The pathogenesis of eosinophilic endomyocardial disease in patients with carcinomas of the lung
Identifieur interne : 000660 ( Main/Exploration ); précédent : 000659; suivant : 000661The pathogenesis of eosinophilic endomyocardial disease in patients with carcinomas of the lung
Auteurs : RBID : ISTEX:380_1985_Article_BF02066412.pdfAbstract
Studies were done on a patient with a carcinoma of the lung induced by hypereosinophilia who was thought to be at risk from developing eosinophilic endomyocardial disease to see whether the development of heart disease could be related to abnormalities in the morphology or kinetics of blood eosinophils. The patient was a 61-year-old man who had a partial resection of a squamous cell bronchial carcinoma of anaplastic large cell type which had spread locally. Seven months later, he developed a blood eosinophil count of 33.9 × 109/l. There were only transient responses to treatment with steroids and tumor irradiation, and he died 15 weeks later. Up to 3 × 109/l blood eosinophils were degranulated, correlating with serum levels of eosinophil cationic protein. The blood half-life of111indium-labeled eosinophils was prolonged to 53 h, but their distribution was normal. Although an unsuccessful search was made during life for the development of endomyocardial damage, at postmortem the left ventricle had features of eosinophilic endomyocardial disease in the acute necrotic stage. Among 13 other reported patients with carcinoma of the lung and hypereosinophilia, three also had endomyocardial disease or myocardial lesions. These findings confirm the suggestion that the presence in the blood of >1×109/l degranulated eosinophils can be used to predict the development of eosinophilic endomyocardial disease before it becomes apparent clinically, and they also add weight to the hypothesis that blood eosinophil degranulation causes this complication of hypereosinophilic states.
DOI: 10.1007/BF02066412
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Weetman</name><affiliation wicri:level="2"><mods:affiliation>Departments of Immunology and Medicine, Royal Postgraduate Medical School, London, England</mods:affiliation><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Departments of Immunology and Medicine, Royal Postgraduate Medical School, London</wicri:cityArea></affiliation></author><author><name>I. Olsson</name><affiliation wicri:level="1"><mods:affiliation>Department of Internal Medicine, University of Lund, Sweden</mods:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Internal Medicine, University of Lund</wicri:regionArea><wicri:noRegion>University of Lund</wicri:noRegion></affiliation></author><author><name>P-C. Tai</name><affiliation wicri:level="2"><mods:affiliation>Departments of Immunology and Medicine, Royal Postgraduate Medical School, London, England</mods:affiliation><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Departments of Immunology and Medicine, Royal Postgraduate Medical School, London</wicri:cityArea></affiliation></author><author><name>E. G. J. Olsen</name><affiliation wicri:level="2"><mods:affiliation>Department of Morbid Pathology and Histochemistry, National Heart Hospital, London, England</mods:affiliation><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Department of Morbid Pathology and Histochemistry, National Heart Hospital, London</wicri:cityArea></affiliation></author></titleStmt><publicationStmt><idno type="RBID">ISTEX:380_1985_Article_BF02066412.pdf</idno><date when="1985">1985</date><idno type="doi">10.1007/BF02066412</idno><idno type="wicri:Area/Main/Corpus">000399</idno><idno type="wicri:Area/Main/Curation">000399</idno><idno type="wicri:Area/Main/Exploration">000660</idno></publicationStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="eng">Studies were done on a patient with a carcinoma of the lung induced by hypereosinophilia who was thought to be at risk from developing eosinophilic endomyocardial disease to see whether the development of heart disease could be related to abnormalities in the morphology or kinetics of blood eosinophils. The patient was a 61-year-old man who had a partial resection of a squamous cell bronchial carcinoma of anaplastic large cell type which had spread locally. Seven months later, he developed a blood eosinophil count of 33.9 × 109/l. There were only transient responses to treatment with steroids and tumor irradiation, and he died 15 weeks later. Up to 3 × 109/l blood eosinophils were degranulated, correlating with serum levels of eosinophil cationic protein. The blood half-life of111indium-labeled eosinophils was prolonged to 53 h, but their distribution was normal. Although an unsuccessful search was made during life for the development of endomyocardial damage, at postmortem the left ventricle had features of eosinophilic endomyocardial disease in the acute necrotic stage. Among 13 other reported patients with carcinoma of the lung and hypereosinophilia, three also had endomyocardial disease or myocardial lesions. These findings confirm the suggestion that the presence in the blood of >1×109/l degranulated eosinophils can be used to predict the development of eosinophilic endomyocardial disease before it becomes apparent clinically, and they also add weight to the hypothesis that blood eosinophil degranulation causes this complication of hypereosinophilic states.</div></front></TEI><mods xsi:schemaLocation="http://www.loc.gov/mods/v3 file:///applis/istex/home/loadistex/home/etc/xsd/mods.xsd" version="3.4" istexId="454c1ad4eec89506040e02796410054f182ca88e"><titleInfo lang="eng"><title>The pathogenesis of eosinophilic endomyocardial disease in patients with carcinomas of the lung</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="given">C. J. F.</namePart><namePart type="family">Spry</namePart><role><roleTerm type="text">author</roleTerm></role><affiliation>Departments of Immunology and Medicine, Royal Postgraduate Medical School, London, England</affiliation></name><name type="personal"><namePart type="termsOfAddress"></namePart><namePart type="given">A. 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J.</namePart><namePart type="family">Olsen</namePart><role><roleTerm type="text">author</roleTerm></role><affiliation>Department of Morbid Pathology and Histochemistry, National Heart Hospital, London, England</affiliation></name><typeOfResource>text</typeOfResource><genre>Originals</genre><genre>Original Paper</genre><originInfo><publisher>Springer-Verlag, Tokyo</publisher><dateValid encoding="w3cdtf">2005-07-25</dateValid><copyrightDate encoding="w3cdtf">1985</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="eng">Studies were done on a patient with a carcinoma of the lung induced by hypereosinophilia who was thought to be at risk from developing eosinophilic endomyocardial disease to see whether the development of heart disease could be related to abnormalities in the morphology or kinetics of blood eosinophils. The patient was a 61-year-old man who had a partial resection of a squamous cell bronchial carcinoma of anaplastic large cell type which had spread locally. Seven months later, he developed a blood eosinophil count of 33.9 × 109/l. There were only transient responses to treatment with steroids and tumor irradiation, and he died 15 weeks later. Up to 3 × 109/l blood eosinophils were degranulated, correlating with serum levels of eosinophil cationic protein. The blood half-life of111indium-labeled eosinophils was prolonged to 53 h, but their distribution was normal. Although an unsuccessful search was made during life for the development of endomyocardial damage, at postmortem the left ventricle had features of eosinophilic endomyocardial disease in the acute necrotic stage. Among 13 other reported patients with carcinoma of the lung and hypereosinophilia, three also had endomyocardial disease or myocardial lesions. These findings confirm the suggestion that the presence in the blood of >1×109/l degranulated eosinophils can be used to predict the development of eosinophilic endomyocardial disease before it becomes apparent clinically, and they also add weight to the hypothesis that blood eosinophil degranulation causes this complication of hypereosinophilic states.</abstract><relatedItem type="series"><titleInfo type="abbreviated"><title>Heart Vessels</title></titleInfo><titleInfo><title>Heart and Vessels</title><subTitle>An International Journal</subTitle><partNumber>Year: 1985</partNumber><partNumber>Volume: 1</partNumber><partNumber>Number: 3</partNumber></titleInfo><genre>Archive Journal</genre><originInfo><dateIssued encoding="w3cdtf">1985-08-01</dateIssued><copyrightDate encoding="w3cdtf">1985</copyrightDate></originInfo><subject usage="primary"><topic>Medicine & Public Health</topic><topic>Biomedical Engineering</topic><topic>Interventional Radiology</topic><topic>Ultrasound</topic><topic>Cardiology</topic><topic>Cardiac Surgery</topic><topic>Vascular Surgery</topic></subject><identifier type="issn">0910-8327</identifier><identifier type="issn">Electronic: 1615-2573</identifier><identifier type="matrixNumber">380</identifier><identifier type="local">IssueArticleCount: 12</identifier><recordInfo><recordOrigin>Springer-Verlag, 1985</recordOrigin></recordInfo></relatedItem><identifier type="doi">10.1007/BF02066412</identifier><identifier type="matrixNumber">Art6</identifier><identifier type="local">BF02066412</identifier><accessCondition type="use and reproduction">MetadataGrant: OpenAccess</accessCondition><accessCondition type="use and reproduction">AbstractGrant: OpenAccess</accessCondition><accessCondition type="restriction on access">BodyPDFGrant: Restricted</accessCondition><accessCondition type="restriction on access">BodyHTMLGrant: Restricted</accessCondition><accessCondition type="restriction on access">BibliographyGrant: Restricted</accessCondition><accessCondition type="restriction on access">ESMGrant: Restricted</accessCondition><part><extent unit="pages"><start>162</start><end>169</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1985</recordOrigin><recordIdentifier>380_1985_Article_BF02066412.pdf</recordIdentifier></recordInfo></mods></record>Pour manipuler ce document sous Unix (Dilib)
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