Endovascular papillary angioendothelioma‐like tumour associated with lymphoedema
Identifieur interne : 006709 ( Istex/Corpus ); précédent : 006708; suivant : 006710Endovascular papillary angioendothelioma‐like tumour associated with lymphoedema
Auteurs : M. Fukunaga ; S. Ushigome ; Y. Shishikura ; K. Yokoi ; E. IshikawaSource :
- Histopathology [ 0309-0167 ] ; 1995-09.
Abstract
A case of endovascular papillary angioendothelioma‐like tumour associated with lymphoedema is described. Microscopically, the tumour was composed of anastomosing vascular channels, some of which contained papillary projections, producing tuft‐like or glomeruloid appearances. The dermis also showed moderate lymphoedema and lymphocyic infiltrate. The tumour resembled endovascular papillary angioendothelioma but also had several features that differed from typical examples: occurrence in an old patient and less prominent endothelial hobnail features and lymphocytic infiltrate. Three types of proliferating cells were observed: 1 mature flattened endothelial cells, which were strongly positive for endothelial markers (factor VIII‐related antigen, CD31, CD34) and bound ulex europaeus agglutinin 1; 2 immature endothelial cells with round nuclei and vacuolated or pale cytoplasm, which were strongly positive for CD31 and muscle‐specific actin (HHF35) and focally positive for other endothelial markers; and 3 stromal spindle cells in papillary or glomeruloid areas, which were positive for vimentin, HHF35, and alpha‐smooth muscle actin but negative for desmin. The tumour was diploid by flow cytometry. The patient was well without disease twelve months after the excision. We postulate that this tumour was caused by circulatory disturbance, namely lymphoedema associated with syringomyelia and a Charcot's joint.
Url:
DOI: 10.1111/j.1365-2559.1995.tb00216.x
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ISTEX:DBF179368886F4C758F2F3A9754F320163955645Le document en format XML
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Ushigome</name><affiliation><mods:affiliation>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Shishikura, Y" sort="Shishikura, Y" uniqKey="Shishikura Y" first="Y." last="Shishikura">Y. Shishikura</name><affiliation><mods:affiliation>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Yokoi, K" sort="Yokoi, K" uniqKey="Yokoi K" first="K." last="Yokoi">K. Yokoi</name><affiliation><mods:affiliation>Departments of Dermatology, The Jikei University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Ishikawa, E" sort="Ishikawa, E" uniqKey="Ishikawa E" first="E." last="Ishikawa">E. 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Fukunaga</name><affiliation><mods:affiliation>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Address for correspondence:The Department of Pathology, The Jikei University School of Medicine, 3‐25‐8, Nishi‐shinbashi, Minato‐ku, Tokyo, 105, Japan.</mods:affiliation></affiliation></author><author><name sortKey="Ushigome, S" sort="Ushigome, S" uniqKey="Ushigome S" first="S." last="Ushigome">S. Ushigome</name><affiliation><mods:affiliation>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Shishikura, Y" sort="Shishikura, Y" uniqKey="Shishikura Y" first="Y." last="Shishikura">Y. Shishikura</name><affiliation><mods:affiliation>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Yokoi, K" sort="Yokoi, K" uniqKey="Yokoi K" first="K." last="Yokoi">K. Yokoi</name><affiliation><mods:affiliation>Departments of Dermatology, The Jikei University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Ishikawa, E" sort="Ishikawa, E" uniqKey="Ishikawa E" first="E." last="Ishikawa">E. Ishikawa</name><affiliation><mods:affiliation>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Histopathology</title><title level="j" type="alt">HISTOPATHOLOGY</title><idno type="ISSN">0309-0167</idno><idno type="eISSN">1365-2559</idno><imprint><biblScope unit="vol">27</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="243">243</biblScope><biblScope unit="page" to="249">249</biblScope><biblScope unit="page-count">7</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1995-09">1995-09</date></imprint><idno type="ISSN">0309-0167</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0309-0167</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">A case of endovascular papillary angioendothelioma‐like tumour associated with lymphoedema is described. Microscopically, the tumour was composed of anastomosing vascular channels, some of which contained papillary projections, producing tuft‐like or glomeruloid appearances. The dermis also showed moderate lymphoedema and lymphocyic infiltrate. The tumour resembled endovascular papillary angioendothelioma but also had several features that differed from typical examples: occurrence in an old patient and less prominent endothelial hobnail features and lymphocytic infiltrate. Three types of proliferating cells were observed: 1 mature flattened endothelial cells, which were strongly positive for endothelial markers (factor VIII‐related antigen, CD31, CD34) and bound ulex europaeus agglutinin 1; 2 immature endothelial cells with round nuclei and vacuolated or pale cytoplasm, which were strongly positive for CD31 and muscle‐specific actin (HHF35) and focally positive for other endothelial markers; and 3 stromal spindle cells in papillary or glomeruloid areas, which were positive for vimentin, HHF35, and alpha‐smooth muscle actin but negative for desmin. The tumour was diploid by flow cytometry. The patient was well without disease twelve months after the excision. We postulate that this tumour was caused by circulatory disturbance, namely lymphoedema associated with syringomyelia and a Charcot's joint.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>tumour</json:string><json:string>endovascular</json:string><json:string>excision</json:string><json:string>lymphoedema</json:string><json:string>glomeruloid</json:string><json:string>angioendothelioma</json:string><json:string>dabska</json:string><json:string>haemangioendothelioma</json:string><json:string>cuboidal</json:string><json:string>angiosarcoma</json:string><json:string>retiform</json:string><json:string>cutaneous</json:string><json:string>nodule</json:string><json:string>endothelial</json:string><json:string>endothelial cells</json:string><json:string>dabska tumour</json:string><json:string>retiform haemangioendothelioma</json:string><json:string>malignant endovascular</json:string><json:string>blackwell science</json:string><json:string>cuboidal cells</json:string><json:string>lesion</json:string><json:string>papillary</json:string><json:string>epithelioid haemangioendothelioma</json:string><json:string>vascular channels</json:string><json:string>stromal spindle cells</json:string><json:string>cutaneous angiosarcoma</json:string><json:string>histological features</json:string><json:string>glomeruloid haemangioma</json:string><json:string>local recurrence</json:string><json:string>glomeruloid structures</json:string><json:string>glomeruloid lesions</json:string><json:string>spindle cells</json:string><json:string>becton dickinson</json:string><json:string>phase fraction</json:string><json:string>post capillary venules</json:string><json:string>ulex europaeus agglutinin</json:string><json:string>case report</json:string><json:string>factor antigen</json:string><json:string>pale cytoplasm</json:string><json:string>cutaneous nodule</json:string><json:string>vascular tumour</json:string><json:string>endothelial hobnail features</json:string><json:string>endothelial markers</json:string><json:string>tissue tumors</json:string><json:string>flow cytometric</json:string></teeft></keywords><author><json:item><name>M. FUKUNAGA</name><affiliations><json:string>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</json:string><json:string>Address for correspondence:The Department of Pathology, The Jikei University School of Medicine, 3‐25‐8, Nishi‐shinbashi, Minato‐ku, Tokyo, 105, Japan.</json:string></affiliations></json:item><json:item><name>S. USHIGOME</name><affiliations><json:string>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Y. SHISHIKURA</name><affiliations><json:string>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>K. YOKOI</name><affiliations><json:string>Departments of Dermatology, The Jikei University School of Medicine, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>E. 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Microscopically, the tumour was composed of anastomosing vascular channels, some of which contained papillary projections, producing tuft‐like or glomeruloid appearances. The dermis also showed moderate lymphoedema and lymphocyic infiltrate. The tumour resembled endovascular papillary angioendothelioma but also had several features that differed from typical examples: occurrence in an old patient and less prominent endothelial hobnail features and lymphocytic infiltrate. Three types of proliferating cells were observed: 1 mature flattened endothelial cells, which were strongly positive for endothelial markers (factor VIII‐related antigen, CD31, CD34) and bound ulex europaeus agglutinin 1; 2 immature endothelial cells with round nuclei and vacuolated or pale cytoplasm, which were strongly positive for CD31 and muscle‐specific actin (HHF35) and focally positive for other endothelial markers; and 3 stromal spindle cells in papillary or glomeruloid areas, which were positive for vimentin, HHF35, and alpha‐smooth muscle actin but negative for desmin. The tumour was diploid by flow cytometry. The patient was well without disease twelve months after the excision. We postulate that this tumour was caused by circulatory disturbance, namely lymphoedema associated with syringomyelia and a Charcot's joint.</abstract><qualityIndicators><score>4.736</score><pdfVersion>1.3</pdfVersion><pdfPageSize>583.2 x 781.2 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1420</abstractCharCount><pdfWordCount>2444</pdfWordCount><pdfCharCount>16297</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>191</abstractWordCount></qualityIndicators><title>Endovascular papillary angioendothelioma‐like tumour associated with 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xml:id="author-0004"><persName><forename type="first">E.</forename><surname>ISHIKAWA</surname></persName><affiliation>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan<address><country key="JP"></country></address></affiliation></author><idno type="istex">DBF179368886F4C758F2F3A9754F320163955645</idno><idno type="DOI">10.1111/j.1365-2559.1995.tb00216.x</idno><idno type="unit">HIS243</idno><idno type="toTypesetVersion">file:HIS.HIS243.pdf</idno></analytic><monogr><title level="j" type="main">Histopathology</title><title level="j" type="alt">HISTOPATHOLOGY</title><idno type="pISSN">0309-0167</idno><idno type="eISSN">1365-2559</idno><idno type="book-DOI">10.1111/(ISSN)1365-2559</idno><idno type="book-part-DOI">10.1111/his.1995.27.issue-3</idno><idno type="product">HIS</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">27</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="243">243</biblScope><biblScope 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Microscopically, the tumour was composed of anastomosing vascular channels, some of which contained papillary projections, producing tuft‐like or glomeruloid appearances. The dermis also showed moderate lymphoedema and lymphocyic infiltrate. The tumour resembled endovascular papillary angioendothelioma but also had several features that differed from typical examples: occurrence in an old patient and less prominent endothelial hobnail features and lymphocytic infiltrate. Three types of proliferating cells were observed: <hi rend="bold">1</hi> mature flattened endothelial cells, which were strongly positive for endothelial markers (factor VIII‐related antigen, CD31, CD34) and bound ulex europaeus agglutinin 1; <hi rend="bold">2</hi> immature endothelial cells with round nuclei and vacuolated or pale cytoplasm, which were strongly positive for CD31 and muscle‐specific actin (HHF35) and focally positive for other endothelial markers; and <hi rend="bold">3</hi> stromal spindle cells in papillary or glomeruloid areas, which were positive for vimentin, HHF35, and alpha‐smooth muscle actin but negative for desmin. The tumour was diploid by flow cytometry. The patient was well without disease twelve months after the excision. We postulate that this tumour was caused by circulatory disturbance, namely lymphoedema associated with syringomyelia and a Charcot's joint.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">endovascular papillary angioendothelioma</term><term xml:id="k2">Dabska tumour</term><term xml:id="k3">vascular tumour</term><term xml:id="k4">lymphoedema</term></keywords></textClass><langUsage><language ident="EN"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/DBF179368886F4C758F2F3A9754F320163955645/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta 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endovascular papillary angioendothelioma‐like tumour associated with lymphoedema is described. Microscopically, the tumour was composed of anastomosing vascular channels, some of which contained papillary projections, producing tuft‐like or glomeruloid appearances. The dermis also showed moderate lymphoedema and lymphocyic infiltrate. The tumour resembled endovascular papillary angioendothelioma but also had several features that differed from typical examples: occurrence in an old patient and less prominent endothelial hobnail features and lymphocytic infiltrate. Three types of proliferating cells were observed: <b>1</b> mature flattened endothelial cells, which were strongly positive for endothelial markers (factor VIII‐related antigen, CD31, CD34) and bound ulex europaeus agglutinin 1; <b>2</b> immature endothelial cells with round nuclei and vacuolated or pale cytoplasm, which were strongly positive for CD31 and muscle‐specific actin (HHF35) and focally positive for other endothelial markers; and <b>3</b> stromal spindle cells in papillary or glomeruloid areas, which were positive for vimentin, HHF35, and alpha‐smooth muscle actin but negative for desmin. The tumour was diploid by flow cytometry. The patient was well without disease twelve months after the excision. We postulate that this tumour was caused by circulatory disturbance, namely lymphoedema associated with syringomyelia and a Charcot's joint.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Endovascular papillary angioendothelioma‐like tumour associated with lymphoedema</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Endovascular papillary angioendothelioma‐like tumour associated with lymphoedema</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">FUKUNAGA</namePart><affiliation>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</affiliation><affiliation>Address for correspondence:The Department of Pathology, The Jikei University School of Medicine, 3‐25‐8, Nishi‐shinbashi, Minato‐ku, Tokyo, 105, Japan.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">USHIGOME</namePart><affiliation>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">SHISHIKURA</namePart><affiliation>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">YOKOI</namePart><affiliation>Departments of Dermatology, The Jikei University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.</namePart><namePart type="family">ISHIKAWA</namePart><affiliation>Departments of Pathology, The Jikei University School of Medicine, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1995-09</dateIssued><edition>Date of submission 19 December 1994 Accepted for publication 2 May 1994</edition><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="references">16</extent></physicalDescription><abstract>A case of endovascular papillary angioendothelioma‐like tumour associated with lymphoedema is described. Microscopically, the tumour was composed of anastomosing vascular channels, some of which contained papillary projections, producing tuft‐like or glomeruloid appearances. The dermis also showed moderate lymphoedema and lymphocyic infiltrate. The tumour resembled endovascular papillary angioendothelioma but also had several features that differed from typical examples: occurrence in an old patient and less prominent endothelial hobnail features and lymphocytic infiltrate. Three types of proliferating cells were observed: 1 mature flattened endothelial cells, which were strongly positive for endothelial markers (factor VIII‐related antigen, CD31, CD34) and bound ulex europaeus agglutinin 1; 2 immature endothelial cells with round nuclei and vacuolated or pale cytoplasm, which were strongly positive for CD31 and muscle‐specific actin (HHF35) and focally positive for other endothelial markers; and 3 stromal spindle cells in papillary or glomeruloid areas, which were positive for vimentin, HHF35, and alpha‐smooth muscle actin but negative for desmin. The tumour was diploid by flow cytometry. The patient was well without disease twelve months after the excision. We postulate that this tumour was caused by circulatory disturbance, namely lymphoedema associated with syringomyelia and a Charcot's joint.</abstract><subject lang="en"><genre>keywords</genre><topic>endovascular papillary angioendothelioma</topic><topic>Dabska tumour</topic><topic>vascular tumour</topic><topic>lymphoedema</topic></subject><relatedItem type="host"><titleInfo><title>Histopathology</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0309-0167</identifier><identifier type="eISSN">1365-2559</identifier><identifier type="DOI">10.1111/(ISSN)1365-2559</identifier><identifier type="PublisherID">HIS</identifier><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>27</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>243</start><end>249</end><total>7</total></extent></part></relatedItem><identifier type="istex">DBF179368886F4C758F2F3A9754F320163955645</identifier><identifier type="DOI">10.1111/j.1365-2559.1995.tb00216.x</identifier><identifier type="ArticleID">HIS243</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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