Lymphatic dysfunction, not aplasia, underlies Milroy disease.
Identifieur interne : 003B64 ( Ncbi/Merge ); précédent : 003B63; suivant : 003B65Lymphatic dysfunction, not aplasia, underlies Milroy disease.
Auteurs : Russell H. Mellor [Royaume-Uni] ; Charlotte E. Hubert ; Anthony W B. Stanton ; Naomi Tate ; Victoria Akhras ; Alberto Smith ; Kevin G. Burnand ; Steve Jeffery ; Taija M Kinen ; J Rodney Levick ; Peter S. MortimerSource :
- Microcirculation (New York, N.Y. : 1994) [ 1549-8719 ] ; 2010.
Descripteurs français
- KwdFr :
- Adulte, Adulte d'âge moyen, Avant-bras, Colorants fluorescents, Dextrane, Femelle, Fluorescéine-5-isothiocyanate (analogues et dérivés), Humains, Immunohistochimie, Jeune adulte, Lymphoedème (anatomopathologie), Lymphoedème (génétique), Lymphoedème (physiopathologie), Lymphoedème (étiologie), Lymphographie (), Mutation, Mâle, Pied, Protéines du transport vésiculaire (métabolisme), Récepteur-3 au facteur croissance endothéliale vasculaire (génétique), Sujet âgé, Système lymphatique (anatomopathologie), Système lymphatique (imagerie diagnostique), Système lymphatique (physiopathologie), Échographie-doppler couleur, Études cas-témoins.
- MESH :
- analogues et dérivés : Fluorescéine-5-isothiocyanate.
- anatomopathologie : Lymphoedème, Système lymphatique.
- génétique : Lymphoedème, Récepteur-3 au facteur croissance endothéliale vasculaire.
- imagerie diagnostique : Système lymphatique.
- métabolisme : Protéines du transport vésiculaire.
- physiopathologie : Lymphoedème, Système lymphatique.
- étiologie : Lymphoedème.
- Adulte, Adulte d'âge moyen, Avant-bras, Colorants fluorescents, Dextrane, Femelle, Humains, Immunohistochimie, Jeune adulte, Lymphographie, Mutation, Mâle, Pied, Sujet âgé, Échographie-doppler couleur, Études cas-témoins.
English descriptors
- KwdEn :
- Adult, Aged, Case-Control Studies, Dextrans, Female, Fluorescein-5-isothiocyanate (analogs & derivatives), Fluorescent Dyes, Foot, Forearm, Humans, Immunohistochemistry, Lymphatic System (diagnostic imaging), Lymphatic System (pathology), Lymphatic System (physiopathology), Lymphedema (etiology), Lymphedema (genetics), Lymphedema (pathology), Lymphedema (physiopathology), Lymphography (methods), Male, Middle Aged, Mutation, Ultrasonography, Doppler, Color, Vascular Endothelial Growth Factor Receptor-3 (genetics), Vesicular Transport Proteins (metabolism), Young Adult.
- MESH :
- chemical , analogs & derivatives : Fluorescein-5-isothiocyanate.
- chemical , genetics : Vascular Endothelial Growth Factor Receptor-3.
- chemical , metabolism : Vesicular Transport Proteins.
- chemical : Dextrans, Fluorescent Dyes.
- diagnostic imaging : Lymphatic System.
- etiology : Lymphedema.
- genetics : Lymphedema.
- methods : Lymphography.
- pathology : Lymphatic System, Lymphedema.
- physiopathology : Lymphatic System, Lymphedema.
- Adult, Aged, Case-Control Studies, Female, Foot, Forearm, Humans, Immunohistochemistry, Male, Middle Aged, Mutation, Ultrasonography, Doppler, Color, Young Adult.
Abstract
Milroy disease is an inherited autosomal dominant lymphoedema caused by mutations in the gene for vascular endothelial growth factor receptor-3 (VEGFR-3, also known as FLT4). The phenotype has to date been ascribed to lymphatic aplasia. We further investigated the structural and functional defects underlying the phenotype in humans.
DOI: 10.1111/j.1549-8719.2010.00030.x
PubMed: 20536741
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 002A43
- to stream PubMed, to step Curation: 002A43
- to stream PubMed, to step Checkpoint: 002A43
Links to Exploration step
pubmed:20536741Le document en format XML
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<term>Lymphoedème (étiologie)</term>
<term>Lymphographie ()</term>
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<front><div type="abstract" xml:lang="en">Milroy disease is an inherited autosomal dominant lymphoedema caused by mutations in the gene for vascular endothelial growth factor receptor-3 (VEGFR-3, also known as FLT4). The phenotype has to date been ascribed to lymphatic aplasia. We further investigated the structural and functional defects underlying the phenotype in humans.</div>
</front>
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<DateCreated><Year>2010</Year>
<Month>06</Month>
<Day>11</Day>
</DateCreated>
<DateCompleted><Year>2010</Year>
<Month>09</Month>
<Day>14</Day>
</DateCompleted>
<DateRevised><Year>2016</Year>
<Month>11</Month>
<Day>25</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1549-8719</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>17</Volume>
<Issue>4</Issue>
<PubDate><Year>2010</Year>
<Month>May</Month>
</PubDate>
</JournalIssue>
<Title>Microcirculation (New York, N.Y. : 1994)</Title>
<ISOAbbreviation>Microcirculation</ISOAbbreviation>
</Journal>
<ArticleTitle>Lymphatic dysfunction, not aplasia, underlies Milroy disease.</ArticleTitle>
<Pagination><MedlinePgn>281-96</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1111/j.1549-8719.2010.00030.x</ELocationID>
<Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Milroy disease is an inherited autosomal dominant lymphoedema caused by mutations in the gene for vascular endothelial growth factor receptor-3 (VEGFR-3, also known as FLT4). The phenotype has to date been ascribed to lymphatic aplasia. We further investigated the structural and functional defects underlying the phenotype in humans.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">The skin of the swollen foot and the non-swollen forearm was examined by (i) fluorescence microlymphangiography, to quantify functional initial lymphatic density in vivo; and (ii) podoplanin and LYVE-1 immunohistochemistry of biopsies, to quantify structural lymphatic density. Leg vein function was assessed by colour Doppler duplex ultrasound.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Milroy patients exhibited profound (86-91%) functional failure of the initial lymphatics in the foot; the forearm was unimpaired. Dermal lymphatics were present in biopsies but density was reduced by 51-61% (foot) and 26-33% (forearm). Saphenous venous reflux was present in 9/10 individuals with VEGFR3 mutations, including two carriers.</AbstractText>
<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">We propose that VEGFR3 mutations in humans cause lymphoedema through a failure of tissue protein and fluid absorption. This is due to a profound functional failure of initial lymphatics and is not explained by microlymphatic hypoplasia alone. The superficial venous valve reflux indicates the dual role of VEGFR-3 in lymphatic and venous development.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mellor</LastName>
<ForeName>Russell H</ForeName>
<Initials>RH</Initials>
<AffiliationInfo><Affiliation>Cardiac & Vascular Sciences (Dermatology), St George's Hospital Medical School, University of London, London, UK.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Hubert</LastName>
<ForeName>Charlotte E</ForeName>
<Initials>CE</Initials>
</Author>
<Author ValidYN="Y"><LastName>Stanton</LastName>
<ForeName>Anthony W B</ForeName>
<Initials>AW</Initials>
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<Author ValidYN="Y"><LastName>Tate</LastName>
<ForeName>Naomi</ForeName>
<Initials>N</Initials>
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<Author ValidYN="Y"><LastName>Akhras</LastName>
<ForeName>Victoria</ForeName>
<Initials>V</Initials>
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<Author ValidYN="Y"><LastName>Smith</LastName>
<ForeName>Alberto</ForeName>
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<Author ValidYN="Y"><LastName>Burnand</LastName>
<ForeName>Kevin G</ForeName>
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<Author ValidYN="Y"><LastName>Jeffery</LastName>
<ForeName>Steve</ForeName>
<Initials>S</Initials>
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<ForeName>Taija</ForeName>
<Initials>T</Initials>
</Author>
<Author ValidYN="Y"><LastName>Levick</LastName>
<ForeName>J Rodney</ForeName>
<Initials>JR</Initials>
</Author>
<Author ValidYN="Y"><LastName>Mortimer</LastName>
<ForeName>Peter S</ForeName>
<Initials>PS</Initials>
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<MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName>
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<ArticleId IdType="doi">10.1111/j.1549-8719.2010.00030.x</ArticleId>
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<affiliations><list><country><li>Royaume-Uni</li>
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<region><li>Angleterre</li>
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<settlement><li>Londres</li>
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<orgName><li>Université de Londres</li>
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<tree><noCountry><name sortKey="Akhras, Victoria" sort="Akhras, Victoria" uniqKey="Akhras V" first="Victoria" last="Akhras">Victoria Akhras</name>
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<name sortKey="Hubert, Charlotte E" sort="Hubert, Charlotte E" uniqKey="Hubert C" first="Charlotte E" last="Hubert">Charlotte E. Hubert</name>
<name sortKey="Jeffery, Steve" sort="Jeffery, Steve" uniqKey="Jeffery S" first="Steve" last="Jeffery">Steve Jeffery</name>
<name sortKey="Levick, J Rodney" sort="Levick, J Rodney" uniqKey="Levick J" first="J Rodney" last="Levick">J Rodney Levick</name>
<name sortKey="M Kinen, Taija" sort="M Kinen, Taija" uniqKey="M Kinen T" first="Taija" last="M Kinen">Taija M Kinen</name>
<name sortKey="Mortimer, Peter S" sort="Mortimer, Peter S" uniqKey="Mortimer P" first="Peter S" last="Mortimer">Peter S. Mortimer</name>
<name sortKey="Smith, Alberto" sort="Smith, Alberto" uniqKey="Smith A" first="Alberto" last="Smith">Alberto Smith</name>
<name sortKey="Stanton, Anthony W B" sort="Stanton, Anthony W B" uniqKey="Stanton A" first="Anthony W B" last="Stanton">Anthony W B. Stanton</name>
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