Causes and consequences of lymphatic disease.
Identifieur interne : 002864 ( PubMed/Corpus ); précédent : 002863; suivant : 002865Causes and consequences of lymphatic disease.
Auteurs : Stanley G. RocksonSource :
- Annals of the New York Academy of Sciences [ 1749-6632 ] ; 2010.
English descriptors
- KwdEn :
- MESH :
- etiology : Lymphatic Diseases.
- pathology : Lymphatic Diseases.
- physiopathology : Lymphatic Diseases.
- Homeostasis, Humans.
Abstract
The visceral manifestations of lymphatic disorders (lymphangiomatosis and lymphangiectasia) are particularly severe. Any pathology of the lymphatic vasculature, whether superficial or internal, regional, or systemic, is predominated by the appearance of lymphedema, the characteristic form of tissue edema that occurs when lymphatic dysfunction supervenes. Disease manifestations may include dysregulation of body fluid homeostasis, immune traffic impairment, and disturbances of lipid and protein reabsorption from the gut lumen. The appearance of lymphatic edema invokes complex biological alterations. Many of these changes seem to relate uniquely to chronic lymphatic edema, including a profound stimulus to collagen and adipose deposition. Despite the recent advances in our understanding of these disorders, substantial knowledge gaps remain; these gaps inhibit our ability to accurately identify, categorize, treat, and prevent these diseases. Future diagnostic, therapeutic, and reproductive decisions for affected individuals require an accurate knowledge of the clinical and laboratory presentation, mode of inheritance, treatment response, outcomes, and prognosis.
DOI: 10.1111/j.1749-6632.2010.05804.x
PubMed: 20961302
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pubmed:20961302Le document en format XML
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Rockson</name><affiliation><nlm:affiliation>Center for Lymphatic and Venous Disorders, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. rockson@stanford.edu</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:20961302</idno><idno type="pmid">20961302</idno><idno type="doi">10.1111/j.1749-6632.2010.05804.x</idno><idno type="wicri:Area/PubMed/Corpus">002864</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002864</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Causes and consequences of lymphatic 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>Center for Lymphatic and Venous Disorders, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. rockson@stanford.edu</nlm:affiliation></affiliation></author></analytic><series><title level="j">Annals of the New York Academy of Sciences</title><idno type="eISSN">1749-6632</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Homeostasis</term><term>Humans</term><term>Lymphatic Diseases (etiology)</term><term>Lymphatic Diseases (pathology)</term><term>Lymphatic Diseases (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Lymphatic Diseases</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lymphatic Diseases</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lymphatic Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Homeostasis</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The visceral manifestations of lymphatic disorders (lymphangiomatosis and lymphangiectasia) are particularly severe. Any pathology of the lymphatic vasculature, whether superficial or internal, regional, or systemic, is predominated by the appearance of lymphedema, the characteristic form of tissue edema that occurs when lymphatic dysfunction supervenes. Disease manifestations may include dysregulation of body fluid homeostasis, immune traffic impairment, and disturbances of lipid and protein reabsorption from the gut lumen. The appearance of lymphatic edema invokes complex biological alterations. Many of these changes seem to relate uniquely to chronic lymphatic edema, including a profound stimulus to collagen and adipose deposition. Despite the recent advances in our understanding of these disorders, substantial knowledge gaps remain; these gaps inhibit our ability to accurately identify, categorize, treat, and prevent these diseases. Future diagnostic, therapeutic, and reproductive decisions for affected individuals require an accurate knowledge of the clinical and laboratory presentation, mode of inheritance, treatment response, outcomes, and prognosis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20961302</PMID><DateCreated><Year>2010</Year><Month>10</Month><Day>21</Day></DateCreated><DateCompleted><Year>2010</Year><Month>11</Month><Day>08</Day></DateCompleted><DateRevised><Year>2010</Year><Month>10</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1749-6632</ISSN><JournalIssue CitedMedium="Internet"><Volume>1207 Suppl 1</Volume><PubDate><Year>2010</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Annals of the New York Academy of Sciences</Title><ISOAbbreviation>Ann. N. Y. Acad. Sci.</ISOAbbreviation></Journal><ArticleTitle>Causes and consequences of lymphatic disease.</ArticleTitle><Pagination><MedlinePgn>E2-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/j.1749-6632.2010.05804.x</ELocationID><Abstract><AbstractText>The visceral manifestations of lymphatic disorders (lymphangiomatosis and lymphangiectasia) are particularly severe. Any pathology of the lymphatic vasculature, whether superficial or internal, regional, or systemic, is predominated by the appearance of lymphedema, the characteristic form of tissue edema that occurs when lymphatic dysfunction supervenes. Disease manifestations may include dysregulation of body fluid homeostasis, immune traffic impairment, and disturbances of lipid and protein reabsorption from the gut lumen. The appearance of lymphatic edema invokes complex biological alterations. Many of these changes seem to relate uniquely to chronic lymphatic edema, including a profound stimulus to collagen and adipose deposition. Despite the recent advances in our understanding of these disorders, substantial knowledge gaps remain; these gaps inhibit our ability to accurately identify, categorize, treat, and prevent these diseases. Future diagnostic, therapeutic, and reproductive decisions for affected individuals require an accurate knowledge of the clinical and laboratory presentation, mode of inheritance, treatment response, outcomes, and prognosis.</AbstractText><CopyrightInformation>© 2010 New York Academy of Sciences.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rockson</LastName><ForeName>Stanley G</ForeName><Initials>SG</Initials><AffiliationInfo><Affiliation>Center for Lymphatic and Venous Disorders, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. rockson@stanford.edu</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Ann N Y Acad Sci</MedlineTA><NlmUniqueID>7506858</NlmUniqueID><ISSNLinking>0077-8923</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D006706" MajorTopicYN="N">Homeostasis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008206" MajorTopicYN="N">Lymphatic Diseases</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>10</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>10</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>11</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">20961302</ArticleId><ArticleId IdType="doi">10.1111/j.1749-6632.2010.05804.x</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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