last="Reske">Sven Reske</name><affiliation><mods:affiliation>Universität Ulm, Ulm, Germany</mods:affiliation></affiliation></author><author><name sortKey="Nahmias, Claude" sort="Nahmias, Claude" uniqKey="Nahmias C" first="Claude" last="Nahmias">Claude Nahmias</name><affiliation><mods:affiliation>McMaster University, Hamilton</mods:affiliation></affiliation></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E." last="Lang">Anthony E. Lang</name><affiliation><mods:affiliation>Division of Neurology, Department of Medicine, University of Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Rascol, Olivier" sort="Rascol, Olivier" uniqKey="Rascol O" first="Olivier" last="Rascol">Olivier Rascol</name><affiliation><mods:affiliation>Department of Clinical Pharmacology, Clinical Investigation Centre, INSERM U455, Toulouse University Hospital, Toulouse</mods:affiliation></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><mods:affiliation>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay, France</mods:affiliation></affiliation></author><author><name sortKey="Remy, Philippe" sort="Remy, Philippe" uniqKey="Remy P" first="Philippe" last="Remy">Philippe Remy</name><affiliation><mods:affiliation>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay, France</mods:affiliation></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><mods:affiliation>Department of Clinical Neurology, University of Innsbruck, Innsbruck, Austria</mods:affiliation></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><mods:affiliation>University of South Florida and Tampa General Healthcare, Tampa, FL</mods:affiliation></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><mods:affiliation>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</mods:affiliation></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><istex><corpusName>wiley</corpusName><author><json:item><name>Alan L. Whone MBChB, MRCP</name><affiliations><json:string>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Ray L. Watts MD</name><affiliations><json:string>Department of Neurology, Emory University School of Medicine, Atlanta, GA</json:string></affiliations></json:item><json:item><name>A. Jon Stoessl MD, FRCPC</name><affiliations><json:string>University of British Columbia, Vancouver, British Columbia, Canada</json:string></affiliations></json:item><json:item><name>Margaret Davis MD</name><affiliations><json:string>Department of Neurology, Emory University School of Medicine, Atlanta, GA</json:string></affiliations></json:item><json:item><name>Sven Reske MD</name><affiliations><json:string>Universität Ulm, Ulm, Germany</json:string></affiliations></json:item><json:item><name>Claude Nahmias PhD</name><affiliations><json:string>McMaster University, Hamilton</json:string></affiliations></json:item><json:item><name>Anthony E. Lang MD, FRCPC</name><affiliations><json:string>Division of Neurology, Department of Medicine, University of Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Olivier Rascol MD, PhD</name><affiliations><json:string>Department of Clinical Pharmacology, Clinical Investigation Centre, INSERM U455, Toulouse University Hospital, Toulouse</json:string></affiliations></json:item><json:item><name>Maria J. Ribeiro MD</name><affiliations><json:string>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay, France</json:string></affiliations></json:item><json:item><name>Philippe Remy MD, PhD</name><affiliations><json:string>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay, France</json:string></affiliations></json:item><json:item><name>Werner H. Poewe MD</name><affiliations><json:string>Department of Clinical Neurology, University of Innsbruck, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Robert A. Hauser MD</name><affiliations><json:string>University of South Florida and Tampa General Healthcare, Tampa, FL</json:string></affiliations></json:item><json:item><name>David J. Brooks MD, DSc, FRCP, FMed Sci</name><affiliations><json:string>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</json:string></affiliations></json:item></author><articleId><json:string>ANA10609</json:string></articleId><language><json:string>eng</json:string></language><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. 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Jon</forename><surname>Stoessl</surname></persName><roleName type="degree">MD, FRCPC</roleName><affiliation>University of British Columbia, Vancouver, British Columbia, Canada</affiliation></author><author><persName><forename type="first">Margaret</forename><surname>Davis</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</affiliation></author><author><persName><forename type="first">Sven</forename><surname>Reske</surname></persName><roleName type="degree">MD</roleName><affiliation>Universität Ulm, Ulm, Germany</affiliation></author><author><persName><forename type="first">Claude</forename><surname>Nahmias</surname></persName><roleName type="degree">PhD</roleName><affiliation>McMaster University, Hamilton</affiliation></author><author><persName><forename type="first">Anthony E.</forename><surname>Lang</surname></persName><roleName type="degree">MD, FRCPC</roleName><affiliation>Division of Neurology, Department of Medicine, University of Toronto, Ontario, Canada</affiliation></author><author><persName><forename type="first">Olivier</forename><surname>Rascol</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Clinical Pharmacology, Clinical Investigation Centre, INSERM U455, Toulouse University Hospital, Toulouse</affiliation></author><author><persName><forename type="first">Maria J.</forename><surname>Ribeiro</surname></persName><roleName type="degree">MD</roleName><affiliation>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay, France</affiliation></author><author><persName><forename type="first">Philippe</forename><surname>Remy</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay, France</affiliation></author><author><persName><forename type="first">Werner H.</forename><surname>Poewe</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Clinical Neurology, University of Innsbruck, Innsbruck, Austria</affiliation></author><author><persName><forename type="first">Robert A.</forename><surname>Hauser</surname></persName><roleName type="degree">MD</roleName><affiliation>University of South Florida and Tampa General Healthcare, Tampa, FL</affiliation></author><author><persName><forename type="first">David J.</forename><surname>Brooks</surname></persName><roleName type="degree">MD, DSc, FRCP, FMed Sci</roleName><note type="correspondence"><p>Correspondence: Faculty of Medicine, Imperial College, Hammersmith Hospital, London, UK</p></note><affiliation>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</affiliation></author></analytic><monogr><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="pISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><idno type="DOI">10.1002/(ISSN)1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="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></monogr><idno type="istex">0787EB91885A5AF7606EBCBF69CF2E45C0539042</idno><idno type="DOI">10.1002/ana.10609</idno><idno type="ArticleID">ANA10609</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2003</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>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</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Original Articles</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2002-08-19">Received</change><change when="2003-03-17">Registration</change><change when="2003-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/0787EB91885A5AF7606EBCBF69CF2E45C0539042/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8249</doi><issn type="print">0364-5134</issn><issn type="electronic">1531-8249</issn><idGroup><id type="product" value="ANA"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="ANNALS OF NEUROLOGY">Annals of Neurology</title><title type="short">Ann Neurol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="10"><doi origin="wiley" registered="yes">10.1002/ana.v54:1</doi><numberingGroup><numbering type="journalVolume" number="54">54</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2003-07">July 2003</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="13" status="forIssue"><doi origin="wiley" registered="yes">10.1002/ana.10609</doi><idGroup><id type="unit" value="ANA10609"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="articleCategory">Original Articles</title><title type="tocHeading1">Original Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2003 American Neurological Association</copyright><eventGroup><event type="manuscriptReceived" date="2002-08-19"></event><event type="manuscriptRevised" date="2003-03-04"></event><event type="manuscriptAccepted" date="2003-03-17"></event><event type="firstOnline" date="2003-05-14"></event><event type="publishedOnlineFinalForm" date="2003-06-25"></event><event type="publishedOnlineAcceptedOrEarlyUnpaginated" date="2003-05-14"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.4.7 mode:FullText source:FullText result:FullText" date="2011-02-24"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-03"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst">93</numbering><numbering type="pageLast">101</numbering></numberingGroup><correspondenceTo>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, UK</correspondenceTo><objectNameGroup><objectName elementName="appendix">Appendix</objectName></objectNameGroup><linkGroup><link type="toTypesetVersion" href="file:ANA.ANA10609.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="5"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="30"></count><count type="wordTotal" number="5540"></count></countGroup><titleGroup><title type="main" xml:lang="en">Slower progression of Parkinson's disease with ropinirole versus levodopa: The REAL‐PET study</title><title type="short" xml:lang="en">The REAL‐PET Study</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Alan L.</givenNames><familyName>Whone</familyName><degrees>MBChB, MRCP</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Ray L.</givenNames><familyName>Watts</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>A. Jon</givenNames><familyName>Stoessl</familyName><degrees>MD, FRCPC</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Margaret</givenNames><familyName>Davis</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Sven</givenNames><familyName>Reske</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Claude</givenNames><familyName>Nahmias</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af6"><personName><givenNames>Anthony E.</givenNames><familyName>Lang</familyName><degrees>MD, FRCPC</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af7"><personName><givenNames>Olivier</givenNames><familyName>Rascol</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af8"><personName><givenNames>Maria J.</givenNames><familyName>Ribeiro</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af8"><personName><givenNames>Philippe</givenNames><familyName>Remy</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af9"><personName><givenNames>Werner H.</givenNames><familyName>Poewe</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au12" creatorRole="author" affiliationRef="#af10"><personName><givenNames>Robert A.</givenNames><familyName>Hauser</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au13" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>David J.</givenNames><familyName>Brooks</familyName><degrees>MD, DSc, FRCP, FMed Sci</degrees></personName><contactDetails><email>david.brooks@csc.mrc.ac.uk</email></contactDetails></creator><creator xml:id="au14" creatorRole="author" noteRef="#fn1"><groupName>REAL‐PET Study Group</groupName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="CA" type="organization"><unparsedAffiliation>University of British Columbia, Vancouver, British Columbia, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>Universität Ulm, Ulm, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="CA" type="organization"><unparsedAffiliation>McMaster University, Hamilton</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="CA" type="organization"><unparsedAffiliation>Division of Neurology, Department of Medicine, University of Toronto, Ontario, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af7" countryCode="FR" type="organization"><unparsedAffiliation>Department of Clinical Pharmacology, Clinical Investigation Centre, INSERM U455, Toulouse University Hospital, Toulouse</unparsedAffiliation></affiliation><affiliation xml:id="af8" countryCode="FR" type="organization"><unparsedAffiliation>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay, France</unparsedAffiliation></affiliation><affiliation xml:id="af9" countryCode="AT" type="organization"><unparsedAffiliation>Department of Clinical Neurology, University of Innsbruck, Innsbruck, Austria</unparsedAffiliation></affiliation><affiliation xml:id="af10" countryCode="US" type="organization"><unparsedAffiliation>University of South Florida and Tampa General Healthcare, Tampa, FL</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>GlaxoSmithKline</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Preclinical studies suggest ropinirole (a D2/D3 dopamine agonist) may be neuroprotective in Parkinson's disease (PD), and a pilot clinical study using <sup>18</sup>F‐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 <sup>18</sup>F‐dopa PET evidence of early PD, randomized 1 to 1 to receive either ropinirole or levodopa. The primary outcome measure was reduction in putamen <sup>18</sup>F‐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 (<i>p</i> = 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 <sup>18</sup>F‐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 (<i>p</i> < 0.001). Ropinirole is associated with slower progression of PD than levodopa as assessed by <sup>18</sup>F‐dopa PET. Ann Neurol 2003</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>REAL‐PET study investigators are listed in the <link href="#app1">Appendix</link> on page 00.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Slower progression of Parkinson's disease with ropinirole versus levodopa: The REAL‐PET study</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>The REAL‐PET Study</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Slower progression of Parkinson's disease with ropinirole versus levodopa: The REAL‐PET study</title></titleInfo><name type="personal"><namePart type="given">Alan L.</namePart><namePart type="family">Whone</namePart><namePart type="termsOfAddress">MBChB, MRCP</namePart><affiliation>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ray L.</namePart><namePart type="family">Watts</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. Jon</namePart><namePart type="family">Stoessl</namePart><namePart type="termsOfAddress">MD, FRCPC</namePart><affiliation>University of British Columbia, Vancouver, British Columbia, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Margaret</namePart><namePart type="family">Davis</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Emory University School of Medicine, Atlanta, GA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sven</namePart><namePart type="family">Reske</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Universität Ulm, Ulm, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Claude</namePart><namePart type="family">Nahmias</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>McMaster University, Hamilton</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anthony E.</namePart><namePart type="family">Lang</namePart><namePart type="termsOfAddress">MD, FRCPC</namePart><affiliation>Division of Neurology, Department of Medicine, University of Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Olivier</namePart><namePart type="family">Rascol</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Clinical Pharmacology, Clinical Investigation Centre, INSERM U455, Toulouse University Hospital, Toulouse</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Maria J.</namePart><namePart type="family">Ribeiro</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Philippe</namePart><namePart type="family">Remy</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>CEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Werner H.</namePart><namePart type="family">Poewe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Clinical Neurology, University of Innsbruck, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert A.</namePart><namePart type="family">Hauser</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of South Florida and Tampa General Healthcare, Tampa, FL</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David J.</namePart><namePart type="family">Brooks</namePart><namePart type="termsOfAddress">MD, DSc, FRCP, FMed Sci</namePart><affiliation>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</affiliation><description>Correspondence: Faculty of Medicine, Imperial College, Hammersmith Hospital, London, UK</description><role><roleTerm type="text">author</roleTerm></role></name><name type="corporate"><namePart>REAL‐PET Study Group</namePart><description>Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United KingdomDepartment of Neurology, Emory University School of Medicine, Atlanta, GAUniversity of British Columbia, Vancouver, British Columbia, CanadaUniversität Ulm, Ulm, GermanyMcMaster University, HamiltonDivision of Neurology, Department of Medicine, University of Toronto, Ontario, CanadaDepartment of Clinical Pharmacology, Clinical Investigation Centre, INSERM U455, Toulouse University Hospital, ToulouseCEA‐CNRS URA 2210, Service Hospitalier F. Joliot, Orsay, FranceDepartment of Clinical Neurology, University of Innsbruck, Innsbruck, AustriaUniversity of South Florida and Tampa General Healthcare, Tampa, FL</description></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2003-07</dateIssued><dateCaptured encoding="w3cdtf">2002-08-19</dateCaptured><dateValid encoding="w3cdtf">2003-03-17</dateValid><copyrightDate encoding="w3cdtf">2003</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent><extent unit="tables">3</extent><extent unit="references">30</extent><extent unit="words">5540</extent></physicalDescription><abstract 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</abstract><note type="funding">GlaxoSmithKline</note><relatedItem type="host"><titleInfo><title>Annals of Neurology</title></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Original Articles</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>54</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>93</start><end>101</end><total>9</total></extent></part></relatedItem><identifier type="istex">0787EB91885A5AF7606EBCBF69CF2E45C0539042</identifier><identifier type="DOI">10.1002/ana.10609</identifier><identifier type="ArticleID">ANA10609</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 American Neurological Association</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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