Serum urate and probability of dopaminergic deficit in early “Parkinson's disease”
Identifieur interne : 000392 ( Main/Corpus ); précédent : 000391; suivant : 000393Serum urate and probability of dopaminergic deficit in early “Parkinson's disease”
Auteurs : Michael A. Schwarzschild ; Kenneth Marek ; Shirley Eberly ; David Oakes ; Ira Shoulson ; Danna Jennings ; John Seibyl ; Alberto AscherioSource :
- Movement Disorders [ 0885-3185 ] ; 2011-08-15.
English descriptors
Abstract
The objective of this study was to investigate whether higher levels of urate, an antioxidant linked to a lower likelihood of developing Parkinson's disease, is also a predictor of having a dopamine transporter brain scan without evidence of dopaminergic deficit. In a cross‐sectional study of 797 mildly affected, untreated parkinsonian subjects diagnosed with early Parkinson's disease in the Parkinson Research Examination of CEP‐1347 Trial, we investigated the relationship at baseline between serum urate and striatal dopamine transporter density, determined by single‐photon emission computed tomography of iodine‐123‐labeled 2‐β‐carboxymethoxy‐3‐β‐(4‐iodophenyl)tropane uptake. A scan without evidence of dopaminergic deficit was defined as lowest putamen iodine‐123‐labeled 2‐β‐carboxymethoxy‐3‐β‐(4‐iodophenyl)tropane > 80% age‐expected putamen dopamine transporter density. The odds of having a scan without evidence of dopaminergic deficit rose across increasing quintiles of urate level, with an age‐ and sex‐adjusted odds ratio of 3.2 comparing the highest to the lowest urate quintile (95% confidence interval, 1.5–7.2; P for trend = .0003), and remained significant after adjusting for potential confounding factors. The association was significant in men but not women, regardless of whether common or sex‐specific quintiles of urate were used. Higher levels of urate were associated with a greater likelihood of a scan without evidence of dopaminergic deficit among subjects with early untreated parkinsonism in the Parkinson Research Examination of CEP‐1347 Trial. The findings support the diagnostic utility of urate in combination with other determinants. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23741
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In a cross‐sectional study of 797 mildly affected, untreated parkinsonian subjects diagnosed with early Parkinson's disease in the Parkinson Research Examination of CEP‐1347 Trial, we investigated the relationship at baseline between serum urate and striatal dopamine transporter density, determined by single‐photon emission computed tomography of iodine‐123‐labeled 2‐β‐carboxymethoxy‐3‐β‐(4‐iodophenyl)tropane uptake. A scan without evidence of dopaminergic deficit was defined as lowest putamen iodine‐123‐labeled 2‐β‐carboxymethoxy‐3‐β‐(4‐iodophenyl)tropane > 80% age‐expected putamen dopamine transporter density. The odds of having a scan without evidence of dopaminergic deficit rose across increasing quintiles of urate level, with an age‐ and sex‐adjusted odds ratio of 3.2 comparing the highest to the lowest urate quintile (95% confidence interval, 1.5–7.2; P for trend = .0003), and remained significant after adjusting for potential confounding factors. The association was significant in men but not women, regardless of whether common or sex‐specific quintiles of urate were used. Higher levels of urate were associated with a greater likelihood of a scan without evidence of dopaminergic deficit among subjects with early untreated parkinsonism in the Parkinson Research Examination of CEP‐1347 Trial. The findings support the diagnostic utility of urate in combination with other determinants. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Michael A. Schwarzschild MD, PhD</name><affiliations><json:string>Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA</json:string></affiliations></json:item><json:item><name>Kenneth Marek MD</name><affiliations><json:string>Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA</json:string></affiliations></json:item><json:item><name>Shirley Eberly MS</name><affiliations><json:string>Departments of Neurology and Biostatistics, University of Rochester, Rochester, New York, USA</json:string></affiliations></json:item><json:item><name>David Oakes PhD</name><affiliations><json:string>Departments of Neurology and Biostatistics, University of Rochester, Rochester, New York, USA</json:string></affiliations></json:item><json:item><name>Ira Shoulson MD</name><affiliations><json:string>Departments of Neurology and Biostatistics, University of Rochester, Rochester, New York, USA</json:string></affiliations></json:item><json:item><name>Danna Jennings MD</name><affiliations><json:string>Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA</json:string></affiliations></json:item><json:item><name>John Seibyl MD</name><affiliations><json:string>Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA</json:string></affiliations></json:item><json:item><name>Alberto Ascherio MD, DrPH,</name><affiliations><json:string>Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</json:string><json:string>Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA</json:string></affiliations></json:item></author><subject><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>urate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dopamine transporter</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neuroimaging</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>diagnosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>biomarker</value></json:item></subject><articleId><json:string>MDS23741</json:string></articleId><language><json:string>eng</json:string></language><abstract>The objective of this study was to investigate whether higher levels of urate, an antioxidant linked to a lower likelihood of developing Parkinson's disease, is also a predictor of having a dopamine transporter brain scan without evidence of dopaminergic deficit. In a cross‐sectional study of 797 mildly affected, untreated parkinsonian subjects diagnosed with early Parkinson's disease in the Parkinson Research Examination of CEP‐1347 Trial, we investigated the relationship at baseline between serum urate and striatal dopamine transporter density, determined by single‐photon emission computed tomography of iodine‐123‐labeled 2‐β‐carboxymethoxy‐3‐β‐(4‐iodophenyl)tropane uptake. A scan without evidence of dopaminergic deficit was defined as lowest putamen iodine‐123‐labeled 2‐β‐carboxymethoxy‐3‐β‐(4‐iodophenyl)tropane > 80% age‐expected putamen dopamine transporter density. The odds of having a scan without evidence of dopaminergic deficit rose across increasing quintiles of urate level, with an age‐ and sex‐adjusted odds ratio of 3.2 comparing the highest to the lowest urate quintile (95% confidence interval, 1.5–7.2; P for trend = .0003), and remained significant after adjusting for potential confounding factors. The association was significant in men but not women, regardless of whether common or sex‐specific quintiles of urate were used. Higher levels of urate were associated with a greater likelihood of a scan without evidence of dopaminergic deficit among subjects with early untreated parkinsonism in the Parkinson Research Examination of CEP‐1347 Trial. The findings support the diagnostic utility of urate in combination with other determinants. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>6.019</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>1708</abstractCharCount><pdfWordCount>3235</pdfWordCount><pdfCharCount>21468</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>232</abstractWordCount></qualityIndicators><title>Serum urate and probability of dopaminergic deficit in early “Parkinson's disease”</title><corporate><json:item><name>on behalf of the Parkinson Study Group PRECEPT Investigators</name></json:item></corporate><genre><json:string>article</json:string></genre><host><volume>26</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>5</total><last>1868</last><first>1864</first></pages><issn><json:string>0885-3185</json:string></issn><issue>10</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/mds.23741</json:string></doi><id>9217CF0BE19CFAC02CAEDB77C00779BAEE40BFC6</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/9217CF0BE19CFAC02CAEDB77C00779BAEE40BFC6/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/9217CF0BE19CFAC02CAEDB77C00779BAEE40BFC6/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/9217CF0BE19CFAC02CAEDB77C00779BAEE40BFC6/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Serum urate and probability of dopaminergic deficit in early “Parkinson's disease”</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Funding agencies: The present study was supported by the NIH (R01NS061858, K24NS060991), DoD (W81XWH‐06‐1‐0679), and RJG Foundation.</note><note type="content">*Relevant conflicts of interest/financial disclosures: The present study is a secondary analysis of the database of a clinical trial PRECEPT, which was sponsored by Cephalon, Inc. (Frazer, PA), and H. Lundbeck A/S (Copenhagen, Denmark). Dr. Ira Shoulson had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Dr. Kenneth Marek is a consultant/AD board member for GE Healthcare, Alseres, EMD Serono, Lilly, Bayer Healthcare, Sanofi, and Biogen and has an ownership interest in Molecular NeuroImaging, LLC. Dr. John Seibyl is a consultant/AD board member for Bayer Healthcare, GE Healthcare, and Neurologica and has an equity interest in Molecular NeuroImaging, LLC.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Serum urate and probability of dopaminergic deficit in early “Parkinson's disease”</title><author><orgName>on behalf of the Parkinson Study Group PRECEPT Investigators</orgName></author><author><persName><forename type="first">Michael A.</forename><surname>Schwarzschild</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA</affiliation></author><author><persName><forename type="first">Kenneth</forename><surname>Marek</surname></persName><roleName type="degree">MD</roleName><affiliation>Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA</affiliation></author><author><persName><forename type="first">Shirley</forename><surname>Eberly</surname></persName><roleName type="degree">MS</roleName><affiliation>Departments of Neurology and Biostatistics, University of Rochester, Rochester, New York, USA</affiliation></author><author><persName><forename type="first">David</forename><surname>Oakes</surname></persName><roleName type="degree">PhD</roleName><affiliation>Departments of Neurology and Biostatistics, University of Rochester, Rochester, New York, USA</affiliation></author><author><persName><forename type="first">Ira</forename><surname>Shoulson</surname></persName><roleName type="degree">MD</roleName><affiliation>Departments of Neurology and Biostatistics, University of Rochester, Rochester, New York, USA</affiliation></author><author><persName><forename type="first">Danna</forename><surname>Jennings</surname></persName><roleName type="degree">MD</roleName><affiliation>Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA</affiliation></author><author><persName><forename type="first">John</forename><surname>Seibyl</surname></persName><roleName type="degree">MD</roleName><affiliation>Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA</affiliation></author><author><persName><forename type="first">Alberto</forename><surname>Ascherio</surname></persName><roleName type="degree">MD, DrPH,</roleName><note type="correspondence"><p>Correspondence: 655 Huntington Ave, 3rd floor, Boston, MA 02115, USA</p></note><affiliation>Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><affiliation>Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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In a cross‐sectional study of 797 mildly affected, untreated parkinsonian subjects diagnosed with early Parkinson's disease in the Parkinson Research Examination of CEP‐1347 Trial, we investigated the relationship at baseline between serum urate and striatal dopamine transporter density, determined by single‐photon emission computed tomography of iodine‐123‐labeled 2‐β‐carboxymethoxy‐3‐β‐(4‐iodophenyl)tropane uptake. A scan without evidence of dopaminergic deficit was defined as lowest putamen iodine‐123‐labeled 2‐β‐carboxymethoxy‐3‐β‐(4‐iodophenyl)tropane > 80% age‐expected putamen dopamine transporter density. The odds of having a scan without evidence of dopaminergic deficit rose across increasing quintiles of urate level, with an age‐ and sex‐adjusted odds ratio of 3.2 comparing the highest to the lowest urate quintile (95% confidence interval, 1.5–7.2; P for trend = .0003), and remained significant after adjusting for potential confounding factors. The association was significant in men but not women, regardless of whether common or sex‐specific quintiles of urate were used. Higher levels of urate were associated with a greater likelihood of a scan without evidence of dopaminergic deficit among subjects with early untreated parkinsonism in the Parkinson Research Examination of CEP‐1347 Trial. The findings support the diagnostic utility of urate in combination with other determinants. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>urate</term></item><item><term>dopamine transporter</term></item><item><term>neuroimaging</term></item><item><term>diagnosis</term></item><item><term>biomarker</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="2010-08-18">Received</change><change when="2011-03-10">Registration</change><change when="2011-08-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/9217CF0BE19CFAC02CAEDB77C00779BAEE40BFC6/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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type="tableTotal" number="3"></count><count type="referenceTotal" number="26"></count><count type="wordTotal" number="5457"></count></countGroup><titleGroup><title type="main" xml:lang="en">Serum urate and probability of dopaminergic deficit in early “Parkinson's disease”<link href="#fn1"></link><link href="#fn2"></link><link href="#fn3"></link></title><title type="short" xml:lang="en">Serum Urate and Dopaminergic Deficit</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Michael A.</givenNames><familyName>Schwarzschild</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Kenneth</givenNames><familyName>Marek</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Shirley</givenNames><familyName>Eberly</familyName><degrees>MS</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>David</givenNames><familyName>Oakes</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Ira</givenNames><familyName>Shoulson</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Danna</givenNames><familyName>Jennings</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>John</givenNames><familyName>Seibyl</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af4 #af5" corresponding="yes"><personName><givenNames>Alberto</givenNames><familyName>Ascherio</familyName><degrees>MD, DrPH,</degrees></personName><contactDetails><email>aascheri@hsph.harvard.edu</email></contactDetails></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af4 #af5"><groupName>on behalf of the Parkinson Study Group PRECEPT Investigators</groupName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Departments of Neurology and Biostatistics, University of Rochester, Rochester, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">urate</keyword><keyword xml:id="kwd3">dopamine transporter</keyword><keyword xml:id="kwd4">neuroimaging</keyword><keyword xml:id="kwd5">diagnosis</keyword><keyword xml:id="kwd6">biomarker</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The objective of this study was to investigate whether higher levels of urate, an antioxidant linked to a lower likelihood of developing Parkinson's disease, is also a predictor of having a dopamine transporter brain scan without evidence of dopaminergic deficit. In a cross‐sectional study of 797 mildly affected, untreated parkinsonian subjects diagnosed with early Parkinson's disease in the Parkinson Research Examination of CEP‐1347 Trial, we investigated the relationship at baseline between serum urate and striatal dopamine transporter density, determined by single‐photon emission computed tomography of iodine‐123‐labeled 2‐β‐carboxymethoxy‐3‐β‐(4‐iodophenyl)tropane uptake. A scan without evidence of dopaminergic deficit was defined as lowest putamen iodine‐123‐labeled 2‐β‐carboxymethoxy‐3‐β‐(4‐iodophenyl)tropane > 80% age‐expected putamen dopamine transporter density. The odds of having a scan without evidence of dopaminergic deficit rose across increasing quintiles of urate level, with an age‐ and sex‐adjusted odds ratio of 3.2 comparing the highest to the lowest urate quintile (95% confidence interval, 1.5–7.2; <i>P</i> for trend = .0003), and remained significant after adjusting for potential confounding factors. The association was significant in men but not women, regardless of whether common or sex‐specific quintiles of urate were used. Higher levels of urate were associated with a greater likelihood of a scan without evidence of dopaminergic deficit among subjects with early untreated parkinsonism in the Parkinson Research Examination of CEP‐1347 Trial. The findings support the diagnostic utility of urate in combination with other determinants. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Funding agencies</b>: The present study was supported by the NIH (R01NS061858, K24NS060991), DoD (W81XWH‐06‐1‐0679), and RJG Foundation.</p></note><note xml:id="fn2"><p><b>Relevant conflicts of interest/financial disclosures</b>: The present study is a secondary analysis of the database of a clinical trial PRECEPT, which was sponsored by Cephalon, Inc. (Frazer, PA), and H. Lundbeck A/S (Copenhagen, Denmark). Dr. Ira Shoulson had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Dr. Kenneth Marek is a consultant/AD board member for GE Healthcare, Alseres, EMD Serono, Lilly, Bayer Healthcare, Sanofi, and Biogen and has an ownership interest in Molecular NeuroImaging, LLC. Dr. John Seibyl is a consultant/AD board member for Bayer Healthcare, GE Healthcare, and Neurologica and has an equity interest in Molecular NeuroImaging, LLC.</p></note><note xml:id="fn3"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Serum urate and probability of dopaminergic deficit in early “Parkinson's disease”</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Serum Urate and Dopaminergic Deficit</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Serum urate and probability of dopaminergic deficit in early “Parkinson's disease”</title></titleInfo><name type="personal"><namePart type="given">Michael A.</namePart><namePart type="family">Schwarzschild</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kenneth</namePart><namePart type="family">Marek</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shirley</namePart><namePart type="family">Eberly</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Departments of Neurology and Biostatistics, 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>Departments of Neurology and Biostatistics, University of Rochester, Rochester, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ira</namePart><namePart type="family">Shoulson</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Departments of Neurology and Biostatistics, University of Rochester, Rochester, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Danna</namePart><namePart type="family">Jennings</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John</namePart><namePart type="family">Seibyl</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alberto</namePart><namePart type="family">Ascherio</namePart><namePart type="termsOfAddress">MD, DrPH,</namePart><affiliation>Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA</affiliation><affiliation>Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA</affiliation><description>Correspondence: 655 Huntington Ave, 3rd floor, Boston, MA 02115, USA</description><role><roleTerm type="text">author</roleTerm></role></name><name type="corporate"><namePart>on behalf of the Parkinson Study Group PRECEPT Investigators</namePart><description>Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USAInstitute for Neurodegenerative Disorders, New Haven, Connecticut, USADepartments of Neurology and Biostatistics, University of Rochester, Rochester, New York, USADepartments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, Massachusetts, USAChanning Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA</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">2011-08-15</dateIssued><dateCaptured encoding="w3cdtf">2010-08-18</dateCaptured><dateValid encoding="w3cdtf">2011-03-10</dateValid><copyrightDate encoding="w3cdtf">2011</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="tables">3</extent><extent unit="references">26</extent><extent unit="words">5457</extent></physicalDescription><abstract lang="en">The objective of this study was to investigate whether higher levels of urate, an antioxidant linked to a lower likelihood of developing Parkinson's disease, is also a predictor of having a dopamine transporter brain scan without evidence of dopaminergic deficit. In a cross‐sectional study of 797 mildly affected, untreated parkinsonian subjects diagnosed with early Parkinson's disease in the Parkinson Research Examination of CEP‐1347 Trial, we investigated the relationship at baseline between serum urate and striatal dopamine transporter density, determined by single‐photon emission computed tomography of iodine‐123‐labeled 2‐β‐carboxymethoxy‐3‐β‐(4‐iodophenyl)tropane uptake. A scan without evidence of dopaminergic deficit was defined as lowest putamen iodine‐123‐labeled 2‐β‐carboxymethoxy‐3‐β‐(4‐iodophenyl)tropane > 80% age‐expected putamen dopamine transporter density. The odds of having a scan without evidence of dopaminergic deficit rose across increasing quintiles of urate level, with an age‐ and sex‐adjusted odds ratio of 3.2 comparing the highest to the lowest urate quintile (95% confidence interval, 1.5–7.2; P for trend = .0003), and remained significant after adjusting for potential confounding factors. The association was significant in men but not women, regardless of whether common or sex‐specific quintiles of urate were used. Higher levels of urate were associated with a greater likelihood of a scan without evidence of dopaminergic deficit among subjects with early untreated parkinsonism in the Parkinson Research Examination of CEP‐1347 Trial. The findings support the diagnostic utility of urate in combination with other determinants. © 2011 Movement Disorder Society</abstract><note type="content">*Funding agencies: The present study was supported by the NIH (R01NS061858, K24NS060991), DoD (W81XWH‐06‐1‐0679), and RJG Foundation.</note><note type="content">*Relevant conflicts of interest/financial disclosures: The present study is a secondary analysis of the database of a clinical trial PRECEPT, which was sponsored by Cephalon, Inc. (Frazer, PA), and H. Lundbeck A/S (Copenhagen, Denmark). Dr. Ira Shoulson had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Dr. Kenneth Marek is a consultant/AD board member for GE Healthcare, Alseres, EMD Serono, Lilly, Bayer Healthcare, Sanofi, and Biogen and has an ownership interest in Molecular NeuroImaging, LLC. Dr. John Seibyl is a consultant/AD board member for Bayer Healthcare, GE Healthcare, and Neurologica and has an equity interest in Molecular NeuroImaging, LLC.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>urate</topic><topic>dopamine transporter</topic><topic>neuroimaging</topic><topic>diagnosis</topic><topic>biomarker</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><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>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1864</start><end>1868</end><total>5</total></extent></part></relatedItem><identifier type="istex">9217CF0BE19CFAC02CAEDB77C00779BAEE40BFC6</identifier><identifier type="DOI">10.1002/mds.23741</identifier><identifier type="ArticleID">MDS23741</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</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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