Autoantibodies’ titre modulation by anti-BlyS treatment in systemic lupus erythematosus
Objective The objective of this study was to analyse autoantibodies’ titres modulation during belimumab treatment in 50 patients with systemic lupus erythematosus (SLE). Methods Sera were collected at belimumab start (T0) and every six months until the 24th month. Disease activity index (SLEDAI-2K)...
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| Veröffentlicht in: | Lupus 2019-08, Vol.28 (9), p.1074-1081 |
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| creator | Cavazzana, I Kumar, R Pozzari, C Ottaviani, R Fredi, M Piantoni, S Andreoli, L Tincani, A Franceschini, F |
| description | Objective
The objective of this study was to analyse autoantibodies’ titres modulation during belimumab treatment in 50 patients with systemic lupus erythematosus (SLE).
Methods
Sera were collected at belimumab start (T0) and every six months until the 24th month. Disease activity index (SLEDAI-2K) was analysed at every timepoint. High avidity anti-dsDNA was detected by radioimmunological method, anti-ENA, anti-cardiolipin antibodies (aCL), anti-β2 glycoprotein I (anti-β2GPI) were analysed by ELISA.
Results
Fifty patients with SLE (mean SLEDAI-2K: 7.18 ± :3), mean age of 39 ± 11 years and mean follow-up of 13 ± 7.8 years were enrolled. A significant decrease of anti-dsDNA and anti-β2GPI IgM titres was observed at all timepoints. IgG aCL titre showed significant decrease only at T18. Anti-dsDNA negativization was detected in 21%, anti-β2GPI IgG in 33% and aCL IgG in 30% of sera, mostly at T6. Anti-ribosomal showed a significant titre decrease at T6 and T12, with negative seroconversion at T18. Anti-Sm titre significantly dropped down at T6, then remained stable during the time. Significant correlations were found between anti-dsDNA and anti-ribosomal titre and between SLEDAI ratio (SLEDAI value/SLEDAI T0) and anti-ribosomal titre ratio (value/value T0).
Conclusions
Belimumab treatment induced a significant reduction of SLE-specific autoantibodies titre and IgM anti-β2GPI. Anti-ribosomal titre decrease correlates with anti-dsDNA titre and disease activity improvement. |
| doi_str_mv | 10.1177/0961203319860191 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2257702982</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1177_0961203319860191</sage_id><sourcerecordid>2257702982</sourcerecordid><originalsourceid>FETCH-LOGICAL-c365t-1168b98173924f113e814da757be9bfb3a2e9e3b68b98c2b3e7e236c1cf8bf83</originalsourceid><addsrcrecordid>eNp10MtKxDAUBuAgio6XvSsJuHFTzUmmTbPUwRsILpyNq5J0TrXSNmOTLLrzNXw9n8TUGRUEV4H83zkJPyGHwE4BpDxjKgPOhACVZwwUbJAJTKVM4j3fJJMxTsZ8h-w698IYizLbJjsCeIymbEIez4O3uvO1sYsa3cfbO_W175G2dhEa7WvbUTPQUSQXzfBAY6Z9i52ndUfd4Dy2dUmbsAyOYj_4Z2y1ty64fbJV6cbhwfrcI_Ory_nsJrm7v76dnd8lpchSnwBkuVE5SKH4tAIQmMN0oWUqDSpTGaE5KhTmS5XcCJTIRVZCWeWmysUeOVmtXfb2NaDzRVu7EptGd2iDKzhPpWRc5TzS4z_0xYa-i5-LKstZmqZqVGylyt4612NVLPu61f1QACvG1ou_rceRo_XiYFpc_Ax81xxBsgJOP-Hvq_8u_ASYEIrZ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2268055592</pqid></control><display><type>article</type><title>Autoantibodies’ titre modulation by anti-BlyS treatment in systemic lupus erythematosus</title><source>Access via SAGE</source><source>MEDLINE</source><creator>Cavazzana, I ; Kumar, R ; Pozzari, C ; Ottaviani, R ; Fredi, M ; Piantoni, S ; Andreoli, L ; Tincani, A ; Franceschini, F</creator><creatorcontrib>Cavazzana, I ; Kumar, R ; Pozzari, C ; Ottaviani, R ; Fredi, M ; Piantoni, S ; Andreoli, L ; Tincani, A ; Franceschini, F</creatorcontrib><description>Objective
The objective of this study was to analyse autoantibodies’ titres modulation during belimumab treatment in 50 patients with systemic lupus erythematosus (SLE).
Methods
Sera were collected at belimumab start (T0) and every six months until the 24th month. Disease activity index (SLEDAI-2K) was analysed at every timepoint. High avidity anti-dsDNA was detected by radioimmunological method, anti-ENA, anti-cardiolipin antibodies (aCL), anti-β2 glycoprotein I (anti-β2GPI) were analysed by ELISA.
Results
Fifty patients with SLE (mean SLEDAI-2K: 7.18 ± :3), mean age of 39 ± 11 years and mean follow-up of 13 ± 7.8 years were enrolled. A significant decrease of anti-dsDNA and anti-β2GPI IgM titres was observed at all timepoints. IgG aCL titre showed significant decrease only at T18. Anti-dsDNA negativization was detected in 21%, anti-β2GPI IgG in 33% and aCL IgG in 30% of sera, mostly at T6. Anti-ribosomal showed a significant titre decrease at T6 and T12, with negative seroconversion at T18. Anti-Sm titre significantly dropped down at T6, then remained stable during the time. Significant correlations were found between anti-dsDNA and anti-ribosomal titre and between SLEDAI ratio (SLEDAI value/SLEDAI T0) and anti-ribosomal titre ratio (value/value T0).
Conclusions
Belimumab treatment induced a significant reduction of SLE-specific autoantibodies titre and IgM anti-β2GPI. Anti-ribosomal titre decrease correlates with anti-dsDNA titre and disease activity improvement.</description><identifier>ISSN: 0961-2033</identifier><identifier>EISSN: 1477-0962</identifier><identifier>DOI: 10.1177/0961203319860191</identifier><identifier>PMID: 31296140</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Adult ; Anti-DNA antibodies ; Antibodies, Anticardiolipin - immunology ; Antibodies, Antinuclear - immunology ; Antibodies, Monoclonal, Humanized - administration & dosage ; Antibodies, Monoclonal, Humanized - pharmacology ; Autoantibodies ; Autoantibodies - immunology ; Avidity ; B-Cell Activating Factor - immunology ; beta 2-Glycoprotein I - immunology ; BLyS protein ; Cardiolipin ; Enzyme-linked immunosorbent assay ; Follow-Up Studies ; Glycoprotein I ; Humans ; Immunoglobulin G ; Immunoglobulin G - immunology ; Immunoglobulin M ; Immunosuppressive Agents - administration & dosage ; Immunosuppressive Agents - pharmacology ; Lupus ; Lupus Erythematosus, Systemic - drug therapy ; Lupus Erythematosus, Systemic - immunology ; Lupus Erythematosus, Systemic - physiopathology ; Middle Aged ; Retrospective Studies ; Seroconversion ; Severity of Illness Index ; Systemic lupus erythematosus</subject><ispartof>Lupus, 2019-08, Vol.28 (9), p.1074-1081</ispartof><rights>The Author(s) 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c365t-1168b98173924f113e814da757be9bfb3a2e9e3b68b98c2b3e7e236c1cf8bf83</citedby><cites>FETCH-LOGICAL-c365t-1168b98173924f113e814da757be9bfb3a2e9e3b68b98c2b3e7e236c1cf8bf83</cites><orcidid>0000-0002-9107-3218 ; 0000-0002-2757-7120</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/0961203319860191$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/0961203319860191$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,780,784,21819,27924,27925,43621,43622</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31296140$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cavazzana, I</creatorcontrib><creatorcontrib>Kumar, R</creatorcontrib><creatorcontrib>Pozzari, C</creatorcontrib><creatorcontrib>Ottaviani, R</creatorcontrib><creatorcontrib>Fredi, M</creatorcontrib><creatorcontrib>Piantoni, S</creatorcontrib><creatorcontrib>Andreoli, L</creatorcontrib><creatorcontrib>Tincani, A</creatorcontrib><creatorcontrib>Franceschini, F</creatorcontrib><title>Autoantibodies’ titre modulation by anti-BlyS treatment in systemic lupus erythematosus</title><title>Lupus</title><addtitle>Lupus</addtitle><description>Objective
The objective of this study was to analyse autoantibodies’ titres modulation during belimumab treatment in 50 patients with systemic lupus erythematosus (SLE).
Methods
Sera were collected at belimumab start (T0) and every six months until the 24th month. Disease activity index (SLEDAI-2K) was analysed at every timepoint. High avidity anti-dsDNA was detected by radioimmunological method, anti-ENA, anti-cardiolipin antibodies (aCL), anti-β2 glycoprotein I (anti-β2GPI) were analysed by ELISA.
Results
Fifty patients with SLE (mean SLEDAI-2K: 7.18 ± :3), mean age of 39 ± 11 years and mean follow-up of 13 ± 7.8 years were enrolled. A significant decrease of anti-dsDNA and anti-β2GPI IgM titres was observed at all timepoints. IgG aCL titre showed significant decrease only at T18. Anti-dsDNA negativization was detected in 21%, anti-β2GPI IgG in 33% and aCL IgG in 30% of sera, mostly at T6. Anti-ribosomal showed a significant titre decrease at T6 and T12, with negative seroconversion at T18. Anti-Sm titre significantly dropped down at T6, then remained stable during the time. Significant correlations were found between anti-dsDNA and anti-ribosomal titre and between SLEDAI ratio (SLEDAI value/SLEDAI T0) and anti-ribosomal titre ratio (value/value T0).
Conclusions
Belimumab treatment induced a significant reduction of SLE-specific autoantibodies titre and IgM anti-β2GPI. Anti-ribosomal titre decrease correlates with anti-dsDNA titre and disease activity improvement.</description><subject>Adult</subject><subject>Anti-DNA antibodies</subject><subject>Antibodies, Anticardiolipin - immunology</subject><subject>Antibodies, Antinuclear - immunology</subject><subject>Antibodies, Monoclonal, Humanized - administration & dosage</subject><subject>Antibodies, Monoclonal, Humanized - pharmacology</subject><subject>Autoantibodies</subject><subject>Autoantibodies - immunology</subject><subject>Avidity</subject><subject>B-Cell Activating Factor - immunology</subject><subject>beta 2-Glycoprotein I - immunology</subject><subject>BLyS protein</subject><subject>Cardiolipin</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Follow-Up Studies</subject><subject>Glycoprotein I</subject><subject>Humans</subject><subject>Immunoglobulin G</subject><subject>Immunoglobulin G - immunology</subject><subject>Immunoglobulin M</subject><subject>Immunosuppressive Agents - administration & dosage</subject><subject>Immunosuppressive Agents - pharmacology</subject><subject>Lupus</subject><subject>Lupus Erythematosus, Systemic - drug therapy</subject><subject>Lupus Erythematosus, Systemic - immunology</subject><subject>Lupus Erythematosus, Systemic - physiopathology</subject><subject>Middle Aged</subject><subject>Retrospective Studies</subject><subject>Seroconversion</subject><subject>Severity of Illness Index</subject><subject>Systemic lupus erythematosus</subject><issn>0961-2033</issn><issn>1477-0962</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10MtKxDAUBuAgio6XvSsJuHFTzUmmTbPUwRsILpyNq5J0TrXSNmOTLLrzNXw9n8TUGRUEV4H83zkJPyGHwE4BpDxjKgPOhACVZwwUbJAJTKVM4j3fJJMxTsZ8h-w698IYizLbJjsCeIymbEIez4O3uvO1sYsa3cfbO_W175G2dhEa7WvbUTPQUSQXzfBAY6Z9i52ndUfd4Dy2dUmbsAyOYj_4Z2y1ty64fbJV6cbhwfrcI_Ory_nsJrm7v76dnd8lpchSnwBkuVE5SKH4tAIQmMN0oWUqDSpTGaE5KhTmS5XcCJTIRVZCWeWmysUeOVmtXfb2NaDzRVu7EptGd2iDKzhPpWRc5TzS4z_0xYa-i5-LKstZmqZqVGylyt4612NVLPu61f1QACvG1ou_rceRo_XiYFpc_Ax81xxBsgJOP-Hvq_8u_ASYEIrZ</recordid><startdate>201908</startdate><enddate>201908</enddate><creator>Cavazzana, I</creator><creator>Kumar, R</creator><creator>Pozzari, C</creator><creator>Ottaviani, R</creator><creator>Fredi, M</creator><creator>Piantoni, S</creator><creator>Andreoli, L</creator><creator>Tincani, A</creator><creator>Franceschini, F</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9107-3218</orcidid><orcidid>https://orcid.org/0000-0002-2757-7120</orcidid></search><sort><creationdate>201908</creationdate><title>Autoantibodies’ titre modulation by anti-BlyS treatment in systemic lupus erythematosus</title><author>Cavazzana, I ; Kumar, R ; Pozzari, C ; Ottaviani, R ; Fredi, M ; Piantoni, S ; Andreoli, L ; Tincani, A ; Franceschini, F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c365t-1168b98173924f113e814da757be9bfb3a2e9e3b68b98c2b3e7e236c1cf8bf83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adult</topic><topic>Anti-DNA antibodies</topic><topic>Antibodies, Anticardiolipin - immunology</topic><topic>Antibodies, Antinuclear - immunology</topic><topic>Antibodies, Monoclonal, Humanized - administration & dosage</topic><topic>Antibodies, Monoclonal, Humanized - pharmacology</topic><topic>Autoantibodies</topic><topic>Autoantibodies - immunology</topic><topic>Avidity</topic><topic>B-Cell Activating Factor - immunology</topic><topic>beta 2-Glycoprotein I - immunology</topic><topic>BLyS protein</topic><topic>Cardiolipin</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Follow-Up Studies</topic><topic>Glycoprotein I</topic><topic>Humans</topic><topic>Immunoglobulin G</topic><topic>Immunoglobulin G - immunology</topic><topic>Immunoglobulin M</topic><topic>Immunosuppressive Agents - administration & dosage</topic><topic>Immunosuppressive Agents - pharmacology</topic><topic>Lupus</topic><topic>Lupus Erythematosus, Systemic - drug therapy</topic><topic>Lupus Erythematosus, Systemic - immunology</topic><topic>Lupus Erythematosus, Systemic - physiopathology</topic><topic>Middle Aged</topic><topic>Retrospective Studies</topic><topic>Seroconversion</topic><topic>Severity of Illness Index</topic><topic>Systemic lupus erythematosus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cavazzana, I</creatorcontrib><creatorcontrib>Kumar, R</creatorcontrib><creatorcontrib>Pozzari, C</creatorcontrib><creatorcontrib>Ottaviani, R</creatorcontrib><creatorcontrib>Fredi, M</creatorcontrib><creatorcontrib>Piantoni, S</creatorcontrib><creatorcontrib>Andreoli, L</creatorcontrib><creatorcontrib>Tincani, A</creatorcontrib><creatorcontrib>Franceschini, F</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Lupus</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cavazzana, I</au><au>Kumar, R</au><au>Pozzari, C</au><au>Ottaviani, R</au><au>Fredi, M</au><au>Piantoni, S</au><au>Andreoli, L</au><au>Tincani, A</au><au>Franceschini, F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autoantibodies’ titre modulation by anti-BlyS treatment in systemic lupus erythematosus</atitle><jtitle>Lupus</jtitle><addtitle>Lupus</addtitle><date>2019-08</date><risdate>2019</risdate><volume>28</volume><issue>9</issue><spage>1074</spage><epage>1081</epage><pages>1074-1081</pages><issn>0961-2033</issn><eissn>1477-0962</eissn><abstract>Objective
The objective of this study was to analyse autoantibodies’ titres modulation during belimumab treatment in 50 patients with systemic lupus erythematosus (SLE).
Methods
Sera were collected at belimumab start (T0) and every six months until the 24th month. Disease activity index (SLEDAI-2K) was analysed at every timepoint. High avidity anti-dsDNA was detected by radioimmunological method, anti-ENA, anti-cardiolipin antibodies (aCL), anti-β2 glycoprotein I (anti-β2GPI) were analysed by ELISA.
Results
Fifty patients with SLE (mean SLEDAI-2K: 7.18 ± :3), mean age of 39 ± 11 years and mean follow-up of 13 ± 7.8 years were enrolled. A significant decrease of anti-dsDNA and anti-β2GPI IgM titres was observed at all timepoints. IgG aCL titre showed significant decrease only at T18. Anti-dsDNA negativization was detected in 21%, anti-β2GPI IgG in 33% and aCL IgG in 30% of sera, mostly at T6. Anti-ribosomal showed a significant titre decrease at T6 and T12, with negative seroconversion at T18. Anti-Sm titre significantly dropped down at T6, then remained stable during the time. Significant correlations were found between anti-dsDNA and anti-ribosomal titre and between SLEDAI ratio (SLEDAI value/SLEDAI T0) and anti-ribosomal titre ratio (value/value T0).
Conclusions
Belimumab treatment induced a significant reduction of SLE-specific autoantibodies titre and IgM anti-β2GPI. Anti-ribosomal titre decrease correlates with anti-dsDNA titre and disease activity improvement.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>31296140</pmid><doi>10.1177/0961203319860191</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-9107-3218</orcidid><orcidid>https://orcid.org/0000-0002-2757-7120</orcidid></addata></record> |
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| ispartof | Lupus, 2019-08, Vol.28 (9), p.1074-1081 |
| issn | 0961-2033 1477-0962 |
| language | eng |
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| source | Access via SAGE; MEDLINE |
| subjects | Adult Anti-DNA antibodies Antibodies, Anticardiolipin - immunology Antibodies, Antinuclear - immunology Antibodies, Monoclonal, Humanized - administration & dosage Antibodies, Monoclonal, Humanized - pharmacology Autoantibodies Autoantibodies - immunology Avidity B-Cell Activating Factor - immunology beta 2-Glycoprotein I - immunology BLyS protein Cardiolipin Enzyme-linked immunosorbent assay Follow-Up Studies Glycoprotein I Humans Immunoglobulin G Immunoglobulin G - immunology Immunoglobulin M Immunosuppressive Agents - administration & dosage Immunosuppressive Agents - pharmacology Lupus Lupus Erythematosus, Systemic - drug therapy Lupus Erythematosus, Systemic - immunology Lupus Erythematosus, Systemic - physiopathology Middle Aged Retrospective Studies Seroconversion Severity of Illness Index Systemic lupus erythematosus |
| title | Autoantibodies’ titre modulation by anti-BlyS treatment in systemic lupus erythematosus |
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