Complement profile in a Cr inhibitor deficient family
Identifieur interne : 000890 ( Istex/Corpus ); précédent : 000889; suivant : 000891Complement profile in a Cr inhibitor deficient family
Auteurs : K. Sayama ; S. Shiraishi ; Y. MikiSource :
- British Journal of Dermatology [ 0007-0963 ] ; 1985-12.
Abstract
Complement components and anaphylatoxins in a Cr inhibitor (CrINH) deficient family were studied. C4a was increased when CrINH was decreased, and C3a was increased in subjects with systemic lupus erythematosus (SLE)‐like symptoms and with angioedema attacks. Danazol was effective in controlling the clinical as well as complement abnormalities including low CH50, CrINH and C4, which increased within 10 days after danazol treatment was started. Two‐dimensional immunoelectrophoresis of CrINH showed that there was no functionally or electrophoretically abnormal CrINH present before or after danazol treatment. C3a and C4a were considered to play important roles in the pathogenesis of angioedema and associated SLE‐like symptoms.
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DOI: 10.1111/j.1365-2133.1985.tb02410.x
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Miki</name><affiliation><mods:affiliation>Department of Dermatology, University of Ehime School of Medicine, Japan</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:6CE538992D4E5C8087CBF3697F6618247A0BB8C4</idno><date when="1985" year="1985">1985</date><idno type="doi">10.1111/j.1365-2133.1985.tb02410.x</idno><idno type="url">https://api.istex.fr/document/6CE538992D4E5C8087CBF3697F6618247A0BB8C4/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000890</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Complement profile in a Cr inhibitor deficient family</title><author><name sortKey="Sayama, K" sort="Sayama, K" uniqKey="Sayama K" first="K." last="Sayama">K. Sayama</name><affiliation><mods:affiliation>Department of Dermatology, University of Ehime School of Medicine, Japan</mods:affiliation></affiliation></author><author><name sortKey="Shiraishi, S" sort="Shiraishi, S" uniqKey="Shiraishi S" first="S." last="Shiraishi">S. Shiraishi</name><affiliation><mods:affiliation>Department of Dermatology, University of Ehime School of Medicine, Japan</mods:affiliation></affiliation></author><author><name sortKey="Miki, Y" sort="Miki, Y" uniqKey="Miki Y" first="Y." last="Miki">Y. Miki</name><affiliation><mods:affiliation>Department of Dermatology, University of Ehime School of Medicine, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">British Journal of Dermatology</title><idno type="ISSN">0007-0963</idno><idno type="eISSN">1365-2133</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1985-12">1985-12</date><biblScope unit="volume">113</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="737">737</biblScope><biblScope unit="page" to="743">743</biblScope></imprint><idno type="ISSN">0007-0963</idno></series><idno type="istex">6CE538992D4E5C8087CBF3697F6618247A0BB8C4</idno><idno type="DOI">10.1111/j.1365-2133.1985.tb02410.x</idno><idno type="ArticleID">BJD737</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0007-0963</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Complement components and anaphylatoxins in a Cr inhibitor (CrINH) deficient family were studied. C4a was increased when CrINH was decreased, and C3a was increased in subjects with systemic lupus erythematosus (SLE)‐like symptoms and with angioedema attacks. Danazol was effective in controlling the clinical as well as complement abnormalities including low CH50, CrINH and C4, which increased within 10 days after danazol treatment was started. Two‐dimensional immunoelectrophoresis of CrINH showed that there was no functionally or electrophoretically abnormal CrINH present before or after danazol treatment. C3a and C4a were considered to play important roles in the pathogenesis of angioedema and associated SLE‐like symptoms.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>K. SAYAMA</name><affiliations><json:string>Department of Dermatology, University of Ehime School of Medicine, Japan</json:string></affiliations></json:item><json:item><name>S. 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Two‐dimensional immunoelectrophoresis of CrINH showed that there was no functionally or electrophoretically abnormal CrINH present before or after danazol treatment. C3a and C4a were considered to play important roles in the pathogenesis of angioedema and associated SLE‐like symptoms.</abstract><qualityIndicators><score>4.985</score><pdfVersion>1.6</pdfVersion><pdfPageSize>462 x 676 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>732</abstractCharCount><pdfWordCount>2261</pdfWordCount><pdfCharCount>12849</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>102</abstractWordCount></qualityIndicators><title>Complement profile in a Cr inhibitor deficient family</title><genre><json:string>case report</json:string></genre><host><volume>113</volume><publisherId><json:string>BJD</json:string></publisherId><pages><total>7</total><last>743</last><first>737</first></pages><issn><json:string>0007-0963</json:string></issn><issue>6</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1365-2133</json:string></eissn><title>British Journal of Dermatology</title><doi><json:string>10.1111/(ISSN)1365-2133</json:string></doi></host><publicationDate>1985</publicationDate><copyrightDate>1985</copyrightDate><doi><json:string>10.1111/j.1365-2133.1985.tb02410.x</json:string></doi><id>6CE538992D4E5C8087CBF3697F6618247A0BB8C4</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/6CE538992D4E5C8087CBF3697F6618247A0BB8C4/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/6CE538992D4E5C8087CBF3697F6618247A0BB8C4/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/6CE538992D4E5C8087CBF3697F6618247A0BB8C4/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Complement profile in a Cr inhibitor deficient family</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>1985</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Complement profile in a Cr inhibitor deficient family</title><author><persName><forename type="first">K.</forename><surname>SAYAMA</surname></persName><note type="correspondence"><p>Correspondence: Dr K. 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Sayama, Department of Dermatology, University of Ehime School of Medicine, Shigenobucho, Onsengun, Ehime, 791‐02, Japan.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:BJD.BJD737.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication 3 May 1985</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="18"></count><count type="linksCrossRef" number="4"></count></countGroup><titleGroup><title type="main">Complement profile in a Cr inhibitor deficient family</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>K.</givenNames><familyName>SAYAMA</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>S.</givenNames><familyName>SHIRAISHI</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Y.</givenNames><familyName>MIKI</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="JP"><unparsedAffiliation>Department of Dermatology, University of Ehime School of Medicine, Japan</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">SUMMARY</title><p>Complement components and anaphylatoxins in a Cr inhibitor (CrINH) deficient family were studied. C4a was increased when CrINH was decreased, and C3a was increased in subjects with systemic lupus erythematosus (SLE)‐like symptoms and with angioedema attacks. Danazol was effective in controlling the clinical as well as complement abnormalities including low CH50, CrINH and C4, which increased within 10 days after danazol treatment was started. Two‐dimensional immunoelectrophoresis of CrINH showed that there was no functionally or electrophoretically abnormal CrINH present before or after danazol treatment. C3a and C4a were considered to play important roles in the pathogenesis of angioedema and associated SLE‐like symptoms.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Complement profile in a Cr inhibitor deficient family</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Complement profile in a Cr inhibitor deficient family</title></titleInfo><name type="personal"><namePart type="given">K.</namePart><namePart type="family">SAYAMA</namePart><affiliation>Department of Dermatology, University of Ehime School of Medicine, Japan</affiliation><description>Correspondence: Dr K. Sayama, Department of Dermatology, University of Ehime School of Medicine, Shigenobucho, Onsengun, Ehime, 791‐02, Japan.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">SHIRAISHI</namePart><affiliation>Department of Dermatology, University of Ehime School of Medicine, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">MIKI</namePart><affiliation>Department of Dermatology, University of Ehime School of Medicine, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="case report" displayLabel="caseStudy"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1985-12</dateIssued><edition>Accepted for publication 3 May 1985</edition><copyrightDate encoding="w3cdtf">1985</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">18</extent></physicalDescription><abstract lang="en">Complement components and anaphylatoxins in a Cr inhibitor (CrINH) deficient family were studied. C4a was increased when CrINH was decreased, and C3a was increased in subjects with systemic lupus erythematosus (SLE)‐like symptoms and with angioedema attacks. Danazol was effective in controlling the clinical as well as complement abnormalities including low CH50, CrINH and C4, which increased within 10 days after danazol treatment was started. Two‐dimensional immunoelectrophoresis of CrINH showed that there was no functionally or electrophoretically abnormal CrINH present before or after danazol treatment. C3a and C4a were considered to play important roles in the pathogenesis of angioedema and associated SLE‐like symptoms.</abstract><relatedItem type="host"><titleInfo><title>British Journal of Dermatology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0007-0963</identifier><identifier type="eISSN">1365-2133</identifier><identifier type="DOI">10.1111/(ISSN)1365-2133</identifier><identifier type="PublisherID">BJD</identifier><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>113</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>737</start><end>743</end><total>7</total></extent></part></relatedItem><identifier type="istex">6CE538992D4E5C8087CBF3697F6618247A0BB8C4</identifier><identifier type="DOI">10.1111/j.1365-2133.1985.tb02410.x</identifier><identifier type="ArticleID">BJD737</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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