Antiphospholipid antibodies: An epiphenomenon in tourette syndrome
Identifieur interne : 001C64 ( Istex/Corpus ); précédent : 001C63; suivant : 001C65Antiphospholipid antibodies: An epiphenomenon in tourette syndrome
Auteurs : Singer ; Andrea Krumholz ; Joseph Giuliano ; Louise S. KiesslingSource :
- Movement Disorders [ 0885-3185 ] ; 1997-09.
English descriptors
- KwdEn :
Abstract
Antiphospholipids (aPLAs) have been previously identified in children with Tourette syndrome (TS), which has led to the speculation that these antibodies might have a pathophysiologic role in this disorder. Therefore, 21 healthy children and adolescents with TS, whose ages ranged from 7 to 17 years, underwent laboratory studies designed to diagnose the lupus anticoagulant, anticardiolipin (aCL) antibodies [immunoglobulin (Ig) G, IgA, and IgM], and antinuclear antibodies. Although five subjects had at least one value that differed from accepted laboratory standards, the changes were marginal in four of them. Lupus anticoagulant was identified in one patients, based on a minimal requirement of a prolonged dilute Russel viper venom time, clotting studies that did not correct after mixture with normal plasma, and an abnormal platelet neutralization procedure. A prolonged (but correctable) activated partial thromboplastin time was found in one individual, and aCL IgG was marginally increased in three subjects. Two (10%) of a control population of 20 same‐age children also had low positive aCL IgG levels. There were no differences in tics (onset, type, frequency, severity, and family history) or comorbid features between children with normal or “abnormal” laboratory study results. Our data suggest that the presence of aPLAs in TS represents an epiphenomenon rather than a pathophysiologic mechanism.
Url:
DOI: 10.1002/mds.870120518
Links to Exploration step
ISTEX:67EEF7037B3A9AD388C3DE8434C21FBE7F183893Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Antiphospholipid antibodies: An epiphenomenon in tourette syndrome</title><author><name sortKey="Singer" sort="Singer" uniqKey="Singer" last="Singer">Singer</name><affiliation><mods:affiliation>Department of Neurology, Baltimore, Maryland</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Krumholz, Andrea" sort="Krumholz, Andrea" uniqKey="Krumholz A" first="Andrea" last="Krumholz">Andrea Krumholz</name><affiliation><mods:affiliation>Department of Neurology, Baltimore, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Giuliano, Joseph" sort="Giuliano, Joseph" uniqKey="Giuliano J" first="Joseph" last="Giuliano">Joseph Giuliano</name><affiliation><mods:affiliation>Department of Neurology, Baltimore, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Kiessling, Louise S" sort="Kiessling, Louise S" uniqKey="Kiessling L" first="Louise S." last="Kiessling">Louise S. Kiessling</name><affiliation><mods:affiliation>Department of Pediatrics and Family Medicine, Brown University, Providence, Rhode Island, U.S.A.</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:67EEF7037B3A9AD388C3DE8434C21FBE7F183893</idno><date when="1997" year="1997">1997</date><idno type="doi">10.1002/mds.870120518</idno><idno type="url">https://api.istex.fr/document/67EEF7037B3A9AD388C3DE8434C21FBE7F183893/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001C64</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Antiphospholipid antibodies: An epiphenomenon in tourette syndrome</title><author><name sortKey="Singer" sort="Singer" uniqKey="Singer" last="Singer">Singer</name><affiliation><mods:affiliation>Department of Neurology, Baltimore, Maryland</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Krumholz, Andrea" sort="Krumholz, Andrea" uniqKey="Krumholz A" first="Andrea" last="Krumholz">Andrea Krumholz</name><affiliation><mods:affiliation>Department of Neurology, Baltimore, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Giuliano, Joseph" sort="Giuliano, Joseph" uniqKey="Giuliano J" first="Joseph" last="Giuliano">Joseph Giuliano</name><affiliation><mods:affiliation>Department of Neurology, Baltimore, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Kiessling, Louise S" sort="Kiessling, Louise S" uniqKey="Kiessling L" first="Louise S." last="Kiessling">Louise S. Kiessling</name><affiliation><mods:affiliation>Department of Pediatrics and Family Medicine, Brown University, Providence, Rhode Island, U.S.A.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1997-09">1997-09</date><biblScope unit="vol">12</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="738">738</biblScope><biblScope unit="page" to="742">742</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">67EEF7037B3A9AD388C3DE8434C21FBE7F183893</idno><idno type="DOI">10.1002/mds.870120518</idno><idno type="ArticleID">MDS870120518</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Anticardiolipin antibody</term><term>Antiphospholipid antibody</term><term>Lupus anticoagulant</term><term>Pathophysiology</term><term>Tourette syndrome</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Antiphospholipids (aPLAs) have been previously identified in children with Tourette syndrome (TS), which has led to the speculation that these antibodies might have a pathophysiologic role in this disorder. Therefore, 21 healthy children and adolescents with TS, whose ages ranged from 7 to 17 years, underwent laboratory studies designed to diagnose the lupus anticoagulant, anticardiolipin (aCL) antibodies [immunoglobulin (Ig) G, IgA, and IgM], and antinuclear antibodies. Although five subjects had at least one value that differed from accepted laboratory standards, the changes were marginal in four of them. Lupus anticoagulant was identified in one patients, based on a minimal requirement of a prolonged dilute Russel viper venom time, clotting studies that did not correct after mixture with normal plasma, and an abnormal platelet neutralization procedure. A prolonged (but correctable) activated partial thromboplastin time was found in one individual, and aCL IgG was marginally increased in three subjects. Two (10%) of a control population of 20 same‐age children also had low positive aCL IgG levels. There were no differences in tics (onset, type, frequency, severity, and family history) or comorbid features between children with normal or “abnormal” laboratory study results. Our data suggest that the presence of aPLAs in TS represents an epiphenomenon rather than a pathophysiologic mechanism.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Singer</name><affiliations><json:string>Department of Neurology, Baltimore, Maryland</json:string><json:string>Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland</json:string></affiliations></json:item><json:item><name>Andrea Krumholz</name><affiliations><json:string>Department of Neurology, Baltimore, Maryland</json:string></affiliations></json:item><json:item><name>Joseph Giuliano</name><affiliations><json:string>Department of Neurology, Baltimore, Maryland</json:string></affiliations></json:item><json:item><name>Louise S. Kiessling</name><affiliations><json:string>Department of Pediatrics and Family Medicine, Brown University, Providence, Rhode Island, U.S.A.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Tourette syndrome</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Antiphospholipid antibody</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Anticardiolipin antibody</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Lupus anticoagulant</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Pathophysiology</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Antiphospholipids (aPLAs) have been previously identified in children with Tourette syndrome (TS), which has led to the speculation that these antibodies might have a pathophysiologic role in this disorder. Therefore, 21 healthy children and adolescents with TS, whose ages ranged from 7 to 17 years, underwent laboratory studies designed to diagnose the lupus anticoagulant, anticardiolipin (aCL) antibodies [immunoglobulin (Ig) G, IgA, and IgM], and antinuclear antibodies. Although five subjects had at least one value that differed from accepted laboratory standards, the changes were marginal in four of them. Lupus anticoagulant was identified in one patients, based on a minimal requirement of a prolonged dilute Russel viper venom time, clotting studies that did not correct after mixture with normal plasma, and an abnormal platelet neutralization procedure. A prolonged (but correctable) activated partial thromboplastin time was found in one individual, and aCL IgG was marginally increased in three subjects. Two (10%) of a control population of 20 same‐age children also had low positive aCL IgG levels. There were no differences in tics (onset, type, frequency, severity, and family history) or comorbid features between children with normal or “abnormal” laboratory study results. Our data suggest that the presence of aPLAs in TS represents an epiphenomenon rather than a pathophysiologic mechanism.</abstract><qualityIndicators><score>5.606</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 827.759 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1415</abstractCharCount><pdfWordCount>3122</pdfWordCount><pdfCharCount>20034</pdfCharCount><pdfPageCount>5</pdfPageCount><abstractWordCount>207</abstractWordCount></qualityIndicators><title>Antiphospholipid antibodies: An epiphenomenon in tourette syndrome</title><genre><json:string>Serial article</json:string></genre><host><volume>12</volume><pages><total>5</total><last>742</last><first>738</first></pages><issn><json:string>0885-3185</json:string></issn><issue>5</issue><subject><json:item><value>Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>1997</publicationDate><copyrightDate>1997</copyrightDate><doi><json:string>10.1002/mds.870120518</json:string></doi><id>67EEF7037B3A9AD388C3DE8434C21FBE7F183893</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/67EEF7037B3A9AD388C3DE8434C21FBE7F183893/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/67EEF7037B3A9AD388C3DE8434C21FBE7F183893/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/67EEF7037B3A9AD388C3DE8434C21FBE7F183893/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Antiphospholipid antibodies: An epiphenomenon in tourette syndrome</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>1997</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Antiphospholipid antibodies: An epiphenomenon in tourette syndrome</title><author><persName><surname>Singer</surname><roleName type="degree">Dr.</roleName></persName><note type="correspondence"><p>Correspondence: Department of Neurology, Johns Hopkins Hospital, Harvey 811, 600 North Wolfe Street, Baltimore, MD 21287–8811, U.S.A.</p></note><affiliation>Department of Neurology, Baltimore, Maryland</affiliation><affiliation>Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland</affiliation></author><author><persName><forename type="first">Andrea</forename><surname>Krumholz</surname></persName><affiliation>Department of Neurology, Baltimore, Maryland</affiliation></author><author><persName><forename type="first">Joseph</forename><surname>Giuliano</surname></persName><affiliation>Department of Neurology, Baltimore, Maryland</affiliation></author><author><persName><forename type="first">Louise S.</forename><surname>Kiessling</surname></persName><affiliation>Department of Pediatrics and Family Medicine, Brown University, Providence, Rhode Island, U.S.A.</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</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="1997-09"></date><biblScope unit="vol">12</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="738">738</biblScope><biblScope unit="page" to="742">742</biblScope></imprint></monogr><idno type="istex">67EEF7037B3A9AD388C3DE8434C21FBE7F183893</idno><idno type="DOI">10.1002/mds.870120518</idno><idno type="ArticleID">MDS870120518</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1997</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Antiphospholipids (aPLAs) have been previously identified in children with Tourette syndrome (TS), which has led to the speculation that these antibodies might have a pathophysiologic role in this disorder. Therefore, 21 healthy children and adolescents with TS, whose ages ranged from 7 to 17 years, underwent laboratory studies designed to diagnose the lupus anticoagulant, anticardiolipin (aCL) antibodies [immunoglobulin (Ig) G, IgA, and IgM], and antinuclear antibodies. Although five subjects had at least one value that differed from accepted laboratory standards, the changes were marginal in four of them. Lupus anticoagulant was identified in one patients, based on a minimal requirement of a prolonged dilute Russel viper venom time, clotting studies that did not correct after mixture with normal plasma, and an abnormal platelet neutralization procedure. A prolonged (but correctable) activated partial thromboplastin time was found in one individual, and aCL IgG was marginally increased in three subjects. Two (10%) of a control population of 20 same‐age children also had low positive aCL IgG levels. There were no differences in tics (onset, type, frequency, severity, and family history) or comorbid features between children with normal or “abnormal” laboratory study results. Our data suggest that the presence of aPLAs in TS represents an epiphenomenon rather than a pathophysiologic mechanism.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Tourette syndrome</term></item><item><term>Antiphospholipid antibody</term></item><item><term>Anticardiolipin antibody</term></item><item><term>Lupus anticoagulant</term></item><item><term>Pathophysiology</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996-02-21">Received</change><change when="1996-08-15">Registration</change><change when="1997-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/67EEF7037B3A9AD388C3DE8434C21FBE7F183893/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="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="50"><doi origin="wiley" registered="yes">10.1002/mds.v12:5</doi><numberingGroup><numbering type="journalVolume" number="12">12</numbering><numbering type="journalIssue">5</numbering></numberingGroup><coverDate startDate="1997-09">September 1997</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="18" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.870120518</doi><idGroup><id type="unit" value="MDS870120518"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 1997 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="1996-02-21"></event><event type="manuscriptRevised" date="1996-07-02"></event><event type="manuscriptAccepted" date="1996-08-15"></event><event type="firstOnline" date="2004-11-04"></event><event type="publishedOnlineFinalForm" date="2004-11-04"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">738</numbering><numbering type="pageLast">742</numbering></numberingGroup><correspondenceTo>Department of Neurology, Johns Hopkins Hospital, Harvey 811, 600 North Wolfe Street, Baltimore, MD 21287–8811, U.S.A.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS870120518.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="44"></count></countGroup><titleGroup><title type="main" xml:lang="en">Antiphospholipid antibodies: An epiphenomenon in tourette syndrome</title><title type="short" xml:lang="en">AMTIPHOSPHOLIPIDS IN TOURETTE SYNDROME</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>Harvey S.</givenNames><familyName>Singer</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Andrea</givenNames><familyName>Krumholz</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Joseph</givenNames><familyName>Giuliano</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Louise S.</givenNames><familyName>Kiessling</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Baltimore, Maryland</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Pediatrics and Family Medicine, Brown University, Providence, Rhode Island, U.S.A.</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Tourette syndrome</keyword><keyword xml:id="kwd2">Antiphospholipid antibody</keyword><keyword xml:id="kwd3">Anticardiolipin antibody</keyword><keyword xml:id="kwd4">Lupus anticoagulant</keyword><keyword xml:id="kwd5">Pathophysiology</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Antiphospholipids (aPLAs) have been previously identified in children with Tourette syndrome (TS), which has led to the speculation that these antibodies might have a pathophysiologic role in this disorder. Therefore, 21 healthy children and adolescents with TS, whose ages ranged from 7 to 17 years, underwent laboratory studies designed to diagnose the lupus anticoagulant, anticardiolipin (aCL) antibodies [immunoglobulin (Ig) G, IgA, and IgM], and antinuclear antibodies. Although five subjects had at least one value that differed from accepted laboratory standards, the changes were marginal in four of them. Lupus anticoagulant was identified in one patients, based on a minimal requirement of a prolonged dilute Russel viper venom time, clotting studies that did not correct after mixture with normal plasma, and an abnormal platelet neutralization procedure. A prolonged (but correctable) activated partial thromboplastin time was found in one individual, and aCL IgG was marginally increased in three subjects. Two (10%) of a control population of 20 same‐age children also had low positive aCL IgG levels. There were no differences in tics (onset, type, frequency, severity, and family history) or comorbid features between children with normal or “abnormal” laboratory study results. Our data suggest that the presence of aPLAs in TS represents an epiphenomenon rather than a pathophysiologic mechanism.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Antiphospholipid antibodies: An epiphenomenon in tourette syndrome</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>AMTIPHOSPHOLIPIDS IN TOURETTE SYNDROME</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Antiphospholipid antibodies: An epiphenomenon in tourette syndrome</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Singer</namePart><affiliation>Department of Neurology, Baltimore, Maryland</affiliation><affiliation>Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland</affiliation><description>Correspondence: Department of Neurology, Johns Hopkins Hospital, Harvey 811, 600 North Wolfe Street, Baltimore, MD 21287–8811, U.S.A.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrea</namePart><namePart type="family">Krumholz</namePart><affiliation>Department of Neurology, Baltimore, Maryland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joseph</namePart><namePart type="family">Giuliano</namePart><affiliation>Department of Neurology, Baltimore, Maryland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Louise S.</namePart><namePart type="family">Kiessling</namePart><affiliation>Department of Pediatrics and Family Medicine, Brown University, Providence, Rhode Island, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></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">1997-09</dateIssued><dateCaptured encoding="w3cdtf">1996-02-21</dateCaptured><dateValid encoding="w3cdtf">1996-08-15</dateValid><copyrightDate encoding="w3cdtf">1997</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">2</extent><extent unit="references">44</extent></physicalDescription><abstract lang="en">Antiphospholipids (aPLAs) have been previously identified in children with Tourette syndrome (TS), which has led to the speculation that these antibodies might have a pathophysiologic role in this disorder. Therefore, 21 healthy children and adolescents with TS, whose ages ranged from 7 to 17 years, underwent laboratory studies designed to diagnose the lupus anticoagulant, anticardiolipin (aCL) antibodies [immunoglobulin (Ig) G, IgA, and IgM], and antinuclear antibodies. Although five subjects had at least one value that differed from accepted laboratory standards, the changes were marginal in four of them. Lupus anticoagulant was identified in one patients, based on a minimal requirement of a prolonged dilute Russel viper venom time, clotting studies that did not correct after mixture with normal plasma, and an abnormal platelet neutralization procedure. A prolonged (but correctable) activated partial thromboplastin time was found in one individual, and aCL IgG was marginally increased in three subjects. Two (10%) of a control population of 20 same‐age children also had low positive aCL IgG levels. There were no differences in tics (onset, type, frequency, severity, and family history) or comorbid features between children with normal or “abnormal” laboratory study results. Our data suggest that the presence of aPLAs in TS represents an epiphenomenon rather than a pathophysiologic mechanism.</abstract><subject lang="en"><genre>Keywords</genre><topic>Tourette syndrome</topic><topic>Antiphospholipid antibody</topic><topic>Anticardiolipin antibody</topic><topic>Lupus anticoagulant</topic><topic>Pathophysiology</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>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>1997</date><detail type="volume"><caption>vol.</caption><number>12</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>738</start><end>742</end><total>5</total></extent></part></relatedItem><identifier type="istex">67EEF7037B3A9AD388C3DE8434C21FBE7F183893</identifier><identifier type="DOI">10.1002/mds.870120518</identifier><identifier type="ArticleID">MDS870120518</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1997 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)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001C64 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 001C64 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:67EEF7037B3A9AD388C3DE8434C21FBE7F183893
|texte= Antiphospholipid antibodies: An epiphenomenon in tourette syndrome
}}
| This area was generated with Dilib version V0.6.23. |  |