The syndrome of deafness-dystonia: clinical and genetic heterogeneity.
Identifieur interne : 000A38 ( PubMed/Corpus ); précédent : 000A37; suivant : 000A39The syndrome of deafness-dystonia: clinical and genetic heterogeneity.
Auteurs : Maja Kojovic ; Isabel Pareés ; Tania Lampreia ; Karolina Pienczk-Reclawowicz ; Georgia Xiromerisiou ; Ignacio Rubio-Agusti ; Milica Kramberger ; Miryam Carecchio ; Anas M. Alazami ; Francesco Brancati ; Jaroslaw Slawek ; Zvezdan Pirtosek ; Enza Maria Valente ; Fowzan S. Alkuraya ; Mark J. Edwards ; Kailash P. BhatiaSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- Adolescent, Adult, Age of Onset, Apoptosis Regulatory Proteins (genetics), DNA-Binding Proteins (genetics), Deaf-Blind Disorders (etiology), Deaf-Blind Disorders (genetics), Disease Progression, Dystonia (etiology), Dystonia (genetics), Family Health, Female, Genetic Heterogeneity, Genetic Testing, Humans, Intellectual Disability (etiology), Intellectual Disability (genetics), Leviviridae, Male, Membrane Transport Proteins (genetics), Middle Aged, Mutation (genetics), Nuclear Proteins (genetics), Optic Atrophy (etiology), Optic Atrophy (genetics), Retrospective Studies, Ubiquitin-Protein Ligase Complexes, Young Adult.
- MESH :
- chemical , genetics : Apoptosis Regulatory Proteins, DNA-Binding Proteins, Membrane Transport Proteins, Nuclear Proteins.
- etiology : Deaf-Blind Disorders, Dystonia, Intellectual Disability, Optic Atrophy.
- genetics : Deaf-Blind Disorders, Dystonia, Intellectual Disability, Mutation, Optic Atrophy.
- Adolescent, Adult, Age of Onset, Disease Progression, Family Health, Female, Genetic Heterogeneity, Genetic Testing, Humans, Leviviridae, Male, Middle Aged, Retrospective Studies, Ubiquitin-Protein Ligase Complexes, Young Adult.
Abstract
The syndrome of deafness-dystonia is rare and refers to the association of hearing impairment and dystonia when these are dominant features of a disease. Known genetic causes include Mohr-Tranebjaerg syndrome, Woodhouse-Sakati syndrome, and mitochondrial disorders, but the cause frequently remains unidentified. The aim of the current study was to better characterize etiological and clinical aspects of deafness-dystonia syndrome. We evaluated 20 patients with deafness-dystonia syndrome who were seen during the period between 1994 and 2011. The cause was identified in only 7 patients and included methylmalonic aciduria, meningoencephalitis, perinatal hypoxic-ischemic injury, large genomic deletion on chromosome 7q21, translocase of inner mitochondrial membrane 8 homolog A (TIMM8A) mutation (Mohr-Tranebjaerg syndrome), and chromosome 2 open reading frame 37 (C2orf37) mutation (Woodhouse-Sakati syndrome). The age of onset and clinical characteristics in these patients varied, depending on the etiology. In 13 patients, the cause remained unexplained despite extensive work-up. In the group of patients who had unknown etiology, a family history for deafness and/or dystonia was present the majority of patients, suggesting a strong genetic component. Sensory-neural deafness always preceded dystonia. Two clinical patterns of deafness-dystonia syndrome were observed: patients who had an onset in childhood had generalized dystonia (10 of 13 patients) with frequent bulbar involvement, whereas patients who had a dystonia onset in adulthood had segmental dystonia (3 of 13 patients) with the invariable presence of laryngeal dystonia. Deafness-dystonia syndrome is etiologically and clinically heterogeneous, and most patients have an unknown cause. The different age at onset and variable family history suggest a heterogeneous genetic background, possibly including currently unidentified genetic conditions.
DOI: 10.1002/mds.25394
PubMed: 23418071
Links to Exploration step
pubmed:23418071Le document en format XML
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Alazami</name></author><author><name sortKey="Brancati, Francesco" sort="Brancati, Francesco" uniqKey="Brancati F" first="Francesco" last="Brancati">Francesco Brancati</name></author><author><name sortKey="Slawek, Jaroslaw" sort="Slawek, Jaroslaw" uniqKey="Slawek J" first="Jaroslaw" last="Slawek">Jaroslaw Slawek</name></author><author><name sortKey="Pirtosek, Zvezdan" sort="Pirtosek, Zvezdan" uniqKey="Pirtosek Z" first="Zvezdan" last="Pirtosek">Zvezdan Pirtosek</name></author><author><name sortKey="Valente, Enza Maria" sort="Valente, Enza Maria" uniqKey="Valente E" first="Enza Maria" last="Valente">Enza Maria Valente</name></author><author><name sortKey="Alkuraya, Fowzan S" sort="Alkuraya, Fowzan S" uniqKey="Alkuraya F" first="Fowzan S" last="Alkuraya">Fowzan S. Alkuraya</name></author><author><name sortKey="Edwards, Mark J" sort="Edwards, Mark J" uniqKey="Edwards M" first="Mark J" last="Edwards">Mark J. 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Bhatia</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="doi">10.1002/mds.25394</idno><idno type="RBID">pubmed:23418071</idno><idno type="pmid">23418071</idno><idno type="wicri:Area/PubMed/Corpus">000A38</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The syndrome of deafness-dystonia: clinical and genetic heterogeneity.</title><author><name sortKey="Kojovic, Maja" sort="Kojovic, Maja" uniqKey="Kojovic M" first="Maja" last="Kojovic">Maja Kojovic</name><affiliation><nlm:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Parees, Isabel" sort="Parees, Isabel" uniqKey="Parees I" first="Isabel" last="Pareés">Isabel Pareés</name></author><author><name sortKey="Lampreia, Tania" sort="Lampreia, Tania" uniqKey="Lampreia T" first="Tania" last="Lampreia">Tania Lampreia</name></author><author><name sortKey="Pienczk Reclawowicz, Karolina" sort="Pienczk Reclawowicz, Karolina" uniqKey="Pienczk Reclawowicz K" first="Karolina" last="Pienczk-Reclawowicz">Karolina Pienczk-Reclawowicz</name></author><author><name sortKey="Xiromerisiou, Georgia" sort="Xiromerisiou, Georgia" uniqKey="Xiromerisiou G" first="Georgia" last="Xiromerisiou">Georgia Xiromerisiou</name></author><author><name sortKey="Rubio Agusti, Ignacio" sort="Rubio Agusti, Ignacio" uniqKey="Rubio Agusti I" first="Ignacio" last="Rubio-Agusti">Ignacio Rubio-Agusti</name></author><author><name sortKey="Kramberger, Milica" sort="Kramberger, Milica" uniqKey="Kramberger M" first="Milica" last="Kramberger">Milica Kramberger</name></author><author><name sortKey="Carecchio, Miryam" sort="Carecchio, Miryam" uniqKey="Carecchio M" first="Miryam" last="Carecchio">Miryam Carecchio</name></author><author><name sortKey="Alazami, Anas M" sort="Alazami, Anas M" uniqKey="Alazami A" first="Anas M" last="Alazami">Anas M. Alazami</name></author><author><name sortKey="Brancati, Francesco" sort="Brancati, Francesco" uniqKey="Brancati F" first="Francesco" last="Brancati">Francesco Brancati</name></author><author><name sortKey="Slawek, Jaroslaw" sort="Slawek, Jaroslaw" uniqKey="Slawek J" first="Jaroslaw" last="Slawek">Jaroslaw Slawek</name></author><author><name sortKey="Pirtosek, Zvezdan" sort="Pirtosek, Zvezdan" uniqKey="Pirtosek Z" first="Zvezdan" last="Pirtosek">Zvezdan Pirtosek</name></author><author><name sortKey="Valente, Enza Maria" sort="Valente, Enza Maria" uniqKey="Valente E" first="Enza Maria" last="Valente">Enza Maria Valente</name></author><author><name sortKey="Alkuraya, Fowzan S" sort="Alkuraya, Fowzan S" uniqKey="Alkuraya F" first="Fowzan S" last="Alkuraya">Fowzan S. Alkuraya</name></author><author><name sortKey="Edwards, Mark J" sort="Edwards, Mark J" uniqKey="Edwards M" first="Mark J" last="Edwards">Mark J. Edwards</name></author><author><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P" last="Bhatia">Kailash P. Bhatia</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="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Age of Onset</term><term>Apoptosis Regulatory Proteins (genetics)</term><term>DNA-Binding Proteins (genetics)</term><term>Deaf-Blind Disorders (etiology)</term><term>Deaf-Blind Disorders (genetics)</term><term>Disease Progression</term><term>Dystonia (etiology)</term><term>Dystonia (genetics)</term><term>Family Health</term><term>Female</term><term>Genetic Heterogeneity</term><term>Genetic Testing</term><term>Humans</term><term>Intellectual Disability (etiology)</term><term>Intellectual Disability (genetics)</term><term>Leviviridae</term><term>Male</term><term>Membrane Transport Proteins (genetics)</term><term>Middle Aged</term><term>Mutation (genetics)</term><term>Nuclear Proteins (genetics)</term><term>Optic Atrophy (etiology)</term><term>Optic Atrophy (genetics)</term><term>Retrospective Studies</term><term>Ubiquitin-Protein Ligase Complexes</term><term>Young Adult</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Apoptosis Regulatory Proteins</term><term>DNA-Binding Proteins</term><term>Membrane Transport Proteins</term><term>Nuclear Proteins</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Deaf-Blind Disorders</term><term>Dystonia</term><term>Intellectual Disability</term><term>Optic Atrophy</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Deaf-Blind Disorders</term><term>Dystonia</term><term>Intellectual Disability</term><term>Mutation</term><term>Optic Atrophy</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Age of Onset</term><term>Disease Progression</term><term>Family Health</term><term>Female</term><term>Genetic Heterogeneity</term><term>Genetic Testing</term><term>Humans</term><term>Leviviridae</term><term>Male</term><term>Middle Aged</term><term>Retrospective Studies</term><term>Ubiquitin-Protein Ligase Complexes</term><term>Young Adult</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The syndrome of deafness-dystonia is rare and refers to the association of hearing impairment and dystonia when these are dominant features of a disease. Known genetic causes include Mohr-Tranebjaerg syndrome, Woodhouse-Sakati syndrome, and mitochondrial disorders, but the cause frequently remains unidentified. The aim of the current study was to better characterize etiological and clinical aspects of deafness-dystonia syndrome. We evaluated 20 patients with deafness-dystonia syndrome who were seen during the period between 1994 and 2011. The cause was identified in only 7 patients and included methylmalonic aciduria, meningoencephalitis, perinatal hypoxic-ischemic injury, large genomic deletion on chromosome 7q21, translocase of inner mitochondrial membrane 8 homolog A (TIMM8A) mutation (Mohr-Tranebjaerg syndrome), and chromosome 2 open reading frame 37 (C2orf37) mutation (Woodhouse-Sakati syndrome). The age of onset and clinical characteristics in these patients varied, depending on the etiology. In 13 patients, the cause remained unexplained despite extensive work-up. In the group of patients who had unknown etiology, a family history for deafness and/or dystonia was present the majority of patients, suggesting a strong genetic component. Sensory-neural deafness always preceded dystonia. Two clinical patterns of deafness-dystonia syndrome were observed: patients who had an onset in childhood had generalized dystonia (10 of 13 patients) with frequent bulbar involvement, whereas patients who had a dystonia onset in adulthood had segmental dystonia (3 of 13 patients) with the invariable presence of laryngeal dystonia. Deafness-dystonia syndrome is etiologically and clinically heterogeneous, and most patients have an unknown cause. The different age at onset and variable family history suggest a heterogeneous genetic background, possibly including currently unidentified genetic conditions.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">23418071</PMID><DateCreated><Year>2013</Year><Month>06</Month><Day>26</Day></DateCreated><DateCompleted><Year>2014</Year><Month>01</Month><Day>30</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>6</Issue><PubDate><Year>2013</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>The syndrome of deafness-dystonia: clinical and genetic heterogeneity.</ArticleTitle><Pagination><MedlinePgn>795-803</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25394</ELocationID><Abstract><AbstractText>The syndrome of deafness-dystonia is rare and refers to the association of hearing impairment and dystonia when these are dominant features of a disease. Known genetic causes include Mohr-Tranebjaerg syndrome, Woodhouse-Sakati syndrome, and mitochondrial disorders, but the cause frequently remains unidentified. The aim of the current study was to better characterize etiological and clinical aspects of deafness-dystonia syndrome. We evaluated 20 patients with deafness-dystonia syndrome who were seen during the period between 1994 and 2011. The cause was identified in only 7 patients and included methylmalonic aciduria, meningoencephalitis, perinatal hypoxic-ischemic injury, large genomic deletion on chromosome 7q21, translocase of inner mitochondrial membrane 8 homolog A (TIMM8A) mutation (Mohr-Tranebjaerg syndrome), and chromosome 2 open reading frame 37 (C2orf37) mutation (Woodhouse-Sakati syndrome). The age of onset and clinical characteristics in these patients varied, depending on the etiology. In 13 patients, the cause remained unexplained despite extensive work-up. In the group of patients who had unknown etiology, a family history for deafness and/or dystonia was present the majority of patients, suggesting a strong genetic component. Sensory-neural deafness always preceded dystonia. Two clinical patterns of deafness-dystonia syndrome were observed: patients who had an onset in childhood had generalized dystonia (10 of 13 patients) with frequent bulbar involvement, whereas patients who had a dystonia onset in adulthood had segmental dystonia (3 of 13 patients) with the invariable presence of laryngeal dystonia. Deafness-dystonia syndrome is etiologically and clinically heterogeneous, and most patients have an unknown cause. The different age at onset and variable family history suggest a heterogeneous genetic background, possibly including currently unidentified genetic conditions.</AbstractText><CopyrightInformation>Copyright © 2013 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kojovic</LastName><ForeName>Maja</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pareés</LastName><ForeName>Isabel</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Lampreia</LastName><ForeName>Tania</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Pienczk-Reclawowicz</LastName><ForeName>Karolina</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Xiromerisiou</LastName><ForeName>Georgia</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Rubio-Agusti</LastName><ForeName>Ignacio</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Kramberger</LastName><ForeName>Milica</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Carecchio</LastName><ForeName>Miryam</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Alazami</LastName><ForeName>Anas M</ForeName><Initials>AM</Initials></Author><Author ValidYN="Y"><LastName>Brancati</LastName><ForeName>Francesco</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Slawek</LastName><ForeName>Jaroslaw</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Pirtosek</LastName><ForeName>Zvezdan</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Valente</LastName><ForeName>Enza Maria</ForeName><Initials>EM</Initials></Author><Author ValidYN="Y"><LastName>Alkuraya</LastName><ForeName>Fowzan S</ForeName><Initials>FS</Initials></Author><Author ValidYN="Y"><LastName>Edwards</LastName><ForeName>Mark J</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Bhatia</LastName><ForeName>Kailash P</ForeName><Initials>KP</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>02</Month><Day>15</Day></ArticleDate></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="D051017">Apoptosis Regulatory Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C556016">DCAF17 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004268">DNA-Binding Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D026901">Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009687">Nuclear Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C474080">THAP1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C118122">TIMM8A protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 6.3.2.19</RegistryNumber><NameOfSubstance UI="D043743">Ubiquitin-Protein Ligase Complexes</NameOfSubstance></Chemical></ChemicalList><SupplMeshList><SupplMeshName Type="Disease" UI="C535808">Mohr-Tranebjaerg syndrome</SupplMeshName></SupplMeshList><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="D017668">Age of Onset</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051017">Apoptosis Regulatory Proteins</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004268">DNA-Binding Proteins</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D054062">Deaf-Blind Disorders</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018450">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004421">Dystonia</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005192">Family Health</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D018740">Genetic Heterogeneity</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005820">Genetic Testing</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008607">Intellectual Disability</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017907">Leviviridae</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D026901">Membrane Transport Proteins</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009154">Mutation</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009687">Nuclear Proteins</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009896">Optic Atrophy</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012189">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D043743">Ubiquitin-Protein Ligase Complexes</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D055815">Young Adult</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>10</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2012</Year><Month>12</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>1</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2013</Year><Month>2</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>2</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>2</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>1</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.25394</ArticleId><ArticleId IdType="pubmed">23418071</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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