Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: The STRIDE‐PD study
Identifieur interne : 000324 ( Main/Corpus ); précédent : 000323; suivant : 000325Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: The STRIDE‐PD study
Auteurs : Fabrizio Stocchi ; Olivier Rascol ; Karl Kieburtz ; Werner Poewe ; Joseph Jankovic ; Eduardo Tolosa ; Paulo Barone ; Anthony E. Lang ; C. Warren OlanowSource :
- Annals of Neurology [ 0364-5134 ] ; 2010-07.
Abstract
Objective: L‐dopa is the most widely used and most effective therapy for Parkinson disease (PD), but chronic treatment is associated with motor complications in the majority of patients. It has been hypothesized that providing more continuous delivery of L‐dopa to the brain would reduce the risk of motor complications, and that this might be accomplished by combining L‐dopa with entacapone, an inhibitor of catechol‐O‐methyltransferase, to extend its elimination half‐life. Methods: We performed a prospective 134‐week double‐blind trial comparing the risk of developing dyskinesia in 747 PD patients randomized to initiate L‐dopa therapy with L‐dopa/carbidopa (LC) or L‐dopa/carbidopa/entacapone (LCE), administered 4× daily at 3.5‐hour intervals. The primary endpoint was time to onset of dyskinesia. Results: In comparison to LC, patients receiving LCE had a shorter time to onset of dyskinesia (hazard ratio, 1.29; p = 0.04) and increased frequency at week 134 (42% vs 32%; p = 0.02). These effects were more pronounced in patients receiving dopamine agonists at baseline. Time to wearing off and motor scores were not significantly different, but trended in favor of LCE treatment. Patients in the LCE group received greater L‐dopa dose equivalents than LC‐treated patients (p < 0.001). Interpretation: Initiating L‐dopa therapy with LCE failed to delay the time of onset or reduce the frequency of dyskinesia compared to LC. In fact, LCE was associated with a shorter time to onset and increased frequency of dyskinesia compared to LC. These results may reflect that the treatment protocol employed did not provide continuous L‐dopa availability and the higher L‐dopa dose equivalents in the LCE group. ANN NEUROL 2010;68:18–27
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DOI: 10.1002/ana.22060
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: The STRIDE‐PD study</title><author><name sortKey="Stocchi, Fabrizio" sort="Stocchi, Fabrizio" uniqKey="Stocchi F" first="Fabrizio" last="Stocchi">Fabrizio Stocchi</name><affiliation><mods:affiliation>Institute of Neurology, IRCCS San Raffaele Pisana, Rome, Italy</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>INSERM U455, Clinical Investigation Center, Faculty of Medicine, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Clinical Pharmacology, Faculty of Medicine, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurosciences, Faculty of Medicine, Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Kieburtz, Karl" sort="Kieburtz, Karl" uniqKey="Kieburtz K" first="Karl" last="Kieburtz">Karl Kieburtz</name><affiliation><mods:affiliation>Department of Neurology, University of Rochester, Rochester, NY</mods:affiliation></affiliation></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation><mods:affiliation>Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, TX</mods:affiliation></affiliation></author><author><name sortKey="Tolosa, Eduardo" sort="Tolosa, Eduardo" uniqKey="Tolosa E" first="Eduardo" last="Tolosa">Eduardo Tolosa</name><affiliation><mods:affiliation>Neurology Service, Hospital Clinic, University of Barcelona, Barcelona, Spain</mods:affiliation></affiliation></author><author><name sortKey="Barone, Paulo" sort="Barone, Paulo" uniqKey="Barone P" first="Paulo" last="Barone">Paulo Barone</name><affiliation><mods:affiliation>Department of Neurological Sciences, University of Naples and IDC‐Hermitage, Naples, Italy</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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Warren Olanow</name><affiliation><mods:affiliation>Institute of Neurology, IRCCS San Raffaele Pisana, Rome, Italy</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, NY</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:3606364AF54F057814BFA79EB847BC4E60B58857</idno><date when="2010" year="2010">2010</date><idno type="doi">10.1002/ana.22060</idno><idno type="url">https://api.istex.fr/document/3606364AF54F057814BFA79EB847BC4E60B58857/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000324</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: The STRIDE‐PD study</title><author><name sortKey="Stocchi, Fabrizio" sort="Stocchi, Fabrizio" uniqKey="Stocchi F" first="Fabrizio" last="Stocchi">Fabrizio Stocchi</name><affiliation><mods:affiliation>Institute of Neurology, IRCCS San Raffaele Pisana, Rome, Italy</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>INSERM U455, Clinical Investigation Center, Faculty of Medicine, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Clinical Pharmacology, Faculty of Medicine, Toulouse, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurosciences, Faculty of Medicine, Toulouse, France</mods:affiliation></affiliation></author><author><name sortKey="Kieburtz, Karl" sort="Kieburtz, Karl" uniqKey="Kieburtz K" first="Karl" last="Kieburtz">Karl Kieburtz</name><affiliation><mods:affiliation>Department of Neurology, University of Rochester, Rochester, NY</mods:affiliation></affiliation></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation><mods:affiliation>Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name><affiliation><mods:affiliation>Department of Neurology, Baylor College of Medicine, Houston, TX</mods:affiliation></affiliation></author><author><name sortKey="Tolosa, Eduardo" sort="Tolosa, Eduardo" uniqKey="Tolosa E" first="Eduardo" last="Tolosa">Eduardo Tolosa</name><affiliation><mods:affiliation>Neurology Service, Hospital Clinic, University of Barcelona, Barcelona, Spain</mods:affiliation></affiliation></author><author><name sortKey="Barone, Paulo" sort="Barone, Paulo" uniqKey="Barone P" first="Paulo" last="Barone">Paulo Barone</name><affiliation><mods:affiliation>Department of Neurological Sciences, University of Naples and IDC‐Hermitage, Naples, Italy</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, University of Toronto, Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Olanow, C Warren" sort="Olanow, C Warren" uniqKey="Olanow C" first="C. Warren" last="Olanow">C. Warren Olanow</name><affiliation><mods:affiliation>Institute of Neurology, IRCCS San Raffaele Pisana, Rome, Italy</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, NY</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="2010-07">2010-07</date><biblScope unit="volume">68</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="18">18</biblScope><biblScope unit="page" to="27">27</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">3606364AF54F057814BFA79EB847BC4E60B58857</idno><idno type="DOI">10.1002/ana.22060</idno><idno type="ArticleID">ANA22060</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">Objective: L‐dopa is the most widely used and most effective therapy for Parkinson disease (PD), but chronic treatment is associated with motor complications in the majority of patients. It has been hypothesized that providing more continuous delivery of L‐dopa to the brain would reduce the risk of motor complications, and that this might be accomplished by combining L‐dopa with entacapone, an inhibitor of catechol‐O‐methyltransferase, to extend its elimination half‐life. Methods: We performed a prospective 134‐week double‐blind trial comparing the risk of developing dyskinesia in 747 PD patients randomized to initiate L‐dopa therapy with L‐dopa/carbidopa (LC) or L‐dopa/carbidopa/entacapone (LCE), administered 4× daily at 3.5‐hour intervals. The primary endpoint was time to onset of dyskinesia. Results: In comparison to LC, patients receiving LCE had a shorter time to onset of dyskinesia (hazard ratio, 1.29; p = 0.04) and increased frequency at week 134 (42% vs 32%; p = 0.02). These effects were more pronounced in patients receiving dopamine agonists at baseline. Time to wearing off and motor scores were not significantly different, but trended in favor of LCE treatment. Patients in the LCE group received greater L‐dopa dose equivalents than LC‐treated patients (p < 0.001). Interpretation: Initiating L‐dopa therapy with LCE failed to delay the time of onset or reduce the frequency of dyskinesia compared to LC. In fact, LCE was associated with a shorter time to onset and increased frequency of dyskinesia compared to LC. These results may reflect that the treatment protocol employed did not provide continuous L‐dopa availability and the higher L‐dopa dose equivalents in the LCE group. ANN NEUROL 2010;68:18–27</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Fabrizio Stocchi MD</name><affiliations><json:string>Institute of Neurology, IRCCS San Raffaele Pisana, Rome, Italy</json:string></affiliations></json:item><json:item><name>Olivier Rascol MD</name><affiliations><json:string>INSERM U455, Clinical Investigation Center, Faculty of Medicine, Toulouse, France</json:string><json:string>Department of Clinical Pharmacology, Faculty of Medicine, Toulouse, France</json:string><json:string>Department of Neurosciences, Faculty of Medicine, Toulouse, France</json:string></affiliations></json:item><json:item><name>Karl Kieburtz MD</name><affiliations><json:string>Department of Neurology, University of Rochester, Rochester, NY</json:string></affiliations></json:item><json:item><name>Werner Poewe MD</name><affiliations><json:string>Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Joseph Jankovic MD</name><affiliations><json:string>Department of Neurology, Baylor College of Medicine, Houston, TX</json:string></affiliations></json:item><json:item><name>Eduardo Tolosa MD</name><affiliations><json:string>Neurology Service, Hospital Clinic, University of Barcelona, Barcelona, Spain</json:string></affiliations></json:item><json:item><name>Paulo Barone MD</name><affiliations><json:string>Department of Neurological Sciences, University of Naples and IDC‐Hermitage, Naples, Italy</json:string></affiliations></json:item><json:item><name>Anthony E. Lang MD</name><affiliations><json:string>Division of Neurology, University of Toronto, Toronto, Canada</json:string></affiliations></json:item><json:item><name>C. Warren Olanow MD</name><affiliations><json:string>Institute of Neurology, IRCCS San Raffaele Pisana, Rome, Italy</json:string><json:string>Department of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, NY</json:string></affiliations></json:item></author><articleId><json:string>ANA22060</json:string></articleId><language><json:string>eng</json:string></language><abstract>Objective: L‐dopa is the most widely used and most effective therapy for Parkinson disease (PD), but chronic treatment is associated with motor complications in the majority of patients. It has been hypothesized that providing more continuous delivery of L‐dopa to the brain would reduce the risk of motor complications, and that this might be accomplished by combining L‐dopa with entacapone, an inhibitor of catechol‐O‐methyltransferase, to extend its elimination half‐life. Methods: We performed a prospective 134‐week double‐blind trial comparing the risk of developing dyskinesia in 747 PD patients randomized to initiate L‐dopa therapy with L‐dopa/carbidopa (LC) or L‐dopa/carbidopa/entacapone (LCE), administered 4× daily at 3.5‐hour intervals. The primary endpoint was time to onset of dyskinesia. Results: In comparison to LC, patients receiving LCE had a shorter time to onset of dyskinesia (hazard ratio, 1.29; p = 0.04) and increased frequency at week 134 (42% vs 32%; p = 0.02). These effects were more pronounced in patients receiving dopamine agonists at baseline. Time to wearing off and motor scores were not significantly different, but trended in favor of LCE treatment. Patients in the LCE group received greater L‐dopa dose equivalents than LC‐treated patients (p > 0.001). Interpretation: Initiating L‐dopa therapy with LCE failed to delay the time of onset or reduce the frequency of dyskinesia compared to LC. In fact, LCE was associated with a shorter time to onset and increased frequency of dyskinesia compared to LC. These results may reflect that the treatment protocol employed did not provide continuous L‐dopa availability and the higher L‐dopa dose equivalents in the LCE group. ANN NEUROL 2010;68:18–27</abstract><qualityIndicators><score>7.948</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 783 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1736</abstractCharCount><pdfWordCount>4948</pdfWordCount><pdfCharCount>32569</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>262</abstractWordCount></qualityIndicators><title>Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: The STRIDE‐PD study</title><genre><json:string>article</json:string></genre><host><volume>68</volume><publisherId><json:string>ANA</json:string></publisherId><pages><total>10</total><last>27</last><first>18</first></pages><issn><json:string>0364-5134</json:string></issn><issue>1</issue><subject><json:item><value>Original Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8249</json:string></eissn><title>Annals of Neurology</title><doi><json:string>10.1002/(ISSN)1531-8249</json:string></doi></host><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1002/ana.22060</json:string></doi><id>3606364AF54F057814BFA79EB847BC4E60B58857</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/3606364AF54F057814BFA79EB847BC4E60B58857/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/3606364AF54F057814BFA79EB847BC4E60B58857/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/3606364AF54F057814BFA79EB847BC4E60B58857/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: The STRIDE‐PD study</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2010</date></publicationStmt><notesStmt><note>Novartis Pharma A.G.</note><note>Orion Copration</note><note>Orion Pharma</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: The STRIDE‐PD study</title><author><persName><forename type="first">Fabrizio</forename><surname>Stocchi</surname></persName><roleName type="degree">MD</roleName><affiliation>Institute of Neurology, IRCCS San Raffaele Pisana, Rome, Italy</affiliation></author><author><persName><forename type="first">Olivier</forename><surname>Rascol</surname></persName><roleName type="degree">MD</roleName><affiliation>INSERM U455, Clinical Investigation Center, Faculty of Medicine, Toulouse, France</affiliation><affiliation>Department of Clinical Pharmacology, Faculty of Medicine, Toulouse, France</affiliation><affiliation>Department of Neurosciences, Faculty of Medicine, Toulouse, France</affiliation></author><author><persName><forename type="first">Karl</forename><surname>Kieburtz</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, University of Rochester, Rochester, NY</affiliation></author><author><persName><forename type="first">Werner</forename><surname>Poewe</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</affiliation></author><author><persName><forename type="first">Joseph</forename><surname>Jankovic</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Baylor College of Medicine, Houston, TX</affiliation></author><author><persName><forename type="first">Eduardo</forename><surname>Tolosa</surname></persName><roleName type="degree">MD</roleName><affiliation>Neurology Service, Hospital Clinic, University of Barcelona, Barcelona, Spain</affiliation></author><author><persName><forename type="first">Paulo</forename><surname>Barone</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurological Sciences, University of Naples and IDC‐Hermitage, Naples, Italy</affiliation></author><author><persName><forename type="first">Anthony E.</forename><surname>Lang</surname></persName><roleName type="degree">MD</roleName><affiliation>Division of Neurology, University of Toronto, Toronto, Canada</affiliation></author><author><persName><forename type="first">C. Warren</forename><surname>Olanow</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Departments of Neurology and Neuroscience, Mount Sinai School of Medicine, 1 Gustave Levy Place, Annenberg 20‐82, New York, NY 10029</p></note><affiliation>Institute of Neurology, IRCCS San Raffaele Pisana, Rome, Italy</affiliation><affiliation>Department of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, NY</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="2010-07"></date><biblScope unit="volume">68</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="18">18</biblScope><biblScope unit="page" to="27">27</biblScope></imprint></monogr><idno type="istex">3606364AF54F057814BFA79EB847BC4E60B58857</idno><idno type="DOI">10.1002/ana.22060</idno><idno type="ArticleID">ANA22060</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Objective: L‐dopa is the most widely used and most effective therapy for Parkinson disease (PD), but chronic treatment is associated with motor complications in the majority of patients. It has been hypothesized that providing more continuous delivery of L‐dopa to the brain would reduce the risk of motor complications, and that this might be accomplished by combining L‐dopa with entacapone, an inhibitor of catechol‐O‐methyltransferase, to extend its elimination half‐life. Methods: We performed a prospective 134‐week double‐blind trial comparing the risk of developing dyskinesia in 747 PD patients randomized to initiate L‐dopa therapy with L‐dopa/carbidopa (LC) or L‐dopa/carbidopa/entacapone (LCE), administered 4× daily at 3.5‐hour intervals. The primary endpoint was time to onset of dyskinesia. Results: In comparison to LC, patients receiving LCE had a shorter time to onset of dyskinesia (hazard ratio, 1.29; p = 0.04) and increased frequency at week 134 (42% vs 32%; p = 0.02). These effects were more pronounced in patients receiving dopamine agonists at baseline. Time to wearing off and motor scores were not significantly different, but trended in favor of LCE treatment. Patients in the LCE group received greater L‐dopa dose equivalents than LC‐treated patients (p < 0.001). Interpretation: Initiating L‐dopa therapy with LCE failed to delay the time of onset or reduce the frequency of dyskinesia compared to LC. In fact, LCE was associated with a shorter time to onset and increased frequency of dyskinesia compared to LC. These results may reflect that the treatment protocol employed did not provide continuous L‐dopa availability and the higher L‐dopa dose equivalents in the LCE group. 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number="10"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">Original Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2010 American Neurological Association</copyright><eventGroup><event type="manuscriptReceived" date="2009-12-22"></event><event type="manuscriptRevised" date="2010-03-17"></event><event type="manuscriptAccepted" date="2010-04-05"></event><event type="publishedOnlineAccepted" date="2010-04-23"></event><event type="firstOnline" date="2010-04-23"></event><event type="publishedOnlineFinalForm" date="2010-06-25"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.15 mode:FullText source:FullText result:FullText" date="2010-07-21"></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">18</numbering><numbering type="pageLast">27</numbering></numberingGroup><correspondenceTo>Departments of Neurology and Neuroscience, Mount Sinai School of Medicine, 1 Gustave Levy Place, Annenberg 20‐82, New York, NY 10029</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANA.ANA22060.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="6"></count><count type="referenceTotal" number="33"></count><count type="wordTotal" number="5961"></count></countGroup><titleGroup><title type="main" xml:lang="en">Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: The STRIDE‐PD study</title><title type="short" xml:lang="en">L‐Dopa/Carbidopa in PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Fabrizio</givenNames><familyName>Stocchi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2 #af3 #af4"><personName><givenNames>Olivier</givenNames><familyName>Rascol</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Karl</givenNames><familyName>Kieburtz</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af6"><personName><givenNames>Werner</givenNames><familyName>Poewe</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af7"><personName><givenNames>Joseph</givenNames><familyName>Jankovic</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af8"><personName><givenNames>Eduardo</givenNames><familyName>Tolosa</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af9"><personName><givenNames>Paulo</givenNames><familyName>Barone</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af10"><personName><givenNames>Anthony E.</givenNames><familyName>Lang</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1 #af11" corresponding="yes"><personName><givenNames>C. Warren</givenNames><familyName>Olanow</familyName><degrees>MD</degrees></personName><contactDetails><email>Warren.olanow@mssm.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="IT" type="organization"><unparsedAffiliation>Institute of Neurology, IRCCS San Raffaele Pisana, Rome, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FR" type="organization"><unparsedAffiliation>INSERM U455, Clinical Investigation Center, Faculty of Medicine, Toulouse, France</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FR" type="organization"><unparsedAffiliation>Department of Clinical Pharmacology, Faculty of Medicine, Toulouse, France</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="FR" type="organization"><unparsedAffiliation>Department of Neurosciences, Faculty of Medicine, Toulouse, France</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, University of Rochester, Rochester, NY</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="AT" type="organization"><unparsedAffiliation>Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</unparsedAffiliation></affiliation><affiliation xml:id="af7" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Baylor College of Medicine, Houston, TX</unparsedAffiliation></affiliation><affiliation xml:id="af8" countryCode="ES" type="organization"><unparsedAffiliation>Neurology Service, Hospital Clinic, University of Barcelona, Barcelona, Spain</unparsedAffiliation></affiliation><affiliation xml:id="af9" countryCode="IT" type="organization"><unparsedAffiliation>Department of Neurological Sciences, University of Naples and IDC‐Hermitage, Naples, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af10" countryCode="CA" type="organization"><unparsedAffiliation>Division of Neurology, University of Toronto, Toronto, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af11" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, NY</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>Novartis Pharma A.G.</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Orion Copration</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Orion Pharma</fundingAgency></fundingInfo><supportingInformation><p> Additional Supporting Information can be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:03645134:media:ana22060:ANA_22060_sm_Supptable"></mediaResource><caption>Supplementary table</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><section xml:id="abs1-1"><title type="main">Objective</title><p>L‐dopa is the most widely used and most effective therapy for Parkinson disease (PD), but chronic treatment is associated with motor complications in the majority of patients. It has been hypothesized that providing more continuous delivery of L‐dopa to the brain would reduce the risk of motor complications, and that this might be accomplished by combining L‐dopa with entacapone, an inhibitor of catechol‐O‐methyltransferase, to extend its elimination half‐life.</p></section><section xml:id="abs1-2"><title type="main">Methods</title><p>We performed a prospective 134‐week double‐blind trial comparing the risk of developing dyskinesia in 747 PD patients randomized to initiate L‐dopa therapy with L‐dopa/carbidopa (LC) or L‐dopa/carbidopa/entacapone (LCE), administered 4× daily at 3.5‐hour intervals. The primary endpoint was time to onset of dyskinesia.</p></section><section xml:id="abs1-3"><title type="main">Results</title><p>In comparison to LC, patients receiving LCE had a shorter time to onset of dyskinesia (hazard ratio, 1.29; <i>p</i> = 0.04) and increased frequency at week 134 (42% vs 32%; <i>p</i> = 0.02). These effects were more pronounced in patients receiving dopamine agonists at baseline. Time to wearing off and motor scores were not significantly different, but trended in favor of LCE treatment. Patients in the LCE group received greater L‐dopa dose equivalents than LC‐treated patients (<i>p</i> < 0.001).</p></section><section xml:id="abs1-4"><title type="main">Interpretation</title><p>Initiating L‐dopa therapy with LCE failed to delay the time of onset or reduce the frequency of dyskinesia compared to LC. In fact, LCE was associated with a shorter time to onset and increased frequency of dyskinesia compared to LC. These results may reflect that the treatment protocol employed did not provide continuous L‐dopa availability and the higher L‐dopa dose equivalents in the LCE group. ANN NEUROL 2010;68:18–27</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: The STRIDE‐PD study</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>L‐Dopa/Carbidopa in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: The STRIDE‐PD study</title></titleInfo><name type="personal"><namePart type="given">Fabrizio</namePart><namePart type="family">Stocchi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute of Neurology, IRCCS San Raffaele Pisana, Rome, Italy</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</namePart><affiliation>INSERM U455, Clinical Investigation Center, Faculty of Medicine, Toulouse, France</affiliation><affiliation>Department of Clinical Pharmacology, Faculty of Medicine, Toulouse, France</affiliation><affiliation>Department of Neurosciences, Faculty of Medicine, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Karl</namePart><namePart type="family">Kieburtz</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Rochester, Rochester, NY</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Werner</namePart><namePart type="family">Poewe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joseph</namePart><namePart type="family">Jankovic</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Baylor College of Medicine, Houston, TX</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eduardo</namePart><namePart type="family">Tolosa</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Neurology Service, Hospital Clinic, University of Barcelona, Barcelona, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paulo</namePart><namePart type="family">Barone</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, University of Naples and IDC‐Hermitage, Naples, Italy</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</namePart><affiliation>Division of Neurology, University of Toronto, Toronto, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. Warren</namePart><namePart type="family">Olanow</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute of Neurology, IRCCS San Raffaele Pisana, Rome, Italy</affiliation><affiliation>Department of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, NY</affiliation><description>Correspondence: Departments of Neurology and Neuroscience, Mount Sinai School of Medicine, 1 Gustave Levy Place, Annenberg 20‐82, New York, NY 10029</description><role><roleTerm type="text">author</roleTerm></role></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">2010-07</dateIssued><dateCaptured encoding="w3cdtf">2009-12-22</dateCaptured><dateValid encoding="w3cdtf">2010-04-05</dateValid><copyrightDate encoding="w3cdtf">2010</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">2</extent><extent unit="tables">6</extent><extent unit="references">33</extent><extent unit="words">5961</extent></physicalDescription><abstract lang="en">Objective: L‐dopa is the most widely used and most effective therapy for Parkinson disease (PD), but chronic treatment is associated with motor complications in the majority of patients. It has been hypothesized that providing more continuous delivery of L‐dopa to the brain would reduce the risk of motor complications, and that this might be accomplished by combining L‐dopa with entacapone, an inhibitor of catechol‐O‐methyltransferase, to extend its elimination half‐life. Methods: We performed a prospective 134‐week double‐blind trial comparing the risk of developing dyskinesia in 747 PD patients randomized to initiate L‐dopa therapy with L‐dopa/carbidopa (LC) or L‐dopa/carbidopa/entacapone (LCE), administered 4× daily at 3.5‐hour intervals. The primary endpoint was time to onset of dyskinesia. Results: In comparison to LC, patients receiving LCE had a shorter time to onset of dyskinesia (hazard ratio, 1.29; p = 0.04) and increased frequency at week 134 (42% vs 32%; p = 0.02). These effects were more pronounced in patients receiving dopamine agonists at baseline. Time to wearing off and motor scores were not significantly different, but trended in favor of LCE treatment. Patients in the LCE group received greater L‐dopa dose equivalents than LC‐treated patients (p < 0.001). Interpretation: Initiating L‐dopa therapy with LCE failed to delay the time of onset or reduce the frequency of dyskinesia compared to LC. In fact, LCE was associated with a shorter time to onset and increased frequency of dyskinesia compared to LC. These results may reflect that the treatment protocol employed did not provide continuous L‐dopa availability and the higher L‐dopa dose equivalents in the LCE group. ANN NEUROL 2010;68:18–27</abstract><note type="funding">Novartis Pharma A.G.</note><note type="funding">Orion Copration</note><note type="funding">Orion Pharma</note><relatedItem type="host"><titleInfo><title>Annals of Neurology</title></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Additional Supporting Information can be found in the online version of this article.Supporting Info Item: Supplementary table - </note><subject><genre>article category</genre><topic>Original Article</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>2010</date><detail type="volume"><caption>vol.</caption><number>68</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>18</start><end>27</end><total>10</total></extent></part></relatedItem><identifier type="istex">3606364AF54F057814BFA79EB847BC4E60B58857</identifier><identifier type="DOI">10.1002/ana.22060</identifier><identifier type="ArticleID">ANA22060</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 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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