“Acquired” antibody hemolytic anemia and familial aberrations in gamma globulins
Identifieur interne : 002B99 ( Istex/Corpus ); précédent : 002B98; suivant : 002C00“Acquired” antibody hemolytic anemia and familial aberrations in gamma globulins
Auteurs : Philip J. Fialkow ; Hugh Fudenberg ; W. V. EpsteinSource :
- The American Journal of Medicine [ 0002-9343 ] ; 1963.
Abstract
This report describes a patient with acquired hemolytic anemia, carditis and thyrotoxicosis. Multiple immunologic abnormalities were found in the patient and in members of his family. The red blood cells of the proband and his mother gave positive direct antiglobulin (Coombs') reactions. Increased levels of gamma globulins and macroglobulins, rheumatoid factors, antinuclear factors and antibodies to cardiac and thyroid tissue were present in various combinations in the serum of proband, his mother and other close relatives. A sibling had died of polyarteritis nodosa.The pertinent clinical and immunologic manifestations are discussed in relation to pathogenetic, etiologic and genetic considerations. The evidence indicates that a genetic predisposition is a necessary but not sufficient condition for the development of diseases associated with immunologic hyperreactivity.
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DOI: 10.1016/0002-9343(64)90082-8
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Fialkow</name><affiliation><mods:affiliation>San Francisco, California, USA</mods:affiliation></affiliation></author><author><name sortKey="Fudenberg, Hugh" sort="Fudenberg, Hugh" uniqKey="Fudenberg H" first="Hugh" last="Fudenberg">Hugh Fudenberg</name><affiliation><mods:affiliation>San Francisco, California, USA</mods:affiliation></affiliation></author><author><name sortKey="Epstein, W V" sort="Epstein, W V" uniqKey="Epstein W" first="W. V." last="Epstein">W. V. Epstein</name><affiliation><mods:affiliation>San Francisco, California, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">The American Journal of Medicine</title><title level="j" type="abbrev">AJM</title><idno type="ISSN">0002-9343</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1963">1963</date><biblScope unit="volume">36</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="188">188</biblScope><biblScope unit="page" to="199">199</biblScope></imprint><idno type="ISSN">0002-9343</idno></series><idno type="istex">CCA30C7D82D2956EAFCF27F6BCCDD5F89C567844</idno><idno type="DOI">10.1016/0002-9343(64)90082-8</idno><idno type="PII">0002-9343(64)90082-8</idno><idno type="ArticleID">64900828</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0002-9343</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">This report describes a patient with acquired hemolytic anemia, carditis and thyrotoxicosis. Multiple immunologic abnormalities were found in the patient and in members of his family. The red blood cells of the proband and his mother gave positive direct antiglobulin (Coombs') reactions. Increased levels of gamma globulins and macroglobulins, rheumatoid factors, antinuclear factors and antibodies to cardiac and thyroid tissue were present in various combinations in the serum of proband, his mother and other close relatives. A sibling had died of polyarteritis nodosa.The pertinent clinical and immunologic manifestations are discussed in relation to pathogenetic, etiologic and genetic considerations. The evidence indicates that a genetic predisposition is a necessary but not sufficient condition for the development of diseases associated with immunologic hyperreactivity.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Philip J. Fialkow M.D.</name><affiliations><json:string>San Francisco, California, USA</json:string></affiliations></json:item><json:item><name>Hugh Fudenberg M.D.</name><affiliations><json:string>San Francisco, California, USA</json:string></affiliations></json:item><json:item><name>W.V. Epstein M.D.</name><affiliations><json:string>San Francisco, California, USA</json:string></affiliations></json:item></author><articleId><json:string>64900828</json:string></articleId><language><json:string>eng</json:string></language><abstract>This report describes a patient with acquired hemolytic anemia, carditis and thyrotoxicosis. Multiple immunologic abnormalities were found in the patient and in members of his family. The red blood cells of the proband and his mother gave positive direct antiglobulin (Coombs') reactions. Increased levels of gamma globulins and macroglobulins, rheumatoid factors, antinuclear factors and antibodies to cardiac and thyroid tissue were present in various combinations in the serum of proband, his mother and other close relatives. A sibling had died of polyarteritis nodosa.The pertinent clinical and immunologic manifestations are discussed in relation to pathogenetic, etiologic and genetic considerations. The evidence indicates that a genetic predisposition is a necessary but not sufficient condition for the development of diseases associated with immunologic hyperreactivity.</abstract><qualityIndicators><score>6.952</score><pdfVersion>1.4</pdfVersion><pdfPageSize>540 x 720 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>881</abstractCharCount><pdfWordCount>5246</pdfWordCount><pdfCharCount>40796</pdfCharCount><pdfPageCount>12</pdfPageCount><abstractWordCount>121</abstractWordCount></qualityIndicators><title>“Acquired” antibody hemolytic anemia and familial aberrations in gamma globulins</title><pii><json:string>0002-9343(64)90082-8</json:string></pii><genre><json:string>research-article</json:string></genre><serie><volume>vol. 2</volume><pages><first>210</first></pages><genre></genre><language><json:string>unknown</json:string></language><title>Progress in Medical 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type="degree">M.D.</roleName><note type="biography">Present address: Department of Medicine, University of Washington School of Medicine, Seattle, Washington.</note><affiliation>Present address: Department of Medicine, University of Washington School of Medicine, Seattle, Washington.</affiliation><affiliation>San Francisco, California, USA</affiliation></author><author><persName><forename type="first">Hugh</forename><surname>Fudenberg</surname></persName><roleName type="degree">M.D.</roleName><note type="biography">From the Department of Medicine, University of California School of Medicine, San Francisco, California.</note><affiliation>From the Department of Medicine, University of California School of Medicine, San Francisco, California.</affiliation><affiliation>San Francisco, California, USA</affiliation></author><author><persName><forename type="first">W.V.</forename><surname>Epstein</surname></persName><roleName type="degree">M.D.</roleName><note type="biography">From the Department of Medicine, University of California School of Medicine, San Francisco, California.</note><affiliation>From the Department of Medicine, University of California School of Medicine, San Francisco, California.</affiliation><affiliation>San Francisco, California, USA</affiliation></author></analytic><monogr><title level="j">The American Journal of Medicine</title><title level="j" type="abbrev">AJM</title><idno type="pISSN">0002-9343</idno><idno type="PII">S0002-9343(00)X0243-4</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1963"></date><biblScope unit="volume">36</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="188">188</biblScope><biblScope unit="page" to="199">199</biblScope></imprint></monogr><idno type="istex">CCA30C7D82D2956EAFCF27F6BCCDD5F89C567844</idno><idno type="DOI">10.1016/0002-9343(64)90082-8</idno><idno type="PII">0002-9343(64)90082-8</idno><idno type="ArticleID">64900828</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1964</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>This report describes a patient with acquired hemolytic anemia, carditis and thyrotoxicosis. Multiple immunologic abnormalities were found in the patient and in members of his family. The red blood cells of the proband and his mother gave positive direct antiglobulin (Coombs') reactions. Increased levels of gamma globulins and macroglobulins, rheumatoid factors, antinuclear factors and antibodies to cardiac and thyroid tissue were present in various combinations in the serum of proband, his mother and other close relatives. A sibling had died of polyarteritis nodosa.The pertinent clinical and immunologic manifestations are discussed in relation to pathogenetic, etiologic and genetic considerations. The evidence indicates that a genetic predisposition is a necessary but not sufficient condition for the development of diseases associated with immunologic hyperreactivity.</p></abstract></profileDesc><revisionDesc><change when="1963-01-16">Received</change><change when="1963">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>AJM</jid><aid>64900828</aid><ce:pii>0002-9343(64)90082-8</ce:pii><ce:doi>10.1016/0002-9343(64)90082-8</ce:doi><ce:copyright type="unknown" year="1964"></ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>This investigation was supported in part by grants (H-5997 and A-1229) from the National Institutes of Health and by funds from The Upjohn Company and the San Francisco Heart Association.</ce:note-para></ce:article-footnote><ce:dochead><ce:textfn>Clinical study</ce:textfn></ce:dochead><ce:title>“Acquired” antibody hemolytic anemia and familial aberrations in gamma globulins</ce:title><ce:author-group><ce:author><ce:given-name>Philip J.</ce:given-name><ce:surname>Fialkow</ce:surname><ce:degrees>M.D.</ce:degrees><ce:cross-ref refid="FN2"><ce:sup loc="post">†</ce:sup></ce:cross-ref><ce:cross-ref refid="FN1"><ce:sup loc="post">1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Hugh</ce:given-name><ce:surname>Fudenberg</ce:surname><ce:degrees>M.D.</ce:degrees><ce:cross-ref refid="FN1"><ce:sup loc="post">1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>W.V.</ce:given-name><ce:surname>Epstein</ce:surname><ce:degrees>M.D.</ce:degrees><ce:cross-ref refid="FN1"><ce:sup loc="post">1</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>San Francisco, California, USA</ce:textfn></ce:affiliation><ce:footnote id="FN2"><ce:label>†</ce:label><ce:note-para>Present address: Department of Medicine, University of Washington School of Medicine, Seattle, Washington.</ce:note-para></ce:footnote><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>From the Department of Medicine, University of California School of Medicine, San Francisco, California.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="16" month="1" year="1963"></ce:date-received><ce:abstract class="author"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">This report describes a patient with acquired hemolytic anemia, carditis and thyrotoxicosis. Multiple immunologic abnormalities were found in the patient and in members of his family. The red blood cells of the proband and his mother gave positive direct antiglobulin (Coombs') reactions. Increased levels of gamma globulins and macroglobulins, rheumatoid factors, antinuclear factors and antibodies to cardiac and thyroid tissue were present in various combinations in the serum of proband, his mother and other close relatives. A sibling had died of polyarteritis nodosa.</ce:simple-para><ce:simple-para view="all" id="simple-para.0015">The pertinent clinical and immunologic manifestations are discussed in relation to pathogenetic, etiologic and genetic considerations. The evidence indicates that a genetic predisposition is a necessary but not sufficient condition for the development of diseases associated with immunologic hyperreactivity.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>“Acquired” antibody hemolytic anemia and familial aberrations in gamma globulins</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>“Acquired” antibody hemolytic anemia and familial aberrations in gamma globulins</title></titleInfo><name type="personal"><namePart type="given">Philip J.</namePart><namePart type="family">Fialkow</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>San Francisco, California, USA</affiliation><description>Present address: Department of Medicine, University of Washington School of Medicine, Seattle, Washington.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hugh</namePart><namePart type="family">Fudenberg</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>San Francisco, California, USA</affiliation><description>From the Department of Medicine, University of California School of Medicine, San Francisco, California.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.V.</namePart><namePart type="family">Epstein</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>San Francisco, California, USA</affiliation><description>From the Department of Medicine, University of California School of Medicine, San Francisco, California.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1963</dateIssued><dateCaptured encoding="w3cdtf">1963-01-16</dateCaptured><copyrightDate encoding="w3cdtf">1964</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">This report describes a patient with acquired hemolytic anemia, carditis and thyrotoxicosis. Multiple immunologic abnormalities were found in the patient and in members of his family. The red blood cells of the proband and his mother gave positive direct antiglobulin (Coombs') reactions. Increased levels of gamma globulins and macroglobulins, rheumatoid factors, antinuclear factors and antibodies to cardiac and thyroid tissue were present in various combinations in the serum of proband, his mother and other close relatives. A sibling had died of polyarteritis nodosa.The pertinent clinical and immunologic manifestations are discussed in relation to pathogenetic, etiologic and genetic considerations. The evidence indicates that a genetic predisposition is a necessary but not sufficient condition for the development of diseases associated with immunologic hyperreactivity.</abstract><note>This investigation was supported in part by grants (H-5997 and A-1229) from the National Institutes of Health and by funds from The Upjohn Company and the San Francisco Heart Association.</note><note type="content">Section title: Clinical study</note><relatedItem type="host"><titleInfo><title>The American Journal of Medicine</title></titleInfo><titleInfo type="abbreviated"><title>AJM</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">196402</dateIssued></originInfo><identifier type="ISSN">0002-9343</identifier><identifier type="PII">S0002-9343(00)X0243-4</identifier><part><date>196402</date><detail type="volume"><number>36</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>A1</start><end>A90</end></extent><extent unit="issue pages"><start>A91</start><end>A156</end></extent><extent unit="issue pages"><start>167</start><end>336</end></extent><extent unit="pages"><start>188</start><end>199</end></extent></part></relatedItem><identifier type="istex">CCA30C7D82D2956EAFCF27F6BCCDD5F89C567844</identifier><identifier type="DOI">10.1016/0002-9343(64)90082-8</identifier><identifier type="PII">0002-9343(64)90082-8</identifier><identifier type="ArticleID">64900828</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:refBibTEI uri="https://api.istex.fr/document/CCA30C7D82D2956EAFCF27F6BCCDD5F89C567844/enrichments/refBib"><teiHeader></teiHeader><text><front></front><body></body><back><listBibl><biblStruct><analytic><title level="a" type="main">Genetics, hypersensitivity and the connective tissue diseases</title><author><persName><forename type="first">M</forename><surname>Ziff</surname></persName></author></analytic><monogr><title level="j">Am. .I. 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