NSAID use and risk of Parkinson disease: a population‐based case‐control study
Identifieur interne : 000086 ( Main/Corpus ); précédent : 000085; suivant : 000087NSAID use and risk of Parkinson disease: a population‐based case‐control study
Auteurs : C. Becker ; S. S. Jick ; C. R. MeierSource :
- European Journal of Neurology [ 1351-5101 ] ; 2011-11.
English descriptors
- KwdEn :
Abstract
Background: Previous epidemiologic studies have produced inconsistent findings regarding the association between the use of non‐steroidal anti‐inflammatory drugs (NSAIDs) and the risk of Parkinson disease (PD). Methods: We conducted a case–control analysis using the General Practice Research Database. Cases (≥40 years) had a new diagnosis of PD between 1994 and 2009. We matched four controls to each PD case on age, sex, general practice, and index date. Use of NSAIDs, aspirin, and acetaminophen was stratified by exposure timing and duration for both cases and controls. We calculated odds ratios (OR) using conditional logistic regression. For additional analyses, the index date was brought backward 1, 2, and 3 years, respectively. Results: We identified 4026 cases with an incident idiopathic PD diagnosis and 15 969 matched controls. Compared with patients without any previous prescription for NSAIDs, those with prior use had no increased risk of a PD diagnosis (OR 1.07, 95% CI 0.99–1.16). Long‐term use (≥15 prescriptions) was associated with a slightly lower PD risk (adjusted OR 0.94, 95% CI 0.83–1.07). The relative PD risks of the use of aspirin or acetaminophen were not materially higher (PD risk of long‐term use: adjusted ORs 1.16, 95% CI 1.03–1.30 and 1.15, 95% CI 1.02–1.30, respectively) compared with those for non‐users. The risk estimate diminished toward the null in subsequent analyses with shifted index dates. Conclusion: In this large observational study with data from the UK primary care, the long‐term use of NSAIDs, aspirin, or acetaminophen was not associated with a substantially altered risk of developing PD.
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DOI: 10.1111/j.1468-1331.2011.03399.x
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Meier</name><affiliation><mods:affiliation>Basel Pharmacoepidemiology Unit, Division of Clinical Pharmacy and Epidemiology, Department of Pharmaceutical Sciences, University of Basel, Switzerland</mods:affiliation></affiliation><affiliation><mods:affiliation>Boston Collaborative Drug Surveillance Program, Boston University Medical Center, Lexington, MA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Hospital Pharmacy, University Hospital, Spitalstrasse 26, Basel, Switzerland</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:2DA69C60955AB3398C85649A97FE5725EE5A60D0</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1111/j.1468-1331.2011.03399.x</idno><idno type="url">https://api.istex.fr/document/2DA69C60955AB3398C85649A97FE5725EE5A60D0/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000086</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">NSAID use and risk of Parkinson disease: a population‐based case‐control study</title><author><name sortKey="Becker, C" sort="Becker, C" uniqKey="Becker C" first="C." last="Becker">C. Becker</name><affiliation><mods:affiliation>Basel Pharmacoepidemiology Unit, Division of Clinical Pharmacy and Epidemiology, Department of Pharmaceutical Sciences, University of Basel, Switzerland</mods:affiliation></affiliation></author><author><name sortKey="Jick, S S" sort="Jick, S S" uniqKey="Jick S" first="S. S." last="Jick">S. S. Jick</name><affiliation><mods:affiliation>Boston Collaborative Drug Surveillance Program, Boston University Medical Center, Lexington, MA, USA</mods:affiliation></affiliation></author><author><name sortKey="Meier, C R" sort="Meier, C R" uniqKey="Meier C" first="C. R." last="Meier">C. R. Meier</name><affiliation><mods:affiliation>Basel Pharmacoepidemiology Unit, Division of Clinical Pharmacy and Epidemiology, Department of Pharmaceutical Sciences, University of Basel, Switzerland</mods:affiliation></affiliation><affiliation><mods:affiliation>Boston Collaborative Drug Surveillance Program, Boston University Medical Center, Lexington, MA, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Hospital Pharmacy, University Hospital, Spitalstrasse 26, Basel, Switzerland</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Neurology</title><idno type="ISSN">1351-5101</idno><idno type="eISSN">1468-1331</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-11">2011-11</date><biblScope unit="volume">18</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="1336">1336</biblScope><biblScope unit="page" to="1342">1342</biblScope></imprint><idno type="ISSN">1351-5101</idno></series><idno type="istex">2DA69C60955AB3398C85649A97FE5725EE5A60D0</idno><idno type="DOI">10.1111/j.1468-1331.2011.03399.x</idno><idno type="ArticleID">ENE3399</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1351-5101</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson disease</term><term>case–control analysis</term><term>epidemiology</term><term>non‐steroidal anti‐inflammatory drugs</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background: Previous epidemiologic studies have produced inconsistent findings regarding the association between the use of non‐steroidal anti‐inflammatory drugs (NSAIDs) and the risk of Parkinson disease (PD). Methods: We conducted a case–control analysis using the General Practice Research Database. Cases (≥40 years) had a new diagnosis of PD between 1994 and 2009. We matched four controls to each PD case on age, sex, general practice, and index date. Use of NSAIDs, aspirin, and acetaminophen was stratified by exposure timing and duration for both cases and controls. We calculated odds ratios (OR) using conditional logistic regression. For additional analyses, the index date was brought backward 1, 2, and 3 years, respectively. Results: We identified 4026 cases with an incident idiopathic PD diagnosis and 15 969 matched controls. Compared with patients without any previous prescription for NSAIDs, those with prior use had no increased risk of a PD diagnosis (OR 1.07, 95% CI 0.99–1.16). Long‐term use (≥15 prescriptions) was associated with a slightly lower PD risk (adjusted OR 0.94, 95% CI 0.83–1.07). The relative PD risks of the use of aspirin or acetaminophen were not materially higher (PD risk of long‐term use: adjusted ORs 1.16, 95% CI 1.03–1.30 and 1.15, 95% CI 1.02–1.30, respectively) compared with those for non‐users. The risk estimate diminished toward the null in subsequent analyses with shifted index dates. Conclusion: In this large observational study with data from the UK primary care, the long‐term use of NSAIDs, aspirin, or acetaminophen was not associated with a substantially altered risk of developing PD.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>C. Becker</name><affiliations><json:string>Basel Pharmacoepidemiology Unit, Division of Clinical Pharmacy and Epidemiology, Department of Pharmaceutical Sciences, University of Basel, Switzerland</json:string></affiliations></json:item><json:item><name>S. S. Jick</name><affiliations><json:string>Boston Collaborative Drug Surveillance Program, Boston University Medical Center, Lexington, MA, USA</json:string></affiliations></json:item><json:item><name>C. R. Meier</name><affiliations><json:string>Basel Pharmacoepidemiology Unit, Division of Clinical Pharmacy and Epidemiology, Department of Pharmaceutical Sciences, University of Basel, Switzerland</json:string><json:string>Boston Collaborative Drug Surveillance Program, Boston University Medical Center, Lexington, MA, USA</json:string><json:string>Hospital Pharmacy, University Hospital, Spitalstrasse 26, Basel, Switzerland</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>case–control analysis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>epidemiology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>non‐steroidal anti‐inflammatory drugs</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson disease</value></json:item></subject><articleId><json:string>ENE3399</json:string></articleId><language><json:string>eng</json:string></language><abstract>Background: Previous epidemiologic studies have produced inconsistent findings regarding the association between the use of non‐steroidal anti‐inflammatory drugs (NSAIDs) and the risk of Parkinson disease (PD). Methods: We conducted a case–control analysis using the General Practice Research Database. Cases (≥40 years) had a new diagnosis of PD between 1994 and 2009. We matched four controls to each PD case on age, sex, general practice, and index date. Use of NSAIDs, aspirin, and acetaminophen was stratified by exposure timing and duration for both cases and controls. We calculated odds ratios (OR) using conditional logistic regression. For additional analyses, the index date was brought backward 1, 2, and 3 years, respectively. Results: We identified 4026 cases with an incident idiopathic PD diagnosis and 15 969 matched controls. Compared with patients without any previous prescription for NSAIDs, those with prior use had no increased risk of a PD diagnosis (OR 1.07, 95% CI 0.99–1.16). Long‐term use (≥15 prescriptions) was associated with a slightly lower PD risk (adjusted OR 0.94, 95% CI 0.83–1.07). The relative PD risks of the use of aspirin or acetaminophen were not materially higher (PD risk of long‐term use: adjusted ORs 1.16, 95% CI 1.03–1.30 and 1.15, 95% CI 1.02–1.30, respectively) compared with those for non‐users. The risk estimate diminished toward the null in subsequent analyses with shifted index dates. 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S.</forename><surname>Jick</surname></persName><affiliation>Boston Collaborative Drug Surveillance Program, Boston University Medical Center, Lexington, MA, USA</affiliation></author><author><persName><forename type="first">C. R.</forename><surname>Meier</surname></persName><affiliation>Basel Pharmacoepidemiology Unit, Division of Clinical Pharmacy and Epidemiology, Department of Pharmaceutical Sciences, University of Basel, Switzerland</affiliation><affiliation>Boston Collaborative Drug Surveillance Program, Boston University Medical Center, Lexington, MA, USA</affiliation><affiliation>Hospital Pharmacy, University Hospital, Spitalstrasse 26, Basel, Switzerland</affiliation></author></analytic><monogr><title level="j">European Journal of Neurology</title><idno type="pISSN">1351-5101</idno><idno type="eISSN">1468-1331</idno><idno type="DOI">10.1111/(ISSN)1468-1331</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-11"></date><biblScope unit="volume">18</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="1336">1336</biblScope><biblScope unit="page" to="1342">1342</biblScope></imprint></monogr><idno type="istex">2DA69C60955AB3398C85649A97FE5725EE5A60D0</idno><idno type="DOI">10.1111/j.1468-1331.2011.03399.x</idno><idno type="ArticleID">ENE3399</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Background: Previous epidemiologic studies have produced inconsistent findings regarding the association between the use of non‐steroidal anti‐inflammatory drugs (NSAIDs) and the risk of Parkinson disease (PD). Methods: We conducted a case–control analysis using the General Practice Research Database. Cases (≥40 years) had a new diagnosis of PD between 1994 and 2009. We matched four controls to each PD case on age, sex, general practice, and index date. Use of NSAIDs, aspirin, and acetaminophen was stratified by exposure timing and duration for both cases and controls. We calculated odds ratios (OR) using conditional logistic regression. For additional analyses, the index date was brought backward 1, 2, and 3 years, respectively. Results: We identified 4026 cases with an incident idiopathic PD diagnosis and 15 969 matched controls. Compared with patients without any previous prescription for NSAIDs, those with prior use had no increased risk of a PD diagnosis (OR 1.07, 95% CI 0.99–1.16). Long‐term use (≥15 prescriptions) was associated with a slightly lower PD risk (adjusted OR 0.94, 95% CI 0.83–1.07). The relative PD risks of the use of aspirin or acetaminophen were not materially higher (PD risk of long‐term use: adjusted ORs 1.16, 95% CI 1.03–1.30 and 1.15, 95% CI 1.02–1.30, respectively) compared with those for non‐users. The risk estimate diminished toward the null in subsequent analyses with shifted index dates. Conclusion: In this large observational study with data from the UK primary care, the long‐term use of NSAIDs, aspirin, or acetaminophen was not associated with a substantially altered risk of developing PD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>case–control analysis</term></item><item><term>epidemiology</term></item><item><term>non‐steroidal anti‐inflammatory drugs</term></item><item><term>Parkinson disease</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2011-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/2DA69C60955AB3398C85649A97FE5725EE5A60D0/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>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1468-1331</doi><issn type="print">1351-5101</issn><issn type="electronic">1468-1331</issn><idGroup><id type="product" value="ENE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROLOGY">European Journal of Neurology</title></titleGroup></publicationMeta><publicationMeta level="part" position="11111"><doi origin="wiley">10.1111/ene.2011.18.issue-11</doi><numberingGroup><numbering type="journalVolume" number="18">18</numbering><numbering type="journalIssue" number="11">11</numbering></numberingGroup><coverDate startDate="2011-11">November 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="10" status="forIssue"><doi origin="wiley">10.1111/j.1468-1331.2011.03399.x</doi><idGroup><id type="unit" value="ENE3399"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><copyright>© 2011 The Author(s). European Journal of Neurology © 2011 EFNS</copyright><eventGroup><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.10 mode:FullText" date="2011-10-11"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-04-04"></event><event type="firstOnline" date="2011-04-04"></event><event type="publishedOnlineFinalForm" date="2011-10-11"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-24"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="1336">1336</numbering><numbering type="pageLast" number="1342">1342</numbering></numberingGroup><correspondenceTo>Dr C. R. Meier, PhD, MSc, Basel Pharmacoepidemiology Unit, Hospital Pharmacy, University Hospital, Spitalstrasse 26, 4031 Basel, CH 4031 Basel, Switzerland (tel.: +41 61 556 53 69; fax: +41 61 265 88 75; e‐mail: <email>Meierch@uhbs.ch</email>).</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ENE.ENE3399.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 6 December 2010 Accepted 3 March 2011</unparsedEditorialHistory><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="4"></count></countGroup><titleGroup><title type="main">NSAID use and risk of Parkinson disease: a population‐based case‐control study</title><title type="shortAuthors">C. Becker <i>et al.</i></title><title type="short">NSAID use and risk of Parkinson disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>C.</givenNames><familyName>Becker</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>S. S.</givenNames><familyName>Jick</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1 #a2 #a3"><personName><givenNames>C. R.</givenNames><familyName>Meier</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="CH"><unparsedAffiliation>Basel Pharmacoepidemiology Unit, Division of Clinical Pharmacy and Epidemiology, Department of Pharmaceutical Sciences, University of Basel, Switzerland</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation>Boston Collaborative Drug Surveillance Program, Boston University Medical Center, Lexington, MA, USA</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="CH"><unparsedAffiliation>Hospital Pharmacy, University Hospital, Spitalstrasse 26, Basel, Switzerland</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">case–control analysis</keyword><keyword xml:id="k2">epidemiology</keyword><keyword xml:id="k3">non‐steroidal anti‐inflammatory drugs</keyword><keyword xml:id="k4">Parkinson disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>Background: </b> Previous epidemiologic studies have produced inconsistent findings regarding the association between the use of non‐steroidal anti‐inflammatory drugs (NSAIDs) and the risk of Parkinson disease (PD).</p><p><b>Methods: </b> We conducted a case–control analysis using the General Practice Research Database. Cases (≥40 years) had a new diagnosis of PD between 1994 and 2009. We matched four controls to each PD case on age, sex, general practice, and index date. Use of NSAIDs, aspirin, and acetaminophen was stratified by exposure timing and duration for both cases and controls. We calculated odds ratios (OR) using conditional logistic regression. For additional analyses, the index date was brought backward 1, 2, and 3 years, respectively.</p><p><b>Results: </b> We identified 4026 cases with an incident idiopathic PD diagnosis and 15 969 matched controls. Compared with patients without any previous prescription for NSAIDs, those with prior use had no increased risk of a PD diagnosis (OR 1.07, 95% CI 0.99–1.16). Long‐term use (≥15 prescriptions) was associated with a slightly lower PD risk (adjusted OR 0.94, 95% CI 0.83–1.07). The relative PD risks of the use of aspirin or acetaminophen were not materially higher (PD risk of long‐term use: adjusted ORs 1.16, 95% CI 1.03–1.30 and 1.15, 95% CI 1.02–1.30, respectively) compared with those for non‐users. The risk estimate diminished toward the null in subsequent analyses with shifted index dates.</p><p><b>Conclusion: </b> In this large observational study with data from the UK primary care, the long‐term use of NSAIDs, aspirin, or acetaminophen was not associated with a substantially altered risk of developing PD.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>NSAID use and risk of Parkinson disease: a population‐based case‐control study</title></titleInfo><titleInfo type="abbreviated"><title>NSAID use and risk of Parkinson disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>NSAID use and risk of Parkinson disease: a population‐based case‐control study</title></titleInfo><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Becker</namePart><affiliation>Basel Pharmacoepidemiology Unit, Division of Clinical Pharmacy and Epidemiology, Department of Pharmaceutical Sciences, University of Basel, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S. S.</namePart><namePart type="family">Jick</namePart><affiliation>Boston Collaborative Drug Surveillance Program, Boston University Medical Center, Lexington, MA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. R.</namePart><namePart type="family">Meier</namePart><affiliation>Basel Pharmacoepidemiology Unit, Division of Clinical Pharmacy and Epidemiology, Department of Pharmaceutical Sciences, University of Basel, Switzerland</affiliation><affiliation>Boston Collaborative Drug Surveillance Program, Boston University Medical Center, Lexington, MA, USA</affiliation><affiliation>Hospital Pharmacy, University Hospital, Spitalstrasse 26, Basel, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2011-11</dateIssued><edition>Received 6 December 2010 Accepted 3 March 2011</edition><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">4</extent></physicalDescription><abstract lang="en">Background: Previous epidemiologic studies have produced inconsistent findings regarding the association between the use of non‐steroidal anti‐inflammatory drugs (NSAIDs) and the risk of Parkinson disease (PD). Methods: We conducted a case–control analysis using the General Practice Research Database. Cases (≥40 years) had a new diagnosis of PD between 1994 and 2009. We matched four controls to each PD case on age, sex, general practice, and index date. Use of NSAIDs, aspirin, and acetaminophen was stratified by exposure timing and duration for both cases and controls. We calculated odds ratios (OR) using conditional logistic regression. For additional analyses, the index date was brought backward 1, 2, and 3 years, respectively. Results: We identified 4026 cases with an incident idiopathic PD diagnosis and 15 969 matched controls. Compared with patients without any previous prescription for NSAIDs, those with prior use had no increased risk of a PD diagnosis (OR 1.07, 95% CI 0.99–1.16). Long‐term use (≥15 prescriptions) was associated with a slightly lower PD risk (adjusted OR 0.94, 95% CI 0.83–1.07). The relative PD risks of the use of aspirin or acetaminophen were not materially higher (PD risk of long‐term use: adjusted ORs 1.16, 95% CI 1.03–1.30 and 1.15, 95% CI 1.02–1.30, respectively) compared with those for non‐users. The risk estimate diminished toward the null in subsequent analyses with shifted index dates. Conclusion: In this large observational study with data from the UK primary care, the long‐term use of NSAIDs, aspirin, or acetaminophen was not associated with a substantially altered risk of developing PD.</abstract><subject lang="en"><genre>Keywords</genre><topic>case–control analysis</topic><topic>epidemiology</topic><topic>non‐steroidal anti‐inflammatory drugs</topic><topic>Parkinson disease</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neurology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1351-5101</identifier><identifier type="eISSN">1468-1331</identifier><identifier type="DOI">10.1111/(ISSN)1468-1331</identifier><identifier type="PublisherID">ENE</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>1336</start><end>1342</end><total>7</total></extent></part></relatedItem><identifier type="istex">2DA69C60955AB3398C85649A97FE5725EE5A60D0</identifier><identifier type="DOI">10.1111/j.1468-1331.2011.03399.x</identifier><identifier type="ArticleID">ENE3399</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2011 The Author(s). 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