Exacerbation of latent lupus: is the culprit acid-fast bacilli or antitubercular therapy?
Identifieur interne : 000E66 ( Istex/Corpus ); précédent : 000E65; suivant : 000E67Exacerbation of latent lupus: is the culprit acid-fast bacilli or antitubercular therapy?
Auteurs : Harpreet Singh ; Sucharita Ray ; Maneet Kaur ; Vikas Gupta ; Harish Kumar ; Paulomi Talapatra ; Rekha Mathur ; Suvrat Arya ; Naveen GhangasSource :
- Clinical Rheumatology [ 0770-3198 ] ; 2013-08-01.
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Abstract
Abstract: Typical as well as atypical presentations of systemic lupus erythematosus are being increasingly recognized due to improved diagnostic methods. In a tuberculosis-endemic country like India, it was traditionally believed that the occurrence of tuberculosis in lupus was due to the chronic immunosuppression caused by lupus or because of the use of steroids or isoniazid-induced lupus. Increasingly several patients with no recorded predisposition to lupus with a history of treatment for tuberculosis are coming with evidence of systemic lupus erythematosus rather than a drug-limited story. Whether the development of an autoimmune state is a mere conjecture or the presence of acid-fast bacilli in the body for a prolonged duration causes complex antigenic interactions leading to an antigenic response needs to be looked into. We present a report of three such patients and review the pathogenetic interactions that could possibly explain the role of mycobacterial antigens as a putative antigen in the pathogenesis of lupus.
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DOI: 10.1007/s10067-013-2250-2
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In a tuberculosis-endemic country like India, it was traditionally believed that the occurrence of tuberculosis in lupus was due to the chronic immunosuppression caused by lupus or because of the use of steroids or isoniazid-induced lupus. Increasingly several patients with no recorded predisposition to lupus with a history of treatment for tuberculosis are coming with evidence of systemic lupus erythematosus rather than a drug-limited story. Whether the development of an autoimmune state is a mere conjecture or the presence of acid-fast bacilli in the body for a prolonged duration causes complex antigenic interactions leading to an antigenic response needs to be looked into. We present a report of three such patients and review the pathogenetic interactions that could possibly explain the role of mycobacterial antigens as a putative antigen in the pathogenesis of lupus.</div></front></TEI><istex><corpusName>springer-journals</corpusName><author><json:item><name>Harpreet Singh</name><affiliations><json:string>Department of Medicine, Pt. B. 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In a tuberculosis-endemic country like India, it was traditionally believed that the occurrence of tuberculosis in lupus was due to the chronic immunosuppression caused by lupus or because of the use of steroids or isoniazid-induced lupus. Increasingly several patients with no recorded predisposition to lupus with a history of treatment for tuberculosis are coming with evidence of systemic lupus erythematosus rather than a drug-limited story. Whether the development of an autoimmune state is a mere conjecture or the presence of acid-fast bacilli in the body for a prolonged duration causes complex antigenic interactions leading to an antigenic response needs to be looked into. We present a report of three such patients and review the pathogenetic interactions that could possibly explain the role of mycobacterial antigens as a putative antigen in the pathogenesis of lupus.</abstract><qualityIndicators><score>6.247</score><pdfWordCount>2399</pdfWordCount><pdfCharCount>15295</pdfCharCount><pdfVersion>1.4</pdfVersion><pdfPageCount>4</pdfPageCount><pdfPageSize>595.276 x 790.866 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractWordCount>154</abstractWordCount><abstractCharCount>1037</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Exacerbation of latent lupus: is the culprit acid-fast bacilli or antitubercular therapy?</title><genre><json:string>review-article</json:string></genre><host><title>Clinical Rheumatology</title><language><json:string>unknown</json:string></language><publicationDate>2013</publicationDate><copyrightDate>2013</copyrightDate><issn><json:string>0770-3198</json:string></issn><eissn><json:string>1434-9949</json:string></eissn><journalId><json:string>10067</json:string></journalId><volume>32</volume><issue>8</issue><pages><first>1233</first><last>1236</last></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Medicine</value></json:item><json:item><value>Medicine & Public Health</value></json:item><json:item><value>Rheumatology</value></json:item></subject></host><ark><json:string>ark:/67375/VQC-P9X3LDR9-G</json:string></ark><publicationDate>2013</publicationDate><copyrightDate>2013</copyrightDate><doi><json:string>10.1007/s10067-013-2250-2</json:string></doi><id>A64025910424F1A5B5EBD465975A5FF3392FF7A7</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-P9X3LDR9-G/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-P9X3LDR9-G/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/VQC-P9X3LDR9-G/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Exacerbation of latent lupus: is the culprit acid-fast bacilli or antitubercular therapy?</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">Springer London</publisher><pubPlace>London</pubPlace><availability><licence><p>Clinical Rheumatology, 2013</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</p></availability><date>2013-01-24</date></publicationStmt><notesStmt><note type="review-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note>Case Based Review</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Exacerbation of latent lupus: is the culprit acid-fast bacilli or antitubercular therapy?</title><author xml:id="author-0000"><persName><forename type="first">Harpreet</forename><surname>Singh</surname></persName><email>drhps1@rediffmail.com</email><affiliation>Department of Medicine, Pt. 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Review</ArticleCategory><ArticleFirstPage>1233</ArticleFirstPage><ArticleLastPage>1236</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2013</Year><Month>3</Month><Day>28</Day></RegistrationDate><Received><Year>2013</Year><Month>1</Month><Day>24</Day></Received><Revised><Year>2013</Year><Month>3</Month><Day>10</Day></Revised><Accepted><Year>2013</Year><Month>3</Month><Day>27</Day></Accepted><OnlineDate><Year>2013</Year><Month>4</Month><Day>10</Day></OnlineDate></ArticleHistory><ArticleCopyright><CopyrightHolderName>Clinical Rheumatology</CopyrightHolderName><CopyrightYear>2013</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Harpreet</GivenName><FamilyName>Singh</FamilyName></AuthorName><Contact><Email>drhps1@rediffmail.com</Email></Contact></Author><Author AffiliationIDS="Aff2" CorrespondingAffiliationID="Aff2"><AuthorName DisplayOrder="Western"><GivenName>Sucharita</GivenName><FamilyName>Ray</FamilyName></AuthorName><Contact><Email>dr.sucharitaray@gmail.com</Email></Contact></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>Maneet</GivenName><FamilyName>Kaur</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Vikas</GivenName><FamilyName>Gupta</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff4"><AuthorName DisplayOrder="Western"><GivenName>Harish</GivenName><FamilyName>Kumar</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff5"><AuthorName DisplayOrder="Western"><GivenName>Paulomi</GivenName><FamilyName>Talapatra</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Rekha</GivenName><FamilyName>Mathur</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Suvrat</GivenName><FamilyName>Arya</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Naveen</GivenName><FamilyName>Ghangas</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Department of Medicine</OrgDivision><OrgName>Pt. B. D Sharma PGIMS</OrgName><OrgAddress><City>Rohtak</City><State>Haryana</State><Country Code="IN">India</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Department of Neurology</OrgDivision><OrgName>Vardhman Mahavir Medical College and Safdarjung Hospital</OrgName><OrgAddress><City>New Delhi</City><Country Code="IN">India</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>Department of Medicine</OrgDivision><OrgName>Dayanand Medical College & Hospital</OrgName><OrgAddress><City>Ludhiana</City><State>Punjab</State><Country Code="IN">India</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Department of Pulmonary Medicine and Critical Care</OrgDivision><OrgName>Vardhman Mahavir Medical College and Safdarjung Hospital</OrgName><OrgAddress><City>New Delhi</City><Country Code="IN">India</Country></OrgAddress></Affiliation><Affiliation ID="Aff5"><OrgDivision>Department of Rheumatology</OrgDivision><OrgName>Pt. B. D. Sharma PGIMS</OrgName><OrgAddress><City>Rohtak</City><State>Haryana</State><Country Code="IN">India</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En" OutputMedium="All"><Heading>Abstract</Heading><Para>Typical as well as atypical presentations of systemic lupus erythematosus are being increasingly recognized due to improved diagnostic methods. In a tuberculosis-endemic country like India, it was traditionally believed that the occurrence of tuberculosis in lupus was due to the chronic immunosuppression caused by lupus or because of the use of steroids or isoniazid-induced lupus. Increasingly several patients with no recorded predisposition to lupus with a history of treatment for tuberculosis are coming with evidence of systemic lupus erythematosus rather than a drug-limited story. Whether the development of an autoimmune state is a mere conjecture or the presence of acid-fast bacilli in the body for a prolonged duration causes complex antigenic interactions leading to an antigenic response needs to be looked into. We present a report of three such patients and review the pathogenetic interactions that could possibly explain the role of mycobacterial antigens as a putative antigen in the pathogenesis of lupus.</Para></Abstract><KeywordGroup Language="En" OutputMedium="All"><Heading>Keywords</Heading><Keyword>Epitope spreading</Keyword><Keyword>Latent lupus</Keyword><Keyword>Lupus</Keyword><Keyword>Pathogenesis</Keyword><Keyword>Tuberculosis</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Exacerbation of latent lupus: is the culprit acid-fast bacilli or antitubercular therapy?</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Exacerbation of latent lupus: is the culprit acid-fast bacilli or antitubercular therapy?</title></titleInfo><name type="personal"><namePart type="given">Harpreet</namePart><namePart type="family">Singh</namePart><affiliation>Department of Medicine, Pt. B. D Sharma PGIMS, Rohtak, Haryana, India</affiliation><affiliation>E-mail: drhps1@rediffmail.com</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Sucharita</namePart><namePart type="family">Ray</namePart><affiliation>Department of Neurology, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India</affiliation><affiliation>E-mail: dr.sucharitaray@gmail.com</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Maneet</namePart><namePart type="family">Kaur</namePart><affiliation>Department of Medicine, Dayanand Medical College & Hospital, Ludhiana, Punjab, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Vikas</namePart><namePart type="family">Gupta</namePart><affiliation>Department of Medicine, Pt. B. D Sharma PGIMS, Rohtak, Haryana, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Harish</namePart><namePart type="family">Kumar</namePart><affiliation>Department of Pulmonary Medicine and Critical Care, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paulomi</namePart><namePart type="family">Talapatra</namePart><affiliation>Department of Rheumatology, Pt. B. D. Sharma PGIMS, Rohtak, Haryana, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rekha</namePart><namePart type="family">Mathur</namePart><affiliation>Department of Medicine, Pt. B. D Sharma PGIMS, Rohtak, Haryana, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Suvrat</namePart><namePart type="family">Arya</namePart><affiliation>Department of Medicine, Pt. B. D Sharma PGIMS, Rohtak, Haryana, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Naveen</namePart><namePart type="family">Ghangas</namePart><affiliation>Department of Medicine, Pt. B. D Sharma PGIMS, Rohtak, Haryana, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="ReviewPaper" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</genre><originInfo><publisher>Springer London</publisher><place><placeTerm type="text">London</placeTerm></place><dateCreated encoding="w3cdtf">2013-01-24</dateCreated><dateIssued encoding="w3cdtf">2013-08-01</dateIssued><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: Typical as well as atypical presentations of systemic lupus erythematosus are being increasingly recognized due to improved diagnostic methods. In a tuberculosis-endemic country like India, it was traditionally believed that the occurrence of tuberculosis in lupus was due to the chronic immunosuppression caused by lupus or because of the use of steroids or isoniazid-induced lupus. Increasingly several patients with no recorded predisposition to lupus with a history of treatment for tuberculosis are coming with evidence of systemic lupus erythematosus rather than a drug-limited story. Whether the development of an autoimmune state is a mere conjecture or the presence of acid-fast bacilli in the body for a prolonged duration causes complex antigenic interactions leading to an antigenic response needs to be looked into. We present a report of three such patients and review the pathogenetic interactions that could possibly explain the role of mycobacterial antigens as a putative antigen in the pathogenesis of lupus.</abstract><note>Case Based Review</note><subject lang="en"><genre>Keywords</genre><topic>Epitope spreading</topic><topic>Latent lupus</topic><topic>Lupus</topic><topic>Pathogenesis</topic><topic>Tuberculosis</topic></subject><relatedItem type="host"><titleInfo><title>Clinical Rheumatology</title><subTitle>Journal of the International League of Associations for Rheumatology</subTitle></titleInfo><titleInfo type="abbreviated"><title>Clin Rheumatol</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>Springer</publisher><dateIssued encoding="w3cdtf">2013-07-27</dateIssued><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><subject><genre>Journal-Subject-Collection</genre><topic authority="SpringerSubjectCodes" authorityURI="SC11">Medicine</topic></subject><subject><genre>Journal-Subject-Group</genre><topic authority="SpringerSubjectCodes" authorityURI="SCH">Medicine & Public Health</topic><topic authority="SpringerSubjectCodes" authorityURI="SCH57009">Rheumatology</topic></subject><identifier type="ISSN">0770-3198</identifier><identifier type="eISSN">1434-9949</identifier><identifier type="JournalID">10067</identifier><identifier type="IssueArticleCount">21</identifier><identifier type="VolumeIssueCount">12</identifier><part><date>2013</date><detail type="volume"><number>32</number><caption>vol.</caption></detail><detail type="issue"><number>8</number><caption>no.</caption></detail><extent unit="pages"><start>1233</start><end>1236</end></extent></part><recordInfo><recordOrigin>Clinical Rheumatology, 2013</recordOrigin></recordInfo></relatedItem><identifier type="istex">A64025910424F1A5B5EBD465975A5FF3392FF7A7</identifier><identifier type="ark">ark:/67375/VQC-P9X3LDR9-G</identifier><identifier type="DOI">10.1007/s10067-013-2250-2</identifier><identifier type="ArticleID">2250</identifier><identifier type="ArticleID">s10067-013-2250-2</identifier><accessCondition type="use and reproduction" contentType="copyright">Clinical Rheumatology, 2013</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Clinical Rheumatology, 2013</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-P9X3LDR9-G/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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