Higher vascular endothelial growth factor-C concentration in plasma is associated with increased forearm capillary filtration capacity in breast cancer-related lymphedema.
Identifieur interne : 000E91 ( PubMed/Checkpoint ); précédent : 000E90; suivant : 000E92Higher vascular endothelial growth factor-C concentration in plasma is associated with increased forearm capillary filtration capacity in breast cancer-related lymphedema.
Auteurs : Mads Radmer Jensen [Danemark] ; Lene Simonsen [Danemark] ; Tonny Karlsmark [Danemark] ; Charlotte Lanng [Danemark] ; Jens Bülow [Danemark]Source :
- Physiological reports [ 2051-817X ] ; 2015.
Abstract
Breast cancer-related lymphedema (BCRL) is a frequent, chronic and debilitating swelling that mainly affects the ipsilateral arm and develops as a complication to breast cancer treatment. The pathophysiology is elusive opposing development of means for prediction and treatment. We have earlier shown that the forearm capillary filtration coefficient (CFC) is increased bilaterally in BCRL. In this study, we aimed to elucidate if increased CFC is associated with low-grade inflammation and/or vascular endothelial growth factor-c (VEGF-C) signaling. Fourteen patients with unilateral BCRL and nine matched breast cancer controls without BCRL participated. Forearm CFC was measured by venous congestion strain gauge plethysmography, and suction blisters were induced medially on the upper arms. Concentrations of 17 selected cytokines, VEGF-C, and total protein were measured in blister fluid and in plasma. Forearm CFC was higher bilaterally in BCRL subjects (P ≤ 0.036). No differences between forearms were found in either group. Plasma VEGF-C concentrations were significantly higher in the BCRL subjects (P < 0.001). In BCRL subjects, monocyte chemotactic protein 1 (MCP-1) (P = 0.009) and total protein (P = 0.035) concentrations were higher in blister fluid from edematous arms compared with nonedematous arms. No differences were found in interstitial cytokine or total protein concentrations between arms in control subjects. Higher plasma concentration of VEGF-C is a possible cause of bilaterally increased forearm CFC in BCRL subjects. Interstitially increased MCP-1 levels may augment local microvascular protein permeability in BCRL.
DOI: 10.14814/phy2.12403
PubMed: 26059032
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forearm capillary filtration capacity in breast cancer-related lymphedema.</title><author><name sortKey="Jensen, Mads Radmer" sort="Jensen, Mads Radmer" uniqKey="Jensen M" first="Mads Radmer" last="Jensen">Mads Radmer Jensen</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Physiology and Nuclear Medicine, Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen, Denmark Department of Dermatology, Copenhagen Wound Healing Centre Copenhagen Lymphoedema Centre Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen, Denmark mads.radmer.jensen@regionh.dk.</nlm:affiliation><country wicri:rule="url">Danemark</country><wicri:regionArea>Department of Clinical Physiology and Nuclear Medicine, Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen, Denmark Department of Dermatology, Copenhagen Wound Healing Centre Copenhagen Lymphoedema Centre Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen</wicri:regionArea><placeName><settlement type="city">Copenhague</settlement><region type="région" nuts="2">Hovedstaden</region></placeName></affiliation></author><author><name sortKey="Simonsen, Lene" sort="Simonsen, Lene" uniqKey="Simonsen L" first="Lene" last="Simonsen">Lene Simonsen</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Physiology and Nuclear Medicine, Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen, Denmark.</nlm:affiliation><country xml:lang="fr">Danemark</country><wicri:regionArea>Department of Clinical Physiology and Nuclear Medicine, Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen</wicri:regionArea><placeName><settlement type="city">Copenhague</settlement><region type="région" nuts="2">Hovedstaden</region></placeName></affiliation></author><author><name sortKey="Karlsmark, Tonny" sort="Karlsmark, Tonny" uniqKey="Karlsmark T" first="Tonny" last="Karlsmark">Tonny Karlsmark</name><affiliation wicri:level="3"><nlm:affiliation>Department of Dermatology, Copenhagen Wound Healing Centre Copenhagen Lymphoedema Centre Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen, Denmark.</nlm:affiliation><country xml:lang="fr">Danemark</country><wicri:regionArea>Department of Dermatology, Copenhagen Wound Healing Centre Copenhagen Lymphoedema Centre Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen</wicri:regionArea><placeName><settlement type="city">Copenhague</settlement><region type="région" nuts="2">Hovedstaden</region></placeName></affiliation></author><author><name sortKey="Lanng, Charlotte" sort="Lanng, Charlotte" uniqKey="Lanng C" first="Charlotte" last="Lanng">Charlotte Lanng</name><affiliation wicri:level="3"><nlm:affiliation>Department of Breast Surgery, Herlev Hospital University Hospital of Copenhagen, Copenhagen, Denmark.</nlm:affiliation><country xml:lang="fr">Danemark</country><wicri:regionArea>Department of Breast Surgery, Herlev Hospital 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nuts="2">Hovedstaden</region></placeName></affiliation></author></analytic><series><title level="j">Physiological reports</title><idno type="ISSN">2051-817X</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Breast cancer-related lymphedema (BCRL) is a frequent, chronic and debilitating swelling that mainly affects the ipsilateral arm and develops as a complication to breast cancer treatment. The pathophysiology is elusive opposing development of means for prediction and treatment. We have earlier shown that the forearm capillary filtration coefficient (CFC) is increased bilaterally in BCRL. In this study, we aimed to elucidate if increased CFC is associated with low-grade inflammation and/or vascular endothelial growth factor-c (VEGF-C) signaling. Fourteen patients with unilateral BCRL and nine matched breast cancer controls without BCRL participated. Forearm CFC was measured by venous congestion strain gauge plethysmography, and suction blisters were induced medially on the upper arms. Concentrations of 17 selected cytokines, VEGF-C, and total protein were measured in blister fluid and in plasma. Forearm CFC was higher bilaterally in BCRL subjects (P ≤ 0.036). No differences between forearms were found in either group. Plasma VEGF-C concentrations were significantly higher in the BCRL subjects (P < 0.001). In BCRL subjects, monocyte chemotactic protein 1 (MCP-1) (P = 0.009) and total protein (P = 0.035) concentrations were higher in blister fluid from edematous arms compared with nonedematous arms. No differences were found in interstitial cytokine or total protein concentrations between arms in control subjects. Higher plasma concentration of VEGF-C is a possible cause of bilaterally increased forearm CFC in BCRL subjects. Interstitially increased MCP-1 levels may augment local microvascular protein permeability in BCRL.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">26059032</PMID><DateCreated><Year>2015</Year><Month>06</Month><Day>10</Day></DateCreated><DateCompleted><Year>2015</Year><Month>06</Month><Day>10</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">2051-817X</ISSN><JournalIssue CitedMedium="Print"><Volume>3</Volume><Issue>6</Issue><PubDate><Year>2015</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Physiological reports</Title><ISOAbbreviation>Physiol Rep</ISOAbbreviation></Journal><ArticleTitle>Higher vascular endothelial growth factor-C concentration in plasma is associated with increased forearm capillary filtration capacity in breast cancer-related lymphedema.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.14814/phy2.12403</ELocationID><ELocationID EIdType="pii" ValidYN="Y">e12403</ELocationID><Abstract><AbstractText>Breast cancer-related lymphedema (BCRL) is a frequent, chronic and debilitating swelling that mainly affects the ipsilateral arm and develops as a complication to breast cancer treatment. The pathophysiology is elusive opposing development of means for prediction and treatment. We have earlier shown that the forearm capillary filtration coefficient (CFC) is increased bilaterally in BCRL. In this study, we aimed to elucidate if increased CFC is associated with low-grade inflammation and/or vascular endothelial growth factor-c (VEGF-C) signaling. Fourteen patients with unilateral BCRL and nine matched breast cancer controls without BCRL participated. Forearm CFC was measured by venous congestion strain gauge plethysmography, and suction blisters were induced medially on the upper arms. Concentrations of 17 selected cytokines, VEGF-C, and total protein were measured in blister fluid and in plasma. Forearm CFC was higher bilaterally in BCRL subjects (P ≤ 0.036). No differences between forearms were found in either group. Plasma VEGF-C concentrations were significantly higher in the BCRL subjects (P < 0.001). In BCRL subjects, monocyte chemotactic protein 1 (MCP-1) (P = 0.009) and total protein (P = 0.035) concentrations were higher in blister fluid from edematous arms compared with nonedematous arms. No differences were found in interstitial cytokine or total protein concentrations between arms in control subjects. Higher plasma concentration of VEGF-C is a possible cause of bilaterally increased forearm CFC in BCRL subjects. Interstitially increased MCP-1 levels may augment local microvascular protein permeability in BCRL.</AbstractText><CopyrightInformation>© 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jensen</LastName><ForeName>Mads Radmer</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>Department of Clinical Physiology and Nuclear Medicine, Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen, Denmark Department of Dermatology, Copenhagen Wound Healing Centre Copenhagen Lymphoedema Centre Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen, Denmark mads.radmer.jensen@regionh.dk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Simonsen</LastName><ForeName>Lene</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Clinical Physiology and Nuclear Medicine, Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Karlsmark</LastName><ForeName>Tonny</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Dermatology, Copenhagen Wound Healing Centre Copenhagen Lymphoedema Centre Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lanng</LastName><ForeName>Charlotte</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Breast Surgery, Herlev Hospital University Hospital of Copenhagen, Copenhagen, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bülow</LastName><ForeName>Jens</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Clinical Physiology and Nuclear Medicine, Bispebjerg Hospital University Hospital of Copenhagen, Copenhagen, Denmark Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Physiol Rep</MedlineTA><NlmUniqueID>101607800</NlmUniqueID><ISSNLinking>2051-817X</ISSNLinking></MedlineJournalInfo><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Cell Physiol. 2012 Jan 15;302(2):C392-404</RefSource><PMID Version="1">21940662</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cancer. 1998 Dec 15;83(12 Suppl American):2798-802</RefSource><PMID Version="1">9874400</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Dermatol. 2004 Jul;13(7):452-60</RefSource><PMID Version="1">15217366</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Lymphat Res Biol. 2012 Dec;10(4):182-8</RefSource><PMID 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Version="1">16992325</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2013 Apr 16;8(4):e60164</RefSource><PMID Version="1">23613720</PMID></CommentsCorrections></CommentsCorrectionsList><OtherID Source="NLM">PMC4510618</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Breast cancer</Keyword><Keyword MajorTopicYN="N">VEGF‐C</Keyword><Keyword MajorTopicYN="N">capillary filtration coefficient</Keyword><Keyword MajorTopicYN="N">cytokine</Keyword><Keyword MajorTopicYN="N">inflammation</Keyword><Keyword MajorTopicYN="N">lymphedema</Keyword><Keyword MajorTopicYN="N">suction blister</Keyword><Keyword MajorTopicYN="N">venous occlusion plethysmography</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>6</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Bülow</name><name sortKey="Karlsmark, Tonny" sort="Karlsmark, Tonny" uniqKey="Karlsmark T" first="Tonny" last="Karlsmark">Tonny Karlsmark</name><name sortKey="Lanng, Charlotte" sort="Lanng, Charlotte" uniqKey="Lanng C" first="Charlotte" last="Lanng">Charlotte Lanng</name><name sortKey="Simonsen, Lene" sort="Simonsen, Lene" uniqKey="Simonsen L" first="Lene" last="Simonsen">Lene Simonsen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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