Levodopa response in early Parkinson's disease
Identifieur interne : 000466 ( Istex/Corpus ); précédent : 000465; suivant : 000467Levodopa response in early Parkinson's disease
Auteurs : Robert A. Hauser ; Peggy Auinger ; David OakesSource :
- Movement Disorders [ 0885-3185 ] ; 2009-12-15.
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- KwdEn :
Abstract
To further characterize the short‐term levodopa response in early PD, we performed a retrospective analysis of the ELLDOPA study which randomized 361 early PD subjects to placebo, levodopa 150, 300, or 600 mg/day. We evaluated change in UPDRS motor scores (UPDRSm) from baseline to weeks 9 and 24, and identified changes in UPDRSm that best discriminated treatment with levodopa from placebo. Linear regressions were used to determine associations between baseline characteristics and changes in UPDRSm. Mean percent improvement in UPDRSm in levodopa‐treated subjects was greater than that for placebo‐treated subjects (27.4% vs. 5.8% at 9 weeks, P < 0.001 and 26.2% vs. 4.0% at 24 weeks, P < 0.001). UPDRSm change at 9 weeks ranged from –92.9% (improvement) to 85.7% (worsening) for levodopa and –86.7% to 160% for placebo, and at 24 weeks ranged from –100.0% to 242.9% for levodopa and –87.5% to 112.5% for placebo. UPDRSm improvements of 22.0% at 9 weeks and 23.8% at 24 weeks best discriminated treatment with levodopa 300 mg/day (a common initial maintenance dosage in clinical practice) from placebo. Significant associations were not observed between baseline subject characteristics and magnitude of response from baseline to week 24. We conclude that although levodopa treatment significantly improved PD signs when compared with placebo, there was a wide range and considerable overlap in clinical responses to levodopa and placebo. A substantial proportion of subjects with early PD did not experience a robust response to levodopa. An improvement in UPDRSm of ∼22% best discriminated levodopa treatment from placebo. © 2009 Movement Disorder Society
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DOI: 10.1002/mds.22759
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ISTEX:9F45EA68C8DD26C12497539861EEF4E613A6FD64Le document en format XML
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Hauser</name><affiliation><mods:affiliation>Departments of Neurology, Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida, USA</mods:affiliation></affiliation></author><author><name sortKey="Auinger, Peggy" sort="Auinger, Peggy" uniqKey="Auinger P" first="Peggy" last="Auinger">Peggy Auinger</name><affiliation><mods:affiliation>Department of Neurology, University of Rochester, Rochester, New York, USA</mods:affiliation></affiliation></author><author><name sortKey="Oakes, David" sort="Oakes, David" uniqKey="Oakes D" first="David" last="Oakes">David Oakes</name><affiliation><mods:affiliation>Department of Biostatistics and Computational Biology, University of Rochester, Rochester, New York, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:9F45EA68C8DD26C12497539861EEF4E613A6FD64</idno><date when="2009" year="2009">2009</date><idno type="doi">10.1002/mds.22759</idno><idno type="url">https://api.istex.fr/document/9F45EA68C8DD26C12497539861EEF4E613A6FD64/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000466</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Levodopa response in early Parkinson's disease</title><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>Departments of Neurology, Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida, USA</mods:affiliation></affiliation></author><author><name sortKey="Auinger, Peggy" sort="Auinger, Peggy" uniqKey="Auinger P" first="Peggy" last="Auinger">Peggy Auinger</name><affiliation><mods:affiliation>Department of Neurology, University of Rochester, Rochester, New York, USA</mods:affiliation></affiliation></author><author><name sortKey="Oakes, David" sort="Oakes, David" uniqKey="Oakes D" first="David" last="Oakes">David Oakes</name><affiliation><mods:affiliation>Department of Biostatistics and Computational Biology, University of Rochester, Rochester, New York, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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We evaluated change in UPDRS motor scores (UPDRSm) from baseline to weeks 9 and 24, and identified changes in UPDRSm that best discriminated treatment with levodopa from placebo. Linear regressions were used to determine associations between baseline characteristics and changes in UPDRSm. Mean percent improvement in UPDRSm in levodopa‐treated subjects was greater than that for placebo‐treated subjects (27.4% vs. 5.8% at 9 weeks, P < 0.001 and 26.2% vs. 4.0% at 24 weeks, P < 0.001). UPDRSm change at 9 weeks ranged from –92.9% (improvement) to 85.7% (worsening) for levodopa and –86.7% to 160% for placebo, and at 24 weeks ranged from –100.0% to 242.9% for levodopa and –87.5% to 112.5% for placebo. UPDRSm improvements of 22.0% at 9 weeks and 23.8% at 24 weeks best discriminated treatment with levodopa 300 mg/day (a common initial maintenance dosage in clinical practice) from placebo. Significant associations were not observed between baseline subject characteristics and magnitude of response from baseline to week 24. We conclude that although levodopa treatment significantly improved PD signs when compared with placebo, there was a wide range and considerable overlap in clinical responses to levodopa and placebo. A substantial proportion of subjects with early PD did not experience a robust response to levodopa. An improvement in UPDRSm of ∼22% best discriminated levodopa treatment from placebo. © 2009 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Robert A. Hauser MD</name><affiliations><json:string>Departments of Neurology, Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida, USA</json:string></affiliations></json:item><json:item><name>Peggy Auinger MS</name><affiliations><json:string>Department of Neurology, University of Rochester, Rochester, New York, USA</json:string></affiliations></json:item><json:item><name>David Oakes PhD</name><affiliations><json:string>Department of Biostatistics and Computational Biology, University of Rochester, Rochester, New York, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>levodopa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>placebo</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>treatment</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>clinical response</value></json:item></subject><language><json:string>eng</json:string></language><abstract>To further characterize the short‐term levodopa response in early PD, we performed a retrospective analysis of the ELLDOPA study which randomized 361 early PD subjects to placebo, levodopa 150, 300, or 600 mg/day. We evaluated change in UPDRS motor scores (UPDRSm) from baseline to weeks 9 and 24, and identified changes in UPDRSm that best discriminated treatment with levodopa from placebo. Linear regressions were used to determine associations between baseline characteristics and changes in UPDRSm. Mean percent improvement in UPDRSm in levodopa‐treated subjects was greater than that for placebo‐treated subjects (27.4% vs. 5.8% at 9 weeks, P > 0.001 and 26.2% vs. 4.0% at 24 weeks, P > 0.001). UPDRSm change at 9 weeks ranged from –92.9% (improvement) to 85.7% (worsening) for levodopa and –86.7% to 160% for placebo, and at 24 weeks ranged from –100.0% to 242.9% for levodopa and –87.5% to 112.5% for placebo. UPDRSm improvements of 22.0% at 9 weeks and 23.8% at 24 weeks best discriminated treatment with levodopa 300 mg/day (a common initial maintenance dosage in clinical practice) from placebo. Significant associations were not observed between baseline subject characteristics and magnitude of response from baseline to week 24. We conclude that although levodopa treatment significantly improved PD signs when compared with placebo, there was a wide range and considerable overlap in clinical responses to levodopa and placebo. A substantial proportion of subjects with early PD did not experience a robust response to levodopa. 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Dr. Hauser has received consulting fees and honoraria related to other levodopa products and other PD medications.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Levodopa response in early Parkinson's disease</title><author><orgName>on behalf of the Parkinson Study Group</orgName></author><author><persName><forename type="first">Robert A.</forename><surname>Hauser</surname><roleName type="degree">MD</roleName></persName><note type="correspondence"><p>Correspondence: Parkinson's Disease and Movement Disorders Center, University of South Florida, 5 Tampa General Circle, Suite 410, Tampa, FL 33606</p></note><affiliation>Departments of Neurology, Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida, USA</affiliation></author><author><persName><forename type="first">Peggy</forename><surname>Auinger</surname><roleName type="degree">MS</roleName></persName><affiliation>Department of Neurology, University of Rochester, Rochester, New York, USA</affiliation></author><author><persName><forename type="first">David</forename><surname>Oakes</surname><roleName type="degree">PhD</roleName></persName><affiliation>Department of Biostatistics and Computational Biology, University of Rochester, Rochester, New York, USA</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-12-15"></date><biblScope unit="vol">24</biblScope><biblScope unit="issue">16</biblScope><biblScope unit="page" from="2328">2328</biblScope><biblScope unit="page" to="2336">2336</biblScope></imprint></monogr><idno type="istex">9F45EA68C8DD26C12497539861EEF4E613A6FD64</idno><idno type="DOI">10.1002/mds.22759</idno><idno type="ArticleID">MDS22759</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2009</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>To further characterize the short‐term levodopa response in early PD, we performed a retrospective analysis of the ELLDOPA study which randomized 361 early PD subjects to placebo, levodopa 150, 300, or 600 mg/day. We evaluated change in UPDRS motor scores (UPDRSm) from baseline to weeks 9 and 24, and identified changes in UPDRSm that best discriminated treatment with levodopa from placebo. Linear regressions were used to determine associations between baseline characteristics and changes in UPDRSm. Mean percent improvement in UPDRSm in levodopa‐treated subjects was greater than that for placebo‐treated subjects (27.4% vs. 5.8% at 9 weeks, P < 0.001 and 26.2% vs. 4.0% at 24 weeks, P < 0.001). UPDRSm change at 9 weeks ranged from –92.9% (improvement) to 85.7% (worsening) for levodopa and –86.7% to 160% for placebo, and at 24 weeks ranged from –100.0% to 242.9% for levodopa and –87.5% to 112.5% for placebo. UPDRSm improvements of 22.0% at 9 weeks and 23.8% at 24 weeks best discriminated treatment with levodopa 300 mg/day (a common initial maintenance dosage in clinical practice) from placebo. Significant associations were not observed between baseline subject characteristics and magnitude of response from baseline to week 24. We conclude that although levodopa treatment significantly improved PD signs when compared with placebo, there was a wide range and considerable overlap in clinical responses to levodopa and placebo. A substantial proportion of subjects with early PD did not experience a robust response to levodopa. An improvement in UPDRSm of ∼22% best discriminated levodopa treatment from placebo. © 2009 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>levodopa</term></item><item><term>placebo</term></item><item><term>treatment</term></item><item><term>Parkinson's disease</term></item><item><term>clinical response</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2008-10-23">Received</change><change when="2009-07-27">Registration</change><change when="2009-12-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/9F45EA68C8DD26C12497539861EEF4E613A6FD64/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)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. 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We evaluated change in UPDRS motor scores (UPDRSm) from baseline to weeks 9 and 24, and identified changes in UPDRSm that best discriminated treatment with levodopa from placebo. Linear regressions were used to determine associations between baseline characteristics and changes in UPDRSm. Mean percent improvement in UPDRSm in levodopa‐treated subjects was greater than that for placebo‐treated subjects (27.4% vs. 5.8% at 9 weeks, <i>P</i> < 0.001 and 26.2% vs. 4.0% at 24 weeks, <i>P</i> < 0.001). UPDRSm change at 9 weeks ranged from –92.9% (improvement) to 85.7% (worsening) for levodopa and –86.7% to 160% for placebo, and at 24 weeks ranged from –100.0% to 242.9% for levodopa and –87.5% to 112.5% for placebo. UPDRSm improvements of 22.0% at 9 weeks and 23.8% at 24 weeks best discriminated treatment with levodopa 300 mg/day (a common initial maintenance dosage in clinical practice) from placebo. Significant associations were not observed between baseline subject characteristics and magnitude of response from baseline to week 24. We conclude that although levodopa treatment significantly improved PD signs when compared with placebo, there was a wide range and considerable overlap in clinical responses to levodopa and placebo. A substantial proportion of subjects with early PD did not experience a robust response to levodopa. An improvement in UPDRSm of ∼22% best discriminated levodopa treatment from placebo. © 2009 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn12"><p>Potential Conflict of Interest: None of the authors has a direct financial conflict of interest with the product (carbidopa/levodopa IR) discussed in this manuscript. Dr. Hauser has received consulting fees and honoraria related to other levodopa products and other PD medications.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Levodopa response in early Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Levodopa in Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Levodopa response in early Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Robert A.</namePart><namePart type="family">Hauser</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Departments of Neurology, Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida, USA</affiliation><description>Correspondence: Parkinson's Disease and Movement Disorders Center, University of South Florida, 5 Tampa General Circle, Suite 410, Tampa, FL 33606</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peggy</namePart><namePart type="family">Auinger</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Department of Neurology, University of Rochester, Rochester, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David</namePart><namePart type="family">Oakes</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Biostatistics and Computational Biology, University of Rochester, Rochester, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="corporate"><namePart>on behalf of the Parkinson Study Group</namePart><description>Departments of Neurology, Molecular Pharmacology and Physiology, University of South Florida, Tampa, Florida, USADepartment of Neurology, University of Rochester, Rochester, New York, USADepartment of Biostatistics and Computational Biology, University of Rochester, Rochester, New York, USA</description></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-12-15</dateIssued><dateCaptured encoding="w3cdtf">2008-10-23</dateCaptured><dateValid encoding="w3cdtf">2009-07-27</dateValid><copyrightDate encoding="w3cdtf">2009</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">3</extent><extent unit="references">14</extent><extent unit="words">6602</extent></physicalDescription><abstract lang="en">To further characterize the short‐term levodopa response in early PD, we performed a retrospective analysis of the ELLDOPA study which randomized 361 early PD subjects to placebo, levodopa 150, 300, or 600 mg/day. We evaluated change in UPDRS motor scores (UPDRSm) from baseline to weeks 9 and 24, and identified changes in UPDRSm that best discriminated treatment with levodopa from placebo. Linear regressions were used to determine associations between baseline characteristics and changes in UPDRSm. Mean percent improvement in UPDRSm in levodopa‐treated subjects was greater than that for placebo‐treated subjects (27.4% vs. 5.8% at 9 weeks, P < 0.001 and 26.2% vs. 4.0% at 24 weeks, P < 0.001). UPDRSm change at 9 weeks ranged from –92.9% (improvement) to 85.7% (worsening) for levodopa and –86.7% to 160% for placebo, and at 24 weeks ranged from –100.0% to 242.9% for levodopa and –87.5% to 112.5% for placebo. UPDRSm improvements of 22.0% at 9 weeks and 23.8% at 24 weeks best discriminated treatment with levodopa 300 mg/day (a common initial maintenance dosage in clinical practice) from placebo. Significant associations were not observed between baseline subject characteristics and magnitude of response from baseline to week 24. We conclude that although levodopa treatment significantly improved PD signs when compared with placebo, there was a wide range and considerable overlap in clinical responses to levodopa and placebo. A substantial proportion of subjects with early PD did not experience a robust response to levodopa. An improvement in UPDRSm of ∼22% best discriminated levodopa treatment from placebo. © 2009 Movement Disorder Society</abstract><note type="content">*Potential Conflict of Interest: None of the authors has a direct financial conflict of interest with the product (carbidopa/levodopa IR) discussed in this manuscript. Dr. Hauser has received consulting fees and honoraria related to other levodopa products and other PD medications.</note><subject lang="en"><genre>Keywords</genre><topic>levodopa</topic><topic>placebo</topic><topic>treatment</topic><topic>Parkinson's disease</topic><topic>clinical response</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><note type="content"> Additional Supporting Information may be found in the online version of this article.</note><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>16</number></detail><extent unit="pages"><start>2328</start><end>2336</end><total>9</total></extent></part></relatedItem><identifier type="istex">9F45EA68C8DD26C12497539861EEF4E613A6FD64</identifier><identifier type="DOI">10.1002/mds.22759</identifier><identifier type="ArticleID">MDS22759</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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