Cardiac involvement in Anderson–Fabry disease
Identifieur interne : 005994 ( Istex/Corpus ); précédent : 005993; suivant : 005995Cardiac involvement in Anderson–Fabry disease
Auteurs : Filippo Maria Cauti ; Constantinos O'Mahony ; Antonis PantazisSource :
- BMJ Case Reports [ 1757-790X ] ; 2010.
Abstract
A normotensive 50-year-old man was evaluated for cardiac symptoms associated with left ventricular hypertrophy (LFH). His symptoms were caused by cardiac involvement from Anderson–Fabry disease (AFD), an X linked lysosomal storage disease caused by mutations in the GLA gene which encodes for the lysosomal enzyme -galactosidase A. He was treated with recombinant enzyme but the clinical course was complicated by arrhythmias and the patient required an internal cardioverter defibrillator. Even though AFD is rare, this case illustrates the importance of considering the diagnosis in selected patients as effective treatment has recently become available. Recognition of AFD also allows for screening of asymptomatic relatives who may benefit from treatment before irreversible life-threatening complications develop.
Url:
DOI: 10.1136/bcr.02.2010.2760
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ISTEX:BF5C03598A2BDE3F4A528527018650927E0DAA1DLe document en format XML
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pub-id-type="other">bcr.02.2010.2760</article-id><article-categories><subj-group subj-group-type="case-report-type"><subject>Rare disease</subject></subj-group><subj-group subj-group-type="search-fields"><subject content-type="sex">Male</subject><subject content-type="age">31–50 years</subject><subject content-type="ethnicity">White</subject><subject content-type="region">Europe (West)</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Cardiomyopathy</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Cardiovascular medicine</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Rare disease</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Echocardiography</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Pacing and electrophysiology</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Arrhythmias</subject></subj-group><series-title>Rare disease</series-title></article-categories><title-group><article-title>Cardiac involvement in Anderson–Fabry disease</article-title><alt-title alt-title-type="running-head">Rare disease</alt-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Cauti</surname><given-names>Filippo Maria</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>O'Mahony</surname><given-names>Constantinos</given-names></name><xref ref-type="aff" rid="aff2">2</xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Pantazis</surname><given-names>Antonis</given-names></name><xref ref-type="aff" rid="aff2">2</xref></contrib></contrib-group><aff id="aff1"><label>1</label><addr-line>Cardiology Department, University of Rome ‘Sapienza’, Via di Grottarossa, Rome, Italy</addr-line></aff><aff id="aff2"><label>2</label><addr-line>Inherited Cardiac Diseases Unit, The Heart Hospital, London, UK</addr-line></aff><author-notes><corresp><label>Correspondence to</label> Filippo Maria Cauti, <email xlink:type="simple">filippocauti@hotmail.it</email></corresp></author-notes><pub-date pub-type="collection"><year>2010</year></pub-date><pub-date pub-type="ppub"><year>2010</year></pub-date><volume>2010</volume><volume-id pub-id-type="other">2010</volume-id><volume-id pub-id-type="other">2010</volume-id><elocation-id>bcr0220102760</elocation-id><permissions><copyright-statement>2010 BMJ Publishing Group Ltd</copyright-statement><copyright-year>2010</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="casereports-2010-bcr-02-2010-2760.pdf"></self-uri><abstract><p>A normotensive 50-year-old man was evaluated for cardiac symptoms associated with left ventricular hypertrophy (LFH). His symptoms were caused by cardiac involvement from Anderson–Fabry disease (AFD), an X linked lysosomal storage disease caused by mutations in the GLA gene which encodes for the lysosomal enzyme -galactosidase A. He was treated with recombinant enzyme but the clinical course was complicated by arrhythmias and the patient required an internal cardioverter defibrillator.</p><p>Even though AFD is rare, this case illustrates the importance of considering the diagnosis in selected patients as effective treatment has recently become available. Recognition of AFD also allows for screening of asymptomatic relatives who may benefit from treatment before irreversible life-threatening complications develop.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Cardiac involvement in Anderson–Fabry disease</title><partName>Rare disease</partName></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Cardiac involvement in Anderson–Fabry disease</title><partName>Rare disease</partName></titleInfo><name type="personal"><namePart type="given">Filippo Maria</namePart><namePart type="family">Cauti</namePart><affiliation>Cardiology Department, University of Rome ‘Sapienza’, Via di Grottarossa, Rome, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Constantinos</namePart><namePart type="family">O'Mahony</namePart><affiliation>Inherited Cardiac Diseases Unit, The Heart Hospital, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Antonis</namePart><namePart type="family">Pantazis</namePart><affiliation>Inherited Cardiac Diseases Unit, The Heart Hospital, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="case-report" displayLabel="case-report"></genre><subject><genre>case-report-type</genre><topic>Rare disease</topic></subject><subject><genre>search-fields</genre><topic>Male</topic><topic>31–50 years</topic><topic>White</topic><geographic>Europe (West)</geographic></subject><subject><genre>hwp-journal-coll</genre><topic>Cardiomyopathy</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Cardiovascular medicine</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Rare disease</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Echocardiography</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Pacing and electrophysiology</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Arrhythmias</topic></subject><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">2010</dateIssued><copyrightDate encoding="w3cdtf">2010</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">A normotensive 50-year-old man was evaluated for cardiac symptoms associated with left ventricular hypertrophy (LFH). His symptoms were caused by cardiac involvement from Anderson–Fabry disease (AFD), an X linked lysosomal storage disease caused by mutations in the GLA gene which encodes for the lysosomal enzyme -galactosidase A. He was treated with recombinant enzyme but the clinical course was complicated by arrhythmias and the patient required an internal cardioverter defibrillator. Even though AFD is rare, this case illustrates the importance of considering the diagnosis in selected patients as effective treatment has recently become available. Recognition of AFD also allows for screening of asymptomatic relatives who may benefit from treatment before irreversible life-threatening complications develop.</abstract><relatedItem type="host"><titleInfo><title>BMJ Case Reports</title></titleInfo><titleInfo type="abbreviated"><title>BMJ Case Reports</title></titleInfo><genre type="journal">journal</genre><identifier type="eISSN">1757-790X</identifier><identifier type="PublisherID">bmjcasereports</identifier><identifier type="PublisherID-hwp">casereports</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>2010</number></detail></part></relatedItem><identifier type="istex">BF5C03598A2BDE3F4A528527018650927E0DAA1D</identifier><identifier type="DOI">10.1136/bcr.02.2010.2760</identifier><identifier type="href">casereports-2010-bcr-02-2010-2760.pdf</identifier><identifier type="ArticleID">bcr.02.2010.2760</identifier><identifier type="local">casereports;2010/aug23_1/bcr0220102760</identifier><accessCondition type="use and reproduction" contentType="copyright">2010 BMJ Publishing Group Ltd</accessCondition><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><annexes><json:item><extension>jpeg</extension><original>true</original><mimetype>image/jpeg</mimetype><uri>https://api.istex.fr/document/BF5C03598A2BDE3F4A528527018650927E0DAA1D/annexes/jpeg</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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