Cerebellar ataxia as a possible organ-specific autoimmune disease.
Identifieur interne : 002183 ( PubMed/Curation ); précédent : 002182; suivant : 002184Cerebellar ataxia as a possible organ-specific autoimmune disease.
Auteurs : Marios Hadjivassiliou [Royaume-Uni] ; Sabrina Boscolo ; Enrico Tongiorgi ; Richard A. Grünewald ; Basil Sharrack ; David S. Sanders ; Nicola Woodroofe ; G Aelwyn B. Davies-JonesSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2008.
English descriptors
- KwdEn :
- Adolescent, Adult, Aged, Aged, 80 and over, Animals, Autoantibodies (blood), Autoimmune Diseases of the Nervous System (blood), Autoimmune Diseases of the Nervous System (genetics), Autoimmune Diseases of the Nervous System (immunology), Brain (immunology), Cerebellar Ataxia (blood), Cerebellar Ataxia (genetics), Cerebellar Ataxia (immunology), Cerebellum (immunology), DNA Mutational Analysis, Diagnostic Imaging, Disease Progression, Female, HLA-DQ Antigens (analysis), HLA-DQ Antigens (genetics), Humans, Male, Middle Aged, Organ Specificity, Prospective Studies, Rats, Rats, Sprague-Dawley.
- MESH :
- chemical , analysis : HLA-DQ Antigens.
- chemical , blood : Autoantibodies.
- blood : Autoimmune Diseases of the Nervous System, Cerebellar Ataxia.
- genetics : Autoimmune Diseases of the Nervous System, Cerebellar Ataxia, HLA-DQ Antigens.
- immunology : Autoimmune Diseases of the Nervous System, Brain, Cerebellar Ataxia, Cerebellum.
- Adolescent, Adult, Aged, Aged, 80 and over, Animals, DNA Mutational Analysis, Diagnostic Imaging, Disease Progression, Female, Humans, Male, Middle Aged, Organ Specificity, Prospective Studies, Rats, Rats, Sprague-Dawley.
Abstract
The purpose of this study was to investigate the possibility that autoimmunity is responsible for some cases of sporadic idiopathic ataxia. We prospectively investigated 400 patients with progressive ataxia and identified a group of patients with idiopathic sporadic ataxia. A comparison of the prevalence of autoimmune diseases, the autoimmunity linked HLA DQ2, and serum anticerebellar antibodies was made between patients with idiopathic sporadic and those with genetically characterized ataxia. Ninety-one of 400 (23%) patients with progressive ataxia had idiopathic sporadic ataxia. The prevalence of autoimmune diseases in this group was 47% as compared with 6% in the group of patients with genetic ataxias (P < 0.0001). The HLA DQ2 was found in 71% of patients with sporadic ataxia, in 34% in patients with genetic ataxia, and in 36% of healthy local population (P = 0.0005 by Chi squared test). Anticerebellar antibodies were detected in 12 out of 20 patients with idiopathic sporadic as opposed to one of 20 patients with genetic ataxia. The significantly higher prevalence of autoimmune diseases, HLA DQ2 and anti-cerebellar antibodies in patients with idiopathic sporadic ataxia compared to genetic ataxia supports the notion that autoimmunity may account for some cases of idiopathic sporadic cerebellar ataxia.
DOI: 10.1002/mds.22129
PubMed: 18546342
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Grünewald</name></author><author><name sortKey="Sharrack, Basil" sort="Sharrack, Basil" uniqKey="Sharrack B" first="Basil" last="Sharrack">Basil Sharrack</name></author><author><name sortKey="Sanders, David S" sort="Sanders, David S" uniqKey="Sanders D" first="David S" last="Sanders">David S. Sanders</name></author><author><name sortKey="Woodroofe, Nicola" sort="Woodroofe, Nicola" uniqKey="Woodroofe N" first="Nicola" last="Woodroofe">Nicola Woodroofe</name></author><author><name sortKey="Davies Jones, G Aelwyn B" sort="Davies Jones, G Aelwyn B" uniqKey="Davies Jones G" first="G Aelwyn B" last="Davies-Jones">G Aelwyn B. Davies-Jones</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="doi">10.1002/mds.22129</idno><idno type="RBID">pubmed:18546342</idno><idno type="pmid">18546342</idno><idno type="wicri:Area/PubMed/Corpus">002183</idno><idno type="wicri:Area/PubMed/Curation">002183</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Cerebellar ataxia as a possible organ-specific autoimmune disease.</title><author><name sortKey="Hadjivassiliou, Marios" sort="Hadjivassiliou, Marios" uniqKey="Hadjivassiliou M" first="Marios" last="Hadjivassiliou">Marios Hadjivassiliou</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, The Royal Hallamshire Hospital, Glossop Road, Sheffield, UK. m.hadjivassiliou@sheffield.ac.uk</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Neurology, The Royal Hallamshire Hospital, Glossop Road, Sheffield</wicri:regionArea></affiliation></author><author><name sortKey="Boscolo, Sabrina" sort="Boscolo, Sabrina" uniqKey="Boscolo S" first="Sabrina" last="Boscolo">Sabrina Boscolo</name></author><author><name sortKey="Tongiorgi, Enrico" sort="Tongiorgi, Enrico" uniqKey="Tongiorgi E" first="Enrico" last="Tongiorgi">Enrico Tongiorgi</name></author><author><name sortKey="Grunewald, Richard A" sort="Grunewald, Richard A" uniqKey="Grunewald R" first="Richard A" last="Grünewald">Richard A. Grünewald</name></author><author><name sortKey="Sharrack, Basil" sort="Sharrack, Basil" uniqKey="Sharrack B" first="Basil" last="Sharrack">Basil Sharrack</name></author><author><name sortKey="Sanders, David S" sort="Sanders, David S" uniqKey="Sanders D" first="David S" last="Sanders">David S. Sanders</name></author><author><name sortKey="Woodroofe, Nicola" sort="Woodroofe, Nicola" uniqKey="Woodroofe N" first="Nicola" last="Woodroofe">Nicola Woodroofe</name></author><author><name sortKey="Davies Jones, G Aelwyn B" sort="Davies Jones, G Aelwyn B" uniqKey="Davies Jones G" first="G Aelwyn B" last="Davies-Jones">G Aelwyn B. Davies-Jones</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>Autoantibodies (blood)</term><term>Autoimmune Diseases of the Nervous System (blood)</term><term>Autoimmune Diseases of the Nervous System (genetics)</term><term>Autoimmune Diseases of the Nervous System (immunology)</term><term>Brain (immunology)</term><term>Cerebellar Ataxia (blood)</term><term>Cerebellar Ataxia (genetics)</term><term>Cerebellar Ataxia (immunology)</term><term>Cerebellum (immunology)</term><term>DNA Mutational Analysis</term><term>Diagnostic Imaging</term><term>Disease Progression</term><term>Female</term><term>HLA-DQ Antigens (analysis)</term><term>HLA-DQ Antigens (genetics)</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Organ Specificity</term><term>Prospective Studies</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>HLA-DQ Antigens</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Autoantibodies</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Autoimmune Diseases of the Nervous System</term><term>Cerebellar Ataxia</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autoimmune Diseases of the Nervous System</term><term>Cerebellar Ataxia</term><term>HLA-DQ Antigens</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Autoimmune Diseases of the Nervous System</term><term>Brain</term><term>Cerebellar Ataxia</term><term>Cerebellum</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>DNA Mutational Analysis</term><term>Diagnostic Imaging</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Organ Specificity</term><term>Prospective Studies</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The purpose of this study was to investigate the possibility that autoimmunity is responsible for some cases of sporadic idiopathic ataxia. We prospectively investigated 400 patients with progressive ataxia and identified a group of patients with idiopathic sporadic ataxia. A comparison of the prevalence of autoimmune diseases, the autoimmunity linked HLA DQ2, and serum anticerebellar antibodies was made between patients with idiopathic sporadic and those with genetically characterized ataxia. Ninety-one of 400 (23%) patients with progressive ataxia had idiopathic sporadic ataxia. The prevalence of autoimmune diseases in this group was 47% as compared with 6% in the group of patients with genetic ataxias (P < 0.0001). The HLA DQ2 was found in 71% of patients with sporadic ataxia, in 34% in patients with genetic ataxia, and in 36% of healthy local population (P = 0.0005 by Chi squared test). Anticerebellar antibodies were detected in 12 out of 20 patients with idiopathic sporadic as opposed to one of 20 patients with genetic ataxia. The significantly higher prevalence of autoimmune diseases, HLA DQ2 and anti-cerebellar antibodies in patients with idiopathic sporadic ataxia compared to genetic ataxia supports the notion that autoimmunity may account for some cases of idiopathic sporadic cerebellar ataxia.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">18546342</PMID><DateCreated><Year>2008</Year><Month>08</Month><Day>05</Day></DateCreated><DateCompleted><Year>2008</Year><Month>11</Month><Day>18</Day></DateCompleted><DateRevised><Year>2011</Year><Month>11</Month><Day>17</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>10</Issue><PubDate><Year>2008</Year><Month>Jul</Month><Day>30</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Cerebellar ataxia as a possible organ-specific autoimmune disease.</ArticleTitle><Pagination><MedlinePgn>1370-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22129</ELocationID><Abstract><AbstractText>The purpose of this study was to investigate the possibility that autoimmunity is responsible for some cases of sporadic idiopathic ataxia. We prospectively investigated 400 patients with progressive ataxia and identified a group of patients with idiopathic sporadic ataxia. A comparison of the prevalence of autoimmune diseases, the autoimmunity linked HLA DQ2, and serum anticerebellar antibodies was made between patients with idiopathic sporadic and those with genetically characterized ataxia. Ninety-one of 400 (23%) patients with progressive ataxia had idiopathic sporadic ataxia. The prevalence of autoimmune diseases in this group was 47% as compared with 6% in the group of patients with genetic ataxias (P < 0.0001). The HLA DQ2 was found in 71% of patients with sporadic ataxia, in 34% in patients with genetic ataxia, and in 36% of healthy local population (P = 0.0005 by Chi squared test). Anticerebellar antibodies were detected in 12 out of 20 patients with idiopathic sporadic as opposed to one of 20 patients with genetic ataxia. The significantly higher prevalence of autoimmune diseases, HLA DQ2 and anti-cerebellar antibodies in patients with idiopathic sporadic ataxia compared to genetic ataxia supports the notion that autoimmunity may account for some cases of idiopathic sporadic cerebellar ataxia.</AbstractText><CopyrightInformation>Copyright 2008 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hadjivassiliou</LastName><ForeName>Marios</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Neurology, The Royal Hallamshire Hospital, Glossop Road, Sheffield, UK. m.hadjivassiliou@sheffield.ac.uk</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boscolo</LastName><ForeName>Sabrina</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Tongiorgi</LastName><ForeName>Enrico</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Grünewald</LastName><ForeName>Richard A</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>Sharrack</LastName><ForeName>Basil</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Sanders</LastName><ForeName>David S</ForeName><Initials>DS</Initials></Author><Author ValidYN="Y"><LastName>Woodroofe</LastName><ForeName>Nicola</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Davies-Jones</LastName><ForeName>G Aelwyn B</ForeName><Initials>GA</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001323">Autoantibodies</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006683">HLA-DQ Antigens</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C053186">HLA-DQ2 antigen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000293">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000328">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000369">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001323">Autoantibodies</DescriptorName><QualifierName MajorTopicYN="N" 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UI="Q000276">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004252">DNA Mutational Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003952">Diagnostic Imaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018450">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006683">HLA-DQ Antigens</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000032">analysis</QualifierName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009928">Organ Specificity</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011446">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017207">Rats, Sprague-Dawley</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>6</Month><Day>12</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>11</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>6</Month><Day>12</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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