Molecular Basis of Vascular Birthmarks
Identifieur interne : 001A42 ( Pmc/Corpus ); précédent : 001A41; suivant : 001A43Molecular Basis of Vascular Birthmarks
Auteurs : Ben Pocock ; Laurence M. Boon ; Miikka VikkulaSource :
- Seminars in Plastic Surgery [ 1535-2188 ] ; 2006.
Abstract
Vascular anomalies affect up to 10% of newborns, largely because of the high incidence of hemangioma of infancy. Vascular anomalies also frequently occur in adults; there is high prevalence of capillary malformations (0.3%). These cutaneous stains often cause psychosocial problems related to their visibility. Venous malformations occur in the skin and in internal organs and may cause destruction. Primary lymphedema causes lifelong morbidity, and arteriovenous malformations, in addition to causing distortion, obstruction, and pain, can be life endangering. The pathophysiology of these anomalies has stayed largely unknown, but genetic studies have revealed clues to their etiology. Genetic defects cause hereditary types of venous malformation, cutaneous and mucosal (VMCM); glomuvenous malformation (GVM); primary congenital lymphedema (Milroy disease); lymphedema-distichiasis syndrome; hypotrichosis-lymphedema-telangiectasia (HLT) syndrome; hereditary hemorrhagic telangiectasia (HHT); cerebral cavernous malformation (CCM); and a newly recognized disorder, capillary malformation–arteriovenous malformation (CM-AVM). These seminal discoveries have not only permitted a more precise clinical classification and diagnosis (a prerequisite for corrective measures for prevention, treatment, and follow-up) but also pointed the way to the identification of factors that play an important role in vasculogenesis or angiogenesis, or both.
Url:
DOI: 10.1055/s-2006-949116
PubMed: NONE
PubMed Central: 2884761
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PMC:2884761Le document en format XML
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<author><name sortKey="Pocock, Ben" sort="Pocock, Ben" uniqKey="Pocock B" first="Ben" last="Pocock">Ben Pocock</name>
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<author><name sortKey="Boon, Laurence M" sort="Boon, Laurence M" uniqKey="Boon L" first="Laurence M." last="Boon">Laurence M. Boon</name>
<affiliation><nlm:aff id="a20149-1">Center for Vascular Anomalies, Cliniques universitaires St. Luc, Brussels, Belgium</nlm:aff>
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<affiliation><nlm:aff id="a20149-2">Human Molecular Genetics, Christian de Duve Institute, Université catholique de Louvain, Brussels, Belgium</nlm:aff>
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<author><name sortKey="Vikkula, Miikka" sort="Vikkula, Miikka" uniqKey="Vikkula M" first="Miikka" last="Vikkula">Miikka Vikkula</name>
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<series><title level="j">Seminars in Plastic Surgery</title>
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<front><div type="abstract" xml:lang="en"><title>ABSTRACT</title>
<p>Vascular anomalies affect up to 10% of newborns, largely because of the high incidence of hemangioma of infancy. Vascular anomalies also frequently occur in adults; there is high prevalence of capillary malformations (0.3%). These cutaneous stains often cause psychosocial problems related to their visibility. Venous malformations occur in the skin and in internal organs and may cause destruction. Primary lymphedema causes lifelong morbidity, and arteriovenous malformations, in addition to causing distortion, obstruction, and pain, can be life endangering. The pathophysiology of these anomalies has stayed largely unknown, but genetic studies have revealed clues to their etiology. Genetic defects cause hereditary types of venous malformation, cutaneous and mucosal (VMCM); glomuvenous malformation (GVM); primary congenital lymphedema (Milroy disease); lymphedema-distichiasis syndrome; hypotrichosis-lymphedema-telangiectasia (HLT) syndrome; hereditary hemorrhagic telangiectasia (HHT); cerebral cavernous malformation (CCM); and a newly recognized disorder, capillary malformation–arteriovenous malformation (CM-AVM). These seminal discoveries have not only permitted a more precise clinical classification and diagnosis (a prerequisite for corrective measures for prevention, treatment, and follow-up) but also pointed the way to the identification of factors that play an important role in vasculogenesis or angiogenesis, or both.</p>
</div>
</front>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Semin Plast Surg</journal-id>
<journal-title>Seminars in Plastic Surgery</journal-title>
<issn pub-type="ppub">1535-2188</issn>
<issn pub-type="epub">1536-0067</issn>
<publisher><publisher-name>Thieme Medical Publishers</publisher-name>
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<article-id pub-id-type="doi">10.1055/s-2006-949116</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
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<title-group><article-title xml:lang="en">Molecular Basis of Vascular Birthmarks</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Pocock</surname>
<given-names>Ben</given-names>
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<xref rid="a20149-1" ref-type="aff">1</xref>
<degrees>M.D.</degrees>
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<contrib contrib-type="author"><name><surname>Boon</surname>
<given-names>Laurence M.</given-names>
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<xref rid="a20149-1" ref-type="aff">1</xref>
<xref rid="a20149-2" ref-type="aff">2</xref>
<degrees>M.D.</degrees>
<degrees>Ph.D.</degrees>
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<contrib contrib-type="author"><name><surname>Vikkula</surname>
<given-names>Miikka</given-names>
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<xref rid="a20149-2" ref-type="aff">2</xref>
<degrees>M.D.</degrees>
<degrees>Ph.D.</degrees>
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<aff id="a20149-1"><label>1</label>
Center for Vascular Anomalies, Cliniques universitaires St. Luc, Brussels, Belgium</aff>
<aff id="a20149-2"><label>2</label>
Human Molecular Genetics, Christian de Duve Institute, Université catholique de Louvain, Brussels, Belgium</aff>
<author-notes><corresp>Address for correspondence and reprint requests: Professor Miikka Vikkula M.D. Ph.D. <institution>Maitre de Recherces du F.N.R.S., Human Molecular Genetics (GEHU), Christian de Duve Institute & Université catholique de Louvain, Avenue Hippocrate 74(+ 5)</institution>
<addr-line>UCL 75.39, B-1200 Brussels, Belgium</addr-line>
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<pub-date pub-type="ppub"><month>8</month>
<year>2006</year>
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<volume>20</volume>
<issue>3</issue>
<fpage>149</fpage>
<lpage>156</lpage>
<copyright-statement>© Thieme Medical Publishers</copyright-statement>
<abstract xml:lang="en"><title>ABSTRACT</title>
<p>Vascular anomalies affect up to 10% of newborns, largely because of the high incidence of hemangioma of infancy. Vascular anomalies also frequently occur in adults; there is high prevalence of capillary malformations (0.3%). These cutaneous stains often cause psychosocial problems related to their visibility. Venous malformations occur in the skin and in internal organs and may cause destruction. Primary lymphedema causes lifelong morbidity, and arteriovenous malformations, in addition to causing distortion, obstruction, and pain, can be life endangering. The pathophysiology of these anomalies has stayed largely unknown, but genetic studies have revealed clues to their etiology. Genetic defects cause hereditary types of venous malformation, cutaneous and mucosal (VMCM); glomuvenous malformation (GVM); primary congenital lymphedema (Milroy disease); lymphedema-distichiasis syndrome; hypotrichosis-lymphedema-telangiectasia (HLT) syndrome; hereditary hemorrhagic telangiectasia (HHT); cerebral cavernous malformation (CCM); and a newly recognized disorder, capillary malformation–arteriovenous malformation (CM-AVM). These seminal discoveries have not only permitted a more precise clinical classification and diagnosis (a prerequisite for corrective measures for prevention, treatment, and follow-up) but also pointed the way to the identification of factors that play an important role in vasculogenesis or angiogenesis, or both.</p>
</abstract>
<kwd-group xml:lang="en"><kwd>Vascular anomaly</kwd>
<kwd>hemangioma</kwd>
<kwd>genetic</kwd>
<kwd>angiogenesis</kwd>
<kwd>mutation</kwd>
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<custom-meta-wrap><custom-meta><meta-name>issue-theme</meta-name>
<meta-value>Dermatology for Plastic Surgeons</meta-value>
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<custom-meta><meta-name>issue-editor</meta-name>
<meta-value>Guest Editor
Moise L. Levy M.D.
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