Antiphospholipid antibodies: An epiphenomenon in tourette syndrome
Identifieur interne : 005402 ( Main/Exploration ); précédent : 005401; suivant : 005403Antiphospholipid antibodies: An epiphenomenon in tourette syndrome
Auteurs : Singer [États-Unis] ; Andrea Krumholz [États-Unis] ; Joseph Giuliano [États-Unis] ; Louise S. Kiessling [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 1997-09.
English descriptors
- KwdEn :
- Adolescent, Antibodies, Anticardiolipin (blood), Antibodies, Antinuclear (blood), Antibodies, Antiphospholipid (blood), Anticardiolipin antibody, Antiphospholipid antibody, Case-Control Studies, Child, Cross-Sectional Studies, Female, Humans, Immunoglobulin G (blood), Lupus Coagulation Inhibitor (blood), Lupus anticoagulant, Male, Pathophysiology, Severity of Illness Index, Tourette Syndrome (blood), Tourette Syndrome (immunology), Tourette syndrome.
- MESH :
- chemical , blood : Antibodies, Anticardiolipin, Antibodies, Antinuclear, Antibodies, Antiphospholipid, Immunoglobulin G, Lupus Coagulation Inhibitor.
- blood : Tourette Syndrome.
- immunology : Tourette Syndrome.
- Adolescent, Case-Control Studies, Child, Cross-Sectional Studies, Female, Humans, Male, Severity of Illness Index.
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
Affiliations:
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Kiessling</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pediatrics and Family Medicine, Brown University, Providence, Rhode Island</wicri:regionArea><placeName><region type="state">Rhode Island</region></placeName></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>Adolescent</term><term>Antibodies, Anticardiolipin (blood)</term><term>Antibodies, Antinuclear (blood)</term><term>Antibodies, Antiphospholipid (blood)</term><term>Anticardiolipin antibody</term><term>Antiphospholipid antibody</term><term>Case-Control Studies</term><term>Child</term><term>Cross-Sectional Studies</term><term>Female</term><term>Humans</term><term>Immunoglobulin G (blood)</term><term>Lupus Coagulation Inhibitor (blood)</term><term>Lupus anticoagulant</term><term>Male</term><term>Pathophysiology</term><term>Severity of Illness Index</term><term>Tourette Syndrome (blood)</term><term>Tourette Syndrome (immunology)</term><term>Tourette syndrome</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Antibodies, Anticardiolipin</term><term>Antibodies, Antinuclear</term><term>Antibodies, Antiphospholipid</term><term>Immunoglobulin G</term><term>Lupus Coagulation Inhibitor</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Tourette Syndrome</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Tourette Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Case-Control Studies</term><term>Child</term><term>Cross-Sectional Studies</term><term>Female</term><term>Humans</term><term>Male</term><term>Severity of Illness Index</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><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li><li>Rhode Island</li></region></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Singer" sort="Singer" uniqKey="Singer" last="Singer">Singer</name></region><name sortKey="Giuliano, Joseph" sort="Giuliano, Joseph" uniqKey="Giuliano J" first="Joseph" last="Giuliano">Joseph Giuliano</name><name sortKey="Kiessling, Louise S" sort="Kiessling, Louise S" uniqKey="Kiessling L" first="Louise S." last="Kiessling">Louise S. Kiessling</name><name sortKey="Krumholz, Andrea" sort="Krumholz, Andrea" uniqKey="Krumholz A" first="Andrea" last="Krumholz">Andrea Krumholz</name><name sortKey="Singer" sort="Singer" uniqKey="Singer" last="Singer">Singer</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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