Antiphospholipid antibodies: an epiphenomenon in Tourette syndrome.
Identifieur interne : 004D84 ( Ncbi/Checkpoint ); précédent : 004D83; suivant : 004D85Antiphospholipid antibodies: an epiphenomenon in Tourette syndrome.
Auteurs : H S Singer [États-Unis] ; A. Krumholz ; J. Giuliano ; L S KiesslingSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1997.
English descriptors
- KwdEn :
- Adolescent, Antibodies, Anticardiolipin (blood), Antibodies, Antinuclear (blood), Antibodies, Antiphospholipid (blood), Case-Control Studies, Child, Cross-Sectional Studies, Female, Humans, Immunoglobulin G (blood), Lupus Coagulation Inhibitor (blood), Male, Severity of Illness Index, Tourette Syndrome (blood), Tourette Syndrome (immunology).
- 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 patient, based on a minimal requirement of a prolonged dilute Russell 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.
DOI: 10.1002/mds.870120518
PubMed: 9380057
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Antiphospholipid antibodies: an epiphenomenon in Tourette syndrome.</title><author><name sortKey="Singer, H S" sort="Singer, H S" uniqKey="Singer H" first="H S" last="Singer">H S Singer</name><affiliation wicri:level="2"><nlm:affiliation>Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Krumholz, A" sort="Krumholz, A" uniqKey="Krumholz A" first="A" last="Krumholz">A. Krumholz</name></author><author><name sortKey="Giuliano, J" sort="Giuliano, J" uniqKey="Giuliano J" first="J" last="Giuliano">J. Giuliano</name></author><author><name sortKey="Kiessling, L S" sort="Kiessling, L S" uniqKey="Kiessling L" first="L S" last="Kiessling">L S Kiessling</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1997">1997</date><idno type="RBID">pubmed:9380057</idno><idno type="pmid">9380057</idno><idno type="doi">10.1002/mds.870120518</idno><idno type="wicri:Area/PubMed/Corpus">004599</idno><idno type="wicri:Area/PubMed/Curation">004599</idno><idno type="wicri:Area/PubMed/Checkpoint">004715</idno><idno type="wicri:Area/Ncbi/Merge">004D84</idno><idno type="wicri:Area/Ncbi/Curation">004D84</idno><idno type="wicri:Area/Ncbi/Checkpoint">004D84</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Antiphospholipid antibodies: an epiphenomenon in Tourette syndrome.</title><author><name sortKey="Singer, H S" sort="Singer, H S" uniqKey="Singer H" first="H S" last="Singer">H S Singer</name><affiliation wicri:level="2"><nlm:affiliation>Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Krumholz, A" sort="Krumholz, A" uniqKey="Krumholz A" first="A" last="Krumholz">A. Krumholz</name></author><author><name sortKey="Giuliano, J" sort="Giuliano, J" uniqKey="Giuliano J" first="J" last="Giuliano">J. Giuliano</name></author><author><name sortKey="Kiessling, L S" sort="Kiessling, L S" uniqKey="Kiessling L" first="L S" last="Kiessling">L S Kiessling</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1997" type="published">1997</date></imprint></series></biblStruct></sourceDesc></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>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>Male</term><term>Severity of Illness Index</term><term>Tourette Syndrome (blood)</term><term>Tourette Syndrome (immunology)</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></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 patient, based on a minimal requirement of a prolonged dilute Russell 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></region></list><tree><noCountry><name sortKey="Giuliano, J" sort="Giuliano, J" uniqKey="Giuliano J" first="J" last="Giuliano">J. Giuliano</name><name sortKey="Kiessling, L S" sort="Kiessling, L S" uniqKey="Kiessling L" first="L S" last="Kiessling">L S Kiessling</name><name sortKey="Krumholz, A" sort="Krumholz, A" uniqKey="Krumholz A" first="A" last="Krumholz">A. Krumholz</name></noCountry><country name="États-Unis"><region name="Maryland"><name sortKey="Singer, H S" sort="Singer, H S" uniqKey="Singer H" first="H S" last="Singer">H S Singer</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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