Diagnosis and management of lymphatic vascular disease.
Identifieur interne : 003160 ( PubMed/Corpus ); précédent : 003159; suivant : 003161Diagnosis and management of lymphatic vascular disease.
Auteurs : Stanley G. RocksonSource :
- Journal of the American College of Cardiology [ 1558-3597 ] ; 2008.
English descriptors
- KwdEn :
- Cardiovascular Diseases (diagnosis), Cardiovascular Diseases (drug therapy), Cardiovascular Diseases (metabolism), Cardiovascular Diseases (therapy), Humans, Lymphangiogenesis, Lymphatic Diseases (diagnosis), Lymphatic Diseases (drug therapy), Lymphatic Diseases (metabolism), Lymphatic Diseases (therapy), Lymphedema (diagnosis), Lymphedema (therapy), Physical Therapy Modalities, Receptors, Vascular Endothelial Growth Factor (metabolism), Vascular Endothelial Growth Factor A (metabolism).
- MESH :
- chemical , metabolism : Receptors, Vascular Endothelial Growth Factor, Vascular Endothelial Growth Factor A.
- diagnosis : Cardiovascular Diseases, Lymphatic Diseases, Lymphedema.
- drug therapy : Cardiovascular Diseases, Lymphatic Diseases.
- metabolism : Cardiovascular Diseases, Lymphatic Diseases.
- therapy : Cardiovascular Diseases, Lymphatic Diseases, Lymphedema.
- Humans, Lymphangiogenesis, Physical Therapy Modalities.
Abstract
The lymphatic vasculature is comprised of a network of vessels that is essential both to fluid homeostasis and to the mediation of regional immune responses. In health, the lymphatic vasculature possesses the requisite transport capacity to accommodate the fluid load placed upon it. The most readily recognizable attribute of lymphatic vascular incompetence is the presence of the characteristic swelling of tissues, called lymphedema, which arises as a consequence of insufficient lymph transport. The diagnosis of lymphatic vascular disease relies heavily upon the physical examination. If the diagnosis remains in question, the presence of lymphatic vascular insufficiency can be ascertained through imaging, including indirect radionuclide lymphoscintigraphy. Beyond lymphoscintigraphy, clinically-relevant imaging modalities include magnetic resonance imaging and computerized axial tomography. The state-of-the-art therapeutic approach to lymphatic edema relies upon physiotherapeutic techniques. Complex decongestive physiotherapy is an empirically-derived, effective, multicomponent technique designed to reduce limb volume and maintain the health of the skin and supporting structures. The application of pharmacological therapies has been notably absent from the management strategies for lymphatic vascular insufficiency states. In general, drug-based approaches have been controversial at best. Surgical approaches to improve lymphatic flow through vascular reanastomosis have been, in large part, unsuccessful, but controlled liposuction affords lasting benefit in selected patients. In the future, specifically engineered molecular therapeutics may be designed to facilitate the controlled regrowth of damaged, dysfunctional, or obliterated lymphatic vasculature in order to circumvent or mitigate the vascular insufficiency that leads to edema and tissue destruction.
DOI: 10.1016/j.jacc.2008.06.005
PubMed: 18755341
Links to Exploration step
pubmed:18755341Le document en format XML
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Rockson</name><affiliation><nlm:affiliation>Stanford Center for Lymphatic and Venous Disorders, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. srockson@cvmed.stanford.edu</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="RBID">pubmed:18755341</idno><idno type="pmid">18755341</idno><idno type="doi">10.1016/j.jacc.2008.06.005</idno><idno type="wicri:Area/PubMed/Corpus">003160</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">003160</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Diagnosis and management of lymphatic vascular disease.</title><author><name sortKey="Rockson, Stanley G" sort="Rockson, Stanley G" uniqKey="Rockson S" first="Stanley G" last="Rockson">Stanley G. Rockson</name><affiliation><nlm:affiliation>Stanford Center for Lymphatic and Venous Disorders, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. srockson@cvmed.stanford.edu</nlm:affiliation></affiliation></author></analytic><series><title level="j">Journal of the American College of Cardiology</title><idno type="eISSN">1558-3597</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cardiovascular Diseases (diagnosis)</term><term>Cardiovascular Diseases (drug therapy)</term><term>Cardiovascular Diseases (metabolism)</term><term>Cardiovascular Diseases (therapy)</term><term>Humans</term><term>Lymphangiogenesis</term><term>Lymphatic Diseases (diagnosis)</term><term>Lymphatic Diseases (drug therapy)</term><term>Lymphatic Diseases (metabolism)</term><term>Lymphatic Diseases (therapy)</term><term>Lymphedema (diagnosis)</term><term>Lymphedema (therapy)</term><term>Physical Therapy Modalities</term><term>Receptors, Vascular Endothelial Growth Factor (metabolism)</term><term>Vascular Endothelial Growth Factor A (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Receptors, Vascular Endothelial Growth Factor</term><term>Vascular Endothelial Growth Factor A</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Cardiovascular Diseases</term><term>Lymphatic Diseases</term><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Cardiovascular Diseases</term><term>Lymphatic Diseases</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cardiovascular Diseases</term><term>Lymphatic Diseases</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Cardiovascular Diseases</term><term>Lymphatic Diseases</term><term>Lymphedema</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Lymphangiogenesis</term><term>Physical Therapy Modalities</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The lymphatic vasculature is comprised of a network of vessels that is essential both to fluid homeostasis and to the mediation of regional immune responses. In health, the lymphatic vasculature possesses the requisite transport capacity to accommodate the fluid load placed upon it. The most readily recognizable attribute of lymphatic vascular incompetence is the presence of the characteristic swelling of tissues, called lymphedema, which arises as a consequence of insufficient lymph transport. The diagnosis of lymphatic vascular disease relies heavily upon the physical examination. If the diagnosis remains in question, the presence of lymphatic vascular insufficiency can be ascertained through imaging, including indirect radionuclide lymphoscintigraphy. Beyond lymphoscintigraphy, clinically-relevant imaging modalities include magnetic resonance imaging and computerized axial tomography. The state-of-the-art therapeutic approach to lymphatic edema relies upon physiotherapeutic techniques. Complex decongestive physiotherapy is an empirically-derived, effective, multicomponent technique designed to reduce limb volume and maintain the health of the skin and supporting structures. The application of pharmacological therapies has been notably absent from the management strategies for lymphatic vascular insufficiency states. In general, drug-based approaches have been controversial at best. Surgical approaches to improve lymphatic flow through vascular reanastomosis have been, in large part, unsuccessful, but controlled liposuction affords lasting benefit in selected patients. In the future, specifically engineered molecular therapeutics may be designed to facilitate the controlled regrowth of damaged, dysfunctional, or obliterated lymphatic vasculature in order to circumvent or mitigate the vascular insufficiency that leads to edema and tissue destruction.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18755341</PMID><DateCreated><Year>2008</Year><Month>08</Month><Day>29</Day></DateCreated><DateCompleted><Year>2008</Year><Month>09</Month><Day>19</Day></DateCompleted><DateRevised><Year>2009</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1558-3597</ISSN><JournalIssue CitedMedium="Internet"><Volume>52</Volume><Issue>10</Issue><PubDate><Year>2008</Year><Month>Sep</Month><Day>02</Day></PubDate></JournalIssue><Title>Journal of the American College of Cardiology</Title><ISOAbbreviation>J. Am. Coll. Cardiol.</ISOAbbreviation></Journal><ArticleTitle>Diagnosis and management of lymphatic vascular disease.</ArticleTitle><Pagination><MedlinePgn>799-806</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jacc.2008.06.005</ELocationID><Abstract><AbstractText>The lymphatic vasculature is comprised of a network of vessels that is essential both to fluid homeostasis and to the mediation of regional immune responses. In health, the lymphatic vasculature possesses the requisite transport capacity to accommodate the fluid load placed upon it. The most readily recognizable attribute of lymphatic vascular incompetence is the presence of the characteristic swelling of tissues, called lymphedema, which arises as a consequence of insufficient lymph transport. The diagnosis of lymphatic vascular disease relies heavily upon the physical examination. If the diagnosis remains in question, the presence of lymphatic vascular insufficiency can be ascertained through imaging, including indirect radionuclide lymphoscintigraphy. Beyond lymphoscintigraphy, clinically-relevant imaging modalities include magnetic resonance imaging and computerized axial tomography. The state-of-the-art therapeutic approach to lymphatic edema relies upon physiotherapeutic techniques. Complex decongestive physiotherapy is an empirically-derived, effective, multicomponent technique designed to reduce limb volume and maintain the health of the skin and supporting structures. The application of pharmacological therapies has been notably absent from the management strategies for lymphatic vascular insufficiency states. In general, drug-based approaches have been controversial at best. Surgical approaches to improve lymphatic flow through vascular reanastomosis have been, in large part, unsuccessful, but controlled liposuction affords lasting benefit in selected patients. In the future, specifically engineered molecular therapeutics may be designed to facilitate the controlled regrowth of damaged, dysfunctional, or obliterated lymphatic vasculature in order to circumvent or mitigate the vascular insufficiency that leads to edema and tissue destruction.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rockson</LastName><ForeName>Stanley G</ForeName><Initials>SG</Initials><AffiliationInfo><Affiliation>Stanford Center for Lymphatic and Venous Disorders, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. srockson@cvmed.stanford.edu</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Am Coll Cardiol</MedlineTA><NlmUniqueID>8301365</NlmUniqueID><ISSNLinking>0735-1097</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042461">Vascular Endothelial Growth Factor A</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D040262">Receptors, Vascular Endothelial Growth Factor</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="N">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="Y">diagnosis</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008206" MajorTopicYN="N">Lymphatic Diseases</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="Y">diagnosis</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D026741" MajorTopicYN="N">Physical Therapy Modalities</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D040262" MajorTopicYN="N">Receptors, Vascular Endothelial Growth Factor</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042461" MajorTopicYN="N">Vascular Endothelial Growth Factor A</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>76</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2008</Year><Month>05</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2008</Year><Month>05</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2008</Year><Month>06</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>8</Month><Day>30</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>9</Month><Day>20</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>8</Month><Day>30</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">18755341</ArticleId><ArticleId IdType="pii">S0735-1097(08)02100-1</ArticleId><ArticleId IdType="doi">10.1016/j.jacc.2008.06.005</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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