Serveur d'exploration sur l'opéra

Attention, ce site est en cours de développement !
Attention, site généré par des moyens informatiques à partir de corpus bruts.
Les informations ne sont donc pas validées.

OP0223 M-ficolin, an activator of the complement system, predicts DAS28 remission in early DMARD naïve rheumatoid arthritis

Identifieur interne : 000905 ( Istex/Corpus ); précédent : 000904; suivant : 000906

OP0223 M-ficolin, an activator of the complement system, predicts DAS28 remission in early DMARD naïve rheumatoid arthritis

Auteurs : C. G. Ammitzb Ll ; J. C. Jensenius ; T. Ellingsen ; S. Thiel ; K. H Rslev-Petersen ; M. Hetland ; P. Junker ; J. Johansen ; M. Stergaard ; J. P Denphant ; K. Stengaard-Pedersen

Source :

RBID : ISTEX:3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B

Abstract

Background M-ficolin is a soluble pattern recognition molecule that activates the complement system. We recently reported a factor 300 difference in the synovial fluid M-ficolin concentration between rheumatoid arthritis (RA) and osteoarthritis, suggesting a pathogenic role of M-ficolin1. Objectives To assess M-ficolin in DMARD naïve early RA patients, investigate correlations between M-ficolin and disease activity markers, and analyze the predictive value of M-ficolin. Methods 180 DMARD naïve RA patients with disease duration <6 months were included in a randomized double blind placebo-controlled trial (OPERA) of methotrexate, intraarticular glucucorticoids + either adalimumab (ADA) or placebo (PLA). A sandwich-type time-resolved immunofluorometric assay using monoclonal antibodies was used for quantification of M-ficolin in the OPERA cohort, 101 healthy adults and 51 chronic RA patients in remission. Concentrations are reported as medians. Spearman test, Students T-test and one-way analysis of variance were used. Logistic regression analyses were performed and adjusted for CRP, treatment group (ADA/PLA), x-ray erosions, anti-CCP, IgM-RF, neutrophils and monocytes. Results The highest M-ficolin levels were measured in the OPERA cohort at baseline (2.84μg/l, CI 2.63-3.09), and during treatment the level decreased 24% (CI 18-31%, p<0.001) at year one (2.31μg/l, CI 2.14-2.50). The healthy adults had significantly lower concentrations (1.88μg/l, CI 1.72-2.06) than the OPERA cohort at baseline (p<0.001) and year one (p<0.001), and the chronic RA patients (2.17μg/l, CI 1.94-2.42) (p=0.03). At baseline M-ficolin correlated to DAS28 (rho=0.29, p<0.001) and the four variables constituting DAS28 (0.001< p≤0.04). At year one M-ficolin correlated to DAS28 (rho=0.36, p<0.001) and 3 of the 4 variables constituting DAS28 (0.001< p≤0.05), except tender joint count 28 (p=0.23). Furthermore M-ficolin correlated to HAQ at debut (rho=0.25, p=0.003) and year one (rho=0.23, p<0.001). Logistic regression analysis determined M-ficolin as the strongest predictor of DAS28<2.6 at year one (coefficient=1.42, p=0.0001) followed by treatment group (PLA/ADA) (coefficient=1.23, p=0.001) and erosions on baseline x-ray (coefficient=-1.19, p=0.02), but M-ficolin was the only variable that predicted DAS28<3.2 at year one (coefficient=0.89, p=0.02). Low baseline M-ficolin level was the only variable associated with low disease activity at year one, and this was further analyzed by comparing the group with the 25% lowest baseline M-ficolin levels with the remaining 75% of patients (cutoff 2.00 μg/l). This resulted in a sensitivity of 29%, a specificity of 96%, and a positive predictive value of 98% in determining a DAS28 score <3.2 at year one. Conclusions The elevated baseline M-ficolin levels in early RA correlated consistently to disease activity markers, most notably DAS28 and HAQ, thus reflecting essential parts of the disease activity. Low M-ficolin levels at baseline predicts a positive predictive value of 98% of a DAS28<3.2 after one year irrespective of treatment and well-known prognostic factors. References Ammitzbøll CG, et al. Rheumatol Int 2011. Disclosure of Interest None Declared

Url:
DOI: 10.1136/annrheumdis-2012-eular.1906

Links to Exploration step

ISTEX:3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B

Le document en format XML

<record>
<TEI wicri:istexFullTextTei="biblStruct">
<teiHeader>
<fileDesc>
<titleStmt>
<title xml:lang="en">OP0223 M-ficolin, an activator of the complement system, predicts DAS28 remission in early DMARD naïve rheumatoid arthritis</title>
<author>
<name sortKey="Ammitzb Ll, C G" sort="Ammitzb Ll, C G" uniqKey="Ammitzb Ll C" first="C. G." last="Ammitzb Ll">C. G. Ammitzb Ll</name>
<affiliation>
<mods:affiliation>Aarhus University Hospital</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Jensenius, J C" sort="Jensenius, J C" uniqKey="Jensenius J" first="J. C." last="Jensenius">J. C. Jensenius</name>
<affiliation>
<mods:affiliation>Aarhus University, Aarhus</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Ellingsen, T" sort="Ellingsen, T" uniqKey="Ellingsen T" first="T." last="Ellingsen">T. Ellingsen</name>
<affiliation>
<mods:affiliation>Silkeborg Regional Hospital, Silkeborg</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Thiel, S" sort="Thiel, S" uniqKey="Thiel S" first="S." last="Thiel">S. Thiel</name>
<affiliation>
<mods:affiliation>Aarhus University, Aarhus</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="H Rslev Petersen, K" sort="H Rslev Petersen, K" uniqKey="H Rslev Petersen K" first="K." last="H Rslev-Petersen">K. H Rslev-Petersen</name>
<affiliation>
<mods:affiliation>King Christian X’s Rheumatism Hospital, Gråsten</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Hetland, M" sort="Hetland, M" uniqKey="Hetland M" first="M." last="Hetland">M. Hetland</name>
<affiliation>
<mods:affiliation>Glostrup Hospital, Glostrup</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Junker, P" sort="Junker, P" uniqKey="Junker P" first="P." last="Junker">P. Junker</name>
<affiliation>
<mods:affiliation>Odense University Hospital, Odense</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Johansen, J" sort="Johansen, J" uniqKey="Johansen J" first="J." last="Johansen">J. Johansen</name>
<affiliation>
<mods:affiliation>Glostrup Hospital, Glostrup</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey=" Stergaard, M" sort=" Stergaard, M" uniqKey=" Stergaard M" first="M." last=" Stergaard">M. Stergaard</name>
<affiliation>
<mods:affiliation>Glostrup Hospital, Glostrup</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="P Denphant, J" sort="P Denphant, J" uniqKey="P Denphant J" first="J." last="P Denphant">J. P Denphant</name>
<affiliation>
<mods:affiliation>Gentofte Hospital, Gentofte, Denmark</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Stengaard Pedersen, K" sort="Stengaard Pedersen, K" uniqKey="Stengaard Pedersen K" first="K." last="Stengaard-Pedersen">K. Stengaard-Pedersen</name>
<affiliation>
<mods:affiliation>Aarhus University Hospital</mods:affiliation>
</affiliation>
</author>
</titleStmt>
<publicationStmt>
<idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B</idno>
<date when="2013" year="2013">2013</date>
<idno type="doi">10.1136/annrheumdis-2012-eular.1906</idno>
<idno type="url">https://api.istex.fr/document/3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B/fulltext/pdf</idno>
<idno type="wicri:Area/Istex/Corpus">000905</idno>
</publicationStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title level="a" type="main" xml:lang="en">OP0223 M-ficolin, an activator of the complement system, predicts DAS28 remission in early DMARD naïve rheumatoid arthritis</title>
<author>
<name sortKey="Ammitzb Ll, C G" sort="Ammitzb Ll, C G" uniqKey="Ammitzb Ll C" first="C. G." last="Ammitzb Ll">C. G. Ammitzb Ll</name>
<affiliation>
<mods:affiliation>Aarhus University Hospital</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Jensenius, J C" sort="Jensenius, J C" uniqKey="Jensenius J" first="J. C." last="Jensenius">J. C. Jensenius</name>
<affiliation>
<mods:affiliation>Aarhus University, Aarhus</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Ellingsen, T" sort="Ellingsen, T" uniqKey="Ellingsen T" first="T." last="Ellingsen">T. Ellingsen</name>
<affiliation>
<mods:affiliation>Silkeborg Regional Hospital, Silkeborg</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Thiel, S" sort="Thiel, S" uniqKey="Thiel S" first="S." last="Thiel">S. Thiel</name>
<affiliation>
<mods:affiliation>Aarhus University, Aarhus</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="H Rslev Petersen, K" sort="H Rslev Petersen, K" uniqKey="H Rslev Petersen K" first="K." last="H Rslev-Petersen">K. H Rslev-Petersen</name>
<affiliation>
<mods:affiliation>King Christian X’s Rheumatism Hospital, Gråsten</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Hetland, M" sort="Hetland, M" uniqKey="Hetland M" first="M." last="Hetland">M. Hetland</name>
<affiliation>
<mods:affiliation>Glostrup Hospital, Glostrup</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Junker, P" sort="Junker, P" uniqKey="Junker P" first="P." last="Junker">P. Junker</name>
<affiliation>
<mods:affiliation>Odense University Hospital, Odense</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Johansen, J" sort="Johansen, J" uniqKey="Johansen J" first="J." last="Johansen">J. Johansen</name>
<affiliation>
<mods:affiliation>Glostrup Hospital, Glostrup</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey=" Stergaard, M" sort=" Stergaard, M" uniqKey=" Stergaard M" first="M." last=" Stergaard">M. Stergaard</name>
<affiliation>
<mods:affiliation>Glostrup Hospital, Glostrup</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="P Denphant, J" sort="P Denphant, J" uniqKey="P Denphant J" first="J." last="P Denphant">J. P Denphant</name>
<affiliation>
<mods:affiliation>Gentofte Hospital, Gentofte, Denmark</mods:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Stengaard Pedersen, K" sort="Stengaard Pedersen, K" uniqKey="Stengaard Pedersen K" first="K." last="Stengaard-Pedersen">K. Stengaard-Pedersen</name>
<affiliation>
<mods:affiliation>Aarhus University Hospital</mods:affiliation>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series>
<title level="j">Annals of the Rheumatic Diseases</title>
<title level="j" type="abbrev">Ann Rheum Dis</title>
<idno type="ISSN">0003-4967</idno>
<idno type="eISSN">1468-2060</idno>
<imprint>
<publisher>BMJ Publishing Group Ltd and European League Against Rheumatism</publisher>
<date type="published" when="2013-06">2013-06</date>
<biblScope unit="volume">71</biblScope>
<biblScope unit="issue">Suppl 3</biblScope>
<biblScope unit="page" from="131">131</biblScope>
</imprint>
<idno type="ISSN">0003-4967</idno>
</series>
<idno type="istex">3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B</idno>
<idno type="DOI">10.1136/annrheumdis-2012-eular.1906</idno>
<idno type="href">annrheumdis-71-131-1.pdf</idno>
<idno type="ArticleID">annrheumdis-2012-eular.1906</idno>
</biblStruct>
</sourceDesc>
<seriesStmt>
<idno type="ISSN">0003-4967</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass></textClass>
<langUsage>
<language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front>
<div type="abstract">Background M-ficolin is a soluble pattern recognition molecule that activates the complement system. We recently reported a factor 300 difference in the synovial fluid M-ficolin concentration between rheumatoid arthritis (RA) and osteoarthritis, suggesting a pathogenic role of M-ficolin1. Objectives To assess M-ficolin in DMARD naïve early RA patients, investigate correlations between M-ficolin and disease activity markers, and analyze the predictive value of M-ficolin. Methods 180 DMARD naïve RA patients with disease duration <6 months were included in a randomized double blind placebo-controlled trial (OPERA) of methotrexate, intraarticular glucucorticoids + either adalimumab (ADA) or placebo (PLA). A sandwich-type time-resolved immunofluorometric assay using monoclonal antibodies was used for quantification of M-ficolin in the OPERA cohort, 101 healthy adults and 51 chronic RA patients in remission. Concentrations are reported as medians. Spearman test, Students T-test and one-way analysis of variance were used. Logistic regression analyses were performed and adjusted for CRP, treatment group (ADA/PLA), x-ray erosions, anti-CCP, IgM-RF, neutrophils and monocytes. Results The highest M-ficolin levels were measured in the OPERA cohort at baseline (2.84μg/l, CI 2.63-3.09), and during treatment the level decreased 24% (CI 18-31%, p<0.001) at year one (2.31μg/l, CI 2.14-2.50). The healthy adults had significantly lower concentrations (1.88μg/l, CI 1.72-2.06) than the OPERA cohort at baseline (p<0.001) and year one (p<0.001), and the chronic RA patients (2.17μg/l, CI 1.94-2.42) (p=0.03). At baseline M-ficolin correlated to DAS28 (rho=0.29, p<0.001) and the four variables constituting DAS28 (0.001< p≤0.04). At year one M-ficolin correlated to DAS28 (rho=0.36, p<0.001) and 3 of the 4 variables constituting DAS28 (0.001< p≤0.05), except tender joint count 28 (p=0.23). Furthermore M-ficolin correlated to HAQ at debut (rho=0.25, p=0.003) and year one (rho=0.23, p<0.001). Logistic regression analysis determined M-ficolin as the strongest predictor of DAS28<2.6 at year one (coefficient=1.42, p=0.0001) followed by treatment group (PLA/ADA) (coefficient=1.23, p=0.001) and erosions on baseline x-ray (coefficient=-1.19, p=0.02), but M-ficolin was the only variable that predicted DAS28<3.2 at year one (coefficient=0.89, p=0.02). Low baseline M-ficolin level was the only variable associated with low disease activity at year one, and this was further analyzed by comparing the group with the 25% lowest baseline M-ficolin levels with the remaining 75% of patients (cutoff 2.00 μg/l). This resulted in a sensitivity of 29%, a specificity of 96%, and a positive predictive value of 98% in determining a DAS28 score <3.2 at year one. Conclusions The elevated baseline M-ficolin levels in early RA correlated consistently to disease activity markers, most notably DAS28 and HAQ, thus reflecting essential parts of the disease activity. Low M-ficolin levels at baseline predicts a positive predictive value of 98% of a DAS28<3.2 after one year irrespective of treatment and well-known prognostic factors. References Ammitzbøll CG, et al. Rheumatol Int 2011. Disclosure of Interest None Declared</div>
</front>
</TEI>
<istex>
<corpusName>bmj</corpusName>
<author>
<json:item>
<name>C.G. Ammitzbøll</name>
<affiliations>
<json:string>Aarhus University Hospital</json:string>
</affiliations>
</json:item>
<json:item>
<name>J.C. Jensenius</name>
<affiliations>
<json:string>Aarhus University, Aarhus</json:string>
</affiliations>
</json:item>
<json:item>
<name>T. Ellingsen</name>
<affiliations>
<json:string>Silkeborg Regional Hospital, Silkeborg</json:string>
</affiliations>
</json:item>
<json:item>
<name>S. Thiel</name>
<affiliations>
<json:string>Aarhus University, Aarhus</json:string>
</affiliations>
</json:item>
<json:item>
<name>K. Hørslev-Petersen</name>
<affiliations>
<json:string>King Christian X’s Rheumatism Hospital, Gråsten</json:string>
</affiliations>
</json:item>
<json:item>
<name>M. Hetland</name>
<affiliations>
<json:string>Glostrup Hospital, Glostrup</json:string>
</affiliations>
</json:item>
<json:item>
<name>P. Junker</name>
<affiliations>
<json:string>Odense University Hospital, Odense</json:string>
</affiliations>
</json:item>
<json:item>
<name>J. Johansen</name>
<affiliations>
<json:string>Glostrup Hospital, Glostrup</json:string>
</affiliations>
</json:item>
<json:item>
<name>M. Østergaard</name>
<affiliations>
<json:string>Glostrup Hospital, Glostrup</json:string>
</affiliations>
</json:item>
<json:item>
<name>J. Pødenphant</name>
<affiliations>
<json:string>Gentofte Hospital, Gentofte, Denmark</json:string>
</affiliations>
</json:item>
<json:item>
<name>K. Stengaard-Pedersen</name>
<affiliations>
<json:string>Aarhus University Hospital</json:string>
</affiliations>
</json:item>
</author>
<subject>
<json:item>
<lang>
<json:string>eng</json:string>
</lang>
<value>Scientific Abstracts</value>
</json:item>
</subject>
<language>
<json:string>eng</json:string>
</language>
<abstract>Background M-ficolin is a soluble pattern recognition molecule that activates the complement system. We recently reported a factor 300 difference in the synovial fluid M-ficolin concentration between rheumatoid arthritis (RA) and osteoarthritis, suggesting a pathogenic role of M-ficolin1. Objectives To assess M-ficolin in DMARD naïve early RA patients, investigate correlations between M-ficolin and disease activity markers, and analyze the predictive value of M-ficolin. Methods 180 DMARD naïve RA patients with disease duration >6 months were included in a randomized double blind placebo-controlled trial (OPERA) of methotrexate, intraarticular glucucorticoids + either adalimumab (ADA) or placebo (PLA). A sandwich-type time-resolved immunofluorometric assay using monoclonal antibodies was used for quantification of M-ficolin in the OPERA cohort, 101 healthy adults and 51 chronic RA patients in remission. Concentrations are reported as medians. Spearman test, Students T-test and one-way analysis of variance were used. Logistic regression analyses were performed and adjusted for CRP, treatment group (ADA/PLA), x-ray erosions, anti-CCP, IgM-RF, neutrophils and monocytes. Results The highest M-ficolin levels were measured in the OPERA cohort at baseline (2.84μg/l, CI 2.63-3.09), and during treatment the level decreased 24% (CI 18-31%, p>0.001) at year one (2.31μg/l, CI 2.14-2.50). The healthy adults had significantly lower concentrations (1.88μg/l, CI 1.72-2.06) than the OPERA cohort at baseline (p>0.001) and year one (p>0.001), and the chronic RA patients (2.17μg/l, CI 1.94-2.42) (p=0.03). At baseline M-ficolin correlated to DAS28 (rho=0.29, p>0.001) and the four variables constituting DAS28 (0.001> p≤0.04). At year one M-ficolin correlated to DAS28 (rho=0.36, p>0.001) and 3 of the 4 variables constituting DAS28 (0.001> p≤0.05), except tender joint count 28 (p=0.23). Furthermore M-ficolin correlated to HAQ at debut (rho=0.25, p=0.003) and year one (rho=0.23, p>0.001). Logistic regression analysis determined M-ficolin as the strongest predictor of DAS28>2.6 at year one (coefficient=1.42, p=0.0001) followed by treatment group (PLA/ADA) (coefficient=1.23, p=0.001) and erosions on baseline x-ray (coefficient=-1.19, p=0.02), but M-ficolin was the only variable that predicted DAS28>3.2 at year one (coefficient=0.89, p=0.02). Low baseline M-ficolin level was the only variable associated with low disease activity at year one, and this was further analyzed by comparing the group with the 25% lowest baseline M-ficolin levels with the remaining 75% of patients (cutoff 2.00 μg/l). This resulted in a sensitivity of 29%, a specificity of 96%, and a positive predictive value of 98% in determining a DAS28 score >3.2 at year one. Conclusions The elevated baseline M-ficolin levels in early RA correlated consistently to disease activity markers, most notably DAS28 and HAQ, thus reflecting essential parts of the disease activity. Low M-ficolin levels at baseline predicts a positive predictive value of 98% of a DAS28>3.2 after one year irrespective of treatment and well-known prognostic factors. References Ammitzbøll CG, et al. Rheumatol Int 2011. Disclosure of Interest None Declared</abstract>
<qualityIndicators>
<score>4.865</score>
<pdfVersion>1.4</pdfVersion>
<pdfPageSize>595 x 842 pts (A4)</pdfPageSize>
<refBibsNative>false</refBibsNative>
<keywordCount>1</keywordCount>
<abstractCharCount>3216</abstractCharCount>
<pdfWordCount>1365</pdfWordCount>
<pdfCharCount>8645</pdfCharCount>
<pdfPageCount>1</pdfPageCount>
<abstractWordCount>453</abstractWordCount>
</qualityIndicators>
<title>OP0223 M-ficolin, an activator of the complement system, predicts DAS28 remission in early DMARD naïve rheumatoid arthritis</title>
<genre>
<json:string>abstract</json:string>
</genre>
<host>
<volume>71</volume>
<pages>
<first>131</first>
</pages>
<issn>
<json:string>0003-4967</json:string>
</issn>
<issue>Suppl 3</issue>
<genre></genre>
<language>
<json:string>unknown</json:string>
</language>
<eissn>
<json:string>1468-2060</json:string>
</eissn>
<title>Annals of the Rheumatic Diseases</title>
</host>
<publicationDate>2013</publicationDate>
<copyrightDate>2013</copyrightDate>
<doi>
<json:string>10.1136/annrheumdis-2012-eular.1906</json:string>
</doi>
<id>3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B</id>
<fulltext>
<json:item>
<original>true</original>
<mimetype>application/pdf</mimetype>
<extension>pdf</extension>
<uri>https://api.istex.fr/document/3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B/fulltext/pdf</uri>
</json:item>
<json:item>
<original>false</original>
<mimetype>application/zip</mimetype>
<extension>zip</extension>
<uri>https://api.istex.fr/document/3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B/fulltext/zip</uri>
</json:item>
<istex:fulltextTEI uri="https://api.istex.fr/document/3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B/fulltext/tei">
<teiHeader>
<fileDesc>
<titleStmt>
<title level="a" type="main" xml:lang="en">OP0223 M-ficolin, an activator of the complement system, predicts DAS28 remission in early DMARD naïve rheumatoid arthritis</title>
<respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt>
<respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt>
</titleStmt>
<publicationStmt>
<authority>ISTEX</authority>
<publisher>BMJ Publishing Group Ltd and European League Against Rheumatism</publisher>
<availability>
<p>BMJ</p>
</availability>
<date>2013</date>
</publicationStmt>
<sourceDesc>
<biblStruct type="inbook">
<analytic>
<title level="a" type="main" xml:lang="en">OP0223 M-ficolin, an activator of the complement system, predicts DAS28 remission in early DMARD naïve rheumatoid arthritis</title>
<author>
<persName>
<forename type="first">C.G.</forename>
<surname>Ammitzbøll</surname>
</persName>
<affiliation>Aarhus University Hospital</affiliation>
</author>
<author>
<persName>
<forename type="first">J.C.</forename>
<surname>Jensenius</surname>
</persName>
<affiliation>Aarhus University, Aarhus</affiliation>
</author>
<author>
<persName>
<forename type="first">T.</forename>
<surname>Ellingsen</surname>
</persName>
<affiliation>Silkeborg Regional Hospital, Silkeborg</affiliation>
</author>
<author>
<persName>
<forename type="first">S.</forename>
<surname>Thiel</surname>
</persName>
<affiliation>Aarhus University, Aarhus</affiliation>
</author>
<author>
<persName>
<forename type="first">K.</forename>
<surname>Hørslev-Petersen</surname>
</persName>
<affiliation>King Christian X’s Rheumatism Hospital, Gråsten</affiliation>
</author>
<author>
<persName>
<forename type="first">M.</forename>
<surname>Hetland</surname>
</persName>
<affiliation>Glostrup Hospital, Glostrup</affiliation>
</author>
<author>
<persName>
<forename type="first">P.</forename>
<surname>Junker</surname>
</persName>
<affiliation>Odense University Hospital, Odense</affiliation>
</author>
<author>
<persName>
<forename type="first">J.</forename>
<surname>Johansen</surname>
</persName>
<affiliation>Glostrup Hospital, Glostrup</affiliation>
</author>
<author>
<persName>
<forename type="first">M.</forename>
<surname>Østergaard</surname>
</persName>
<affiliation>Glostrup Hospital, Glostrup</affiliation>
</author>
<author>
<persName>
<forename type="first">J.</forename>
<surname>Pødenphant</surname>
</persName>
<affiliation>Gentofte Hospital, Gentofte, Denmark</affiliation>
</author>
<author>
<persName>
<forename type="first">K.</forename>
<surname>Stengaard-Pedersen</surname>
</persName>
<affiliation>Aarhus University Hospital</affiliation>
</author>
</analytic>
<monogr>
<title level="j">Annals of the Rheumatic Diseases</title>
<title level="j" type="abbrev">Ann Rheum Dis</title>
<idno type="JournalID">ard</idno>
<idno type="pISSN">0003-4967</idno>
<idno type="eISSN">1468-2060</idno>
<imprint>
<publisher>BMJ Publishing Group Ltd and European League Against Rheumatism</publisher>
<date type="published" when="2013-06"></date>
<biblScope unit="volume">71</biblScope>
<biblScope unit="issue">Suppl 3</biblScope>
<biblScope unit="page" from="131">131</biblScope>
</imprint>
</monogr>
<idno type="istex">3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B</idno>
<idno type="DOI">10.1136/annrheumdis-2012-eular.1906</idno>
<idno type="href">annrheumdis-71-131-1.pdf</idno>
<idno type="ArticleID">annrheumdis-2012-eular.1906</idno>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc>
<creation>
<date>2013</date>
</creation>
<langUsage>
<language ident="en">en</language>
</langUsage>
<abstract>
<p>Background M-ficolin is a soluble pattern recognition molecule that activates the complement system. We recently reported a factor 300 difference in the synovial fluid M-ficolin concentration between rheumatoid arthritis (RA) and osteoarthritis, suggesting a pathogenic role of M-ficolin1. Objectives To assess M-ficolin in DMARD naïve early RA patients, investigate correlations between M-ficolin and disease activity markers, and analyze the predictive value of M-ficolin. Methods 180 DMARD naïve RA patients with disease duration <6 months were included in a randomized double blind placebo-controlled trial (OPERA) of methotrexate, intraarticular glucucorticoids + either adalimumab (ADA) or placebo (PLA). A sandwich-type time-resolved immunofluorometric assay using monoclonal antibodies was used for quantification of M-ficolin in the OPERA cohort, 101 healthy adults and 51 chronic RA patients in remission. Concentrations are reported as medians. Spearman test, Students T-test and one-way analysis of variance were used. Logistic regression analyses were performed and adjusted for CRP, treatment group (ADA/PLA), x-ray erosions, anti-CCP, IgM-RF, neutrophils and monocytes. Results The highest M-ficolin levels were measured in the OPERA cohort at baseline (2.84μg/l, CI 2.63-3.09), and during treatment the level decreased 24% (CI 18-31%, p<0.001) at year one (2.31μg/l, CI 2.14-2.50). The healthy adults had significantly lower concentrations (1.88μg/l, CI 1.72-2.06) than the OPERA cohort at baseline (p<0.001) and year one (p<0.001), and the chronic RA patients (2.17μg/l, CI 1.94-2.42) (p=0.03). At baseline M-ficolin correlated to DAS28 (rho=0.29, p<0.001) and the four variables constituting DAS28 (0.001< p≤0.04). At year one M-ficolin correlated to DAS28 (rho=0.36, p<0.001) and 3 of the 4 variables constituting DAS28 (0.001< p≤0.05), except tender joint count 28 (p=0.23). Furthermore M-ficolin correlated to HAQ at debut (rho=0.25, p=0.003) and year one (rho=0.23, p<0.001). Logistic regression analysis determined M-ficolin as the strongest predictor of DAS28<2.6 at year one (coefficient=1.42, p=0.0001) followed by treatment group (PLA/ADA) (coefficient=1.23, p=0.001) and erosions on baseline x-ray (coefficient=-1.19, p=0.02), but M-ficolin was the only variable that predicted DAS28<3.2 at year one (coefficient=0.89, p=0.02). Low baseline M-ficolin level was the only variable associated with low disease activity at year one, and this was further analyzed by comparing the group with the 25% lowest baseline M-ficolin levels with the remaining 75% of patients (cutoff 2.00 μg/l). This resulted in a sensitivity of 29%, a specificity of 96%, and a positive predictive value of 98% in determining a DAS28 score <3.2 at year one. Conclusions The elevated baseline M-ficolin levels in early RA correlated consistently to disease activity markers, most notably DAS28 and HAQ, thus reflecting essential parts of the disease activity. Low M-ficolin levels at baseline predicts a positive predictive value of 98% of a DAS28<3.2 after one year irrespective of treatment and well-known prognostic factors. References Ammitzbøll CG, et al. Rheumatol Int 2011. Disclosure of Interest None Declared</p>
</abstract>
<textClass>
<keywords scheme="keyword">
<list>
<head>heading</head>
<item>
<term>Scientific Abstracts</term>
</item>
</list>
</keywords>
</textClass>
</profileDesc>
<revisionDesc>
<change when="2013-06">Published</change>
<change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-0-25">References added</change>
<change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-1-2">References added</change>
</revisionDesc>
</teiHeader>
</istex:fulltextTEI>
<json:item>
<original>false</original>
<mimetype>text/plain</mimetype>
<extension>txt</extension>
<uri>https://api.istex.fr/document/3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B/fulltext/txt</uri>
</json:item>
</fulltext>
<metadata>
<istex:metadataXml wicri:clean="corpus bmj" wicri:toSee="no header">
<istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="no"</istex:xmlDeclaration>
<istex:docType PUBLIC="-//NLM//DTD Journal Archiving and Interchange DTD v2.3 20070202//EN" URI="archivearticle.dtd" name="istex:docType"></istex:docType>
<istex:document>
<article article-type="abstract" xml:lang="EN">
<front>
<journal-meta>
<journal-id journal-id-type="hwp">annrheumdis</journal-id>
<journal-id journal-id-type="nlm-ta">Ann Rheum Dis</journal-id>
<journal-id journal-id-type="publisher-id">ard</journal-id>
<journal-title>Annals of the Rheumatic Diseases</journal-title>
<abbrev-journal-title abbrev-type="publisher">Ann Rheum Dis</abbrev-journal-title>
<abbrev-journal-title>Ann Rheum Dis</abbrev-journal-title>
<issn pub-type="ppub">0003-4967</issn>
<issn pub-type="epub">1468-2060</issn>
<publisher>
<publisher-name>BMJ Publishing Group Ltd and European League Against Rheumatism</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="publisher-id">annrheumdis-2012-eular.1906</article-id>
<article-id pub-id-type="doi">10.1136/annrheumdis-2012-eular.1906</article-id>
<article-id pub-id-type="other">annrheumdis;71/Suppl_3/131-a</article-id>
<article-id pub-id-type="other">annrheumdis;annrheumdis-2012-eular.1906</article-id>
<article-id pub-id-type="other">131.1</article-id>
<article-id pub-id-type="other">annrheumdis-2012-eular.1906</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Scientific Abstracts</subject>
<subj-group>
<subject>Oral Presentations</subject>
<subj-group>
<subject>Abstract Session: Innate and adaptive immunity</subject>
</subj-group>
</subj-group>
</subj-group>
</article-categories>
<title-group>
<article-title>OP0223 M-ficolin, an activator of the complement system, predicts DAS28 remission in early DMARD naïve rheumatoid arthritis</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Ammitzbøll</surname>
<given-names>C.G.</given-names>
</name>
<xref ref-type="aff" rid="AFF_1">
<sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Jensenius</surname>
<given-names>J.C.</given-names>
</name>
<xref ref-type="aff" rid="AFF_2">
<sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Ellingsen</surname>
<given-names>T.</given-names>
</name>
<xref ref-type="aff" rid="AFF_3">
<sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Thiel</surname>
<given-names>S.</given-names>
</name>
<xref ref-type="aff" rid="AFF_2">
<sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Hørslev-Petersen</surname>
<given-names>K.</given-names>
</name>
<xref ref-type="aff" rid="AFF_4">
<sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Hetland</surname>
<given-names>M.</given-names>
</name>
<xref ref-type="aff" rid="AFF_5">
<sup>5</sup>
</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Junker</surname>
<given-names>P.</given-names>
</name>
<xref ref-type="aff" rid="AFF_6">
<sup>6</sup>
</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Johansen</surname>
<given-names>J.</given-names>
</name>
<xref ref-type="aff" rid="AFF_5">
<sup>5</sup>
</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Østergaard</surname>
<given-names>M.</given-names>
</name>
<xref ref-type="aff" rid="AFF_5">
<sup>5</sup>
</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Pødenphant</surname>
<given-names>J.</given-names>
</name>
<xref ref-type="aff" rid="AFF_7">
<sup>7</sup>
</xref>
</contrib>
<contrib contrib-type="author" xlink:type="simple">
<name name-style="western">
<surname>Stengaard-Pedersen</surname>
<given-names>K.</given-names>
</name>
<xref ref-type="aff" rid="AFF_1">
<sup>1</sup>
</xref>
</contrib>
<on-behalf-of>and the OPERA Study Group </on-behalf-of>
</contrib-group>
<aff id="AFF_1">
<sup>1</sup>
Aarhus University Hospital</aff>
<aff id="AFF_2">
<sup>2</sup>
Aarhus University, Aarhus</aff>
<aff id="AFF_3">
<sup>3</sup>
Silkeborg Regional Hospital, Silkeborg</aff>
<aff id="AFF_4">
<sup>4</sup>
King Christian X’s Rheumatism Hospital, Gråsten</aff>
<aff id="AFF_5">
<sup>5</sup>
Glostrup Hospital, Glostrup</aff>
<aff id="AFF_6">
<sup>6</sup>
Odense University Hospital, Odense</aff>
<aff id="AFF_7">
<sup>7</sup>
Gentofte Hospital, Gentofte, Denmark</aff>
<pub-date pub-type="ppub">
<month>6</month>
<year>2013</year>
</pub-date>
<volume>71</volume>
<volume-id pub-id-type="other">71</volume-id>
<volume-id pub-id-type="other">71</volume-id>
<issue>Suppl 3</issue>
<issue-id pub-id-type="other">annrheumdis;71/Suppl_3</issue-id>
<issue-id pub-id-type="other" content-type="supplement">Suppl_3</issue-id>
<issue-id pub-id-type="other">71/Suppl_3</issue-id>
<issue-title>Annual European Congress of Rheumatology EULAR abstracts 2012, 6 – 9 June 2012, Berlin, Germany</issue-title>
<fpage seq="1">131</fpage>
<permissions>
<copyright-statement>© 2013, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</copyright-statement>
<copyright-year>2013</copyright-year>
</permissions>
<self-uri content-type="pdf" xlink:role="full-text" xlink:href="annrheumdis-71-131-1.pdf"></self-uri>
<abstract>
<sec>
<title>Background</title>
<p>M-ficolin is a soluble pattern recognition molecule that activates the complement system. We recently reported a factor 300 difference in the synovial fluid M-ficolin concentration between rheumatoid arthritis (RA) and osteoarthritis, suggesting a pathogenic role of M-ficolin
<sup>1</sup>
.</p>
</sec>
<sec>
<title>Objectives</title>
<p>To assess M-ficolin in DMARD naïve early RA patients, investigate correlations between M-ficolin and disease activity markers, and analyze the predictive value of M-ficolin.</p>
</sec>
<sec>
<title>Methods</title>
<p>180 DMARD naïve RA patients with disease duration <6 months were included in a randomized double blind placebo-controlled trial (OPERA) of methotrexate, intraarticular glucucorticoids + either adalimumab (ADA) or placebo (PLA). A sandwich-type time-resolved immunofluorometric assay using monoclonal antibodies was used for quantification of M-ficolin in the OPERA cohort, 101 healthy adults and 51 chronic RA patients in remission. Concentrations are reported as medians. Spearman test, Students T-test and one-way analysis of variance were used. Logistic regression analyses were performed and adjusted for CRP, treatment group (ADA/PLA), x-ray erosions, anti-CCP, IgM-RF, neutrophils and monocytes.</p>
</sec>
<sec>
<title>Results</title>
<p>The highest M-ficolin levels were measured in the OPERA cohort at baseline (2.84μg/l, CI 2.63-3.09), and during treatment the level decreased 24% (CI 18-31%, p<0.001) at year one (2.31μg/l, CI 2.14-2.50). The healthy adults had significantly lower concentrations (1.88μg/l, CI 1.72-2.06) than the OPERA cohort at baseline (p<0.001) and year one (p<0.001), and the chronic RA patients (2.17μg/l, CI 1.94-2.42) (p=0.03).</p>
<p>At baseline M-ficolin correlated to DAS28 (rho=0.29, p<0.001) and the four variables constituting DAS28 (0.001< p≤0.04). At year one M-ficolin correlated to DAS28 (rho=0.36, p<0.001) and 3 of the 4 variables constituting DAS28 (0.001< p≤0.05), except tender joint count 28 (p=0.23). Furthermore M-ficolin correlated to HAQ at debut (rho=0.25, p=0.003) and year one (rho=0.23, p<0.001).</p>
<p>Logistic regression analysis determined M-ficolin as the strongest predictor of DAS28<2.6 at year one (coefficient=1.42, p=0.0001) followed by treatment group (PLA/ADA) (coefficient=1.23, p=0.001) and erosions on baseline x-ray (coefficient=-1.19, p=0.02), but M-ficolin was the only variable that predicted DAS28<3.2 at year one (coefficient=0.89, p=0.02).</p>
<p>Low baseline M-ficolin level was the only variable associated with low disease activity at year one, and this was further analyzed by comparing the group with the 25% lowest baseline M-ficolin levels with the remaining 75% of patients (cutoff 2.00 μg/l). This resulted in a sensitivity of 29%, a specificity of 96%, and a positive predictive value of 98% in determining a DAS28 score <3.2 at year one.</p>
</sec>
<sec>
<title>Conclusions</title>
<p>The elevated baseline M-ficolin levels in early RA correlated consistently to disease activity markers, most notably DAS28 and HAQ, thus reflecting essential parts of the disease activity. Low M-ficolin levels at baseline predicts a positive predictive value of 98% of a DAS28<3.2 after one year irrespective of treatment and well-known prognostic factors.</p>
</sec>
<sec>
<title>References</title>
<p>
<list list-type="order">
<list-item>
<p>Ammitzbøll CG, et al. Rheumatol Int 2011.</p>
</list-item>
</list>
</p>
</sec>
<sec>
<title>Disclosure of Interest</title>
<p>None Declared</p>
</sec>
</abstract>
</article-meta>
</front>
</article>
</istex:document>
</istex:metadataXml>
<mods version="3.6">
<titleInfo lang="en">
<title>OP0223 M-ficolin, an activator of the complement system, predicts DAS28 remission in early DMARD naïve rheumatoid arthritis</title>
</titleInfo>
<titleInfo type="alternative" lang="en" contentType="CDATA">
<title>OP0223 M-ficolin, an activator of the complement system, predicts DAS28 remission in early DMARD naïve rheumatoid arthritis</title>
</titleInfo>
<name type="personal">
<namePart type="given">C.G.</namePart>
<namePart type="family">Ammitzbøll</namePart>
<affiliation>Aarhus University Hospital</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">J.C.</namePart>
<namePart type="family">Jensenius</namePart>
<affiliation>Aarhus University, Aarhus</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">T.</namePart>
<namePart type="family">Ellingsen</namePart>
<affiliation>Silkeborg Regional Hospital, Silkeborg</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">S.</namePart>
<namePart type="family">Thiel</namePart>
<affiliation>Aarhus University, Aarhus</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">K.</namePart>
<namePart type="family">Hørslev-Petersen</namePart>
<affiliation>King Christian X’s Rheumatism Hospital, Gråsten</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">M.</namePart>
<namePart type="family">Hetland</namePart>
<affiliation>Glostrup Hospital, Glostrup</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">P.</namePart>
<namePart type="family">Junker</namePart>
<affiliation>Odense University Hospital, Odense</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">J.</namePart>
<namePart type="family">Johansen</namePart>
<affiliation>Glostrup Hospital, Glostrup</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">M.</namePart>
<namePart type="family">Østergaard</namePart>
<affiliation>Glostrup Hospital, Glostrup</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">J.</namePart>
<namePart type="family">Pødenphant</namePart>
<affiliation>Gentofte Hospital, Gentofte, Denmark</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">K.</namePart>
<namePart type="family">Stengaard-Pedersen</namePart>
<affiliation>Aarhus University Hospital</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<typeOfResource>text</typeOfResource>
<genre type="abstract">abstract</genre>
<subject>
<genre>heading</genre>
<topic>Scientific Abstracts</topic>
</subject>
<originInfo>
<publisher>BMJ Publishing Group Ltd and European League Against Rheumatism</publisher>
<dateIssued encoding="w3cdtf">2013-06</dateIssued>
<copyrightDate encoding="w3cdtf">2013</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>Background M-ficolin is a soluble pattern recognition molecule that activates the complement system. We recently reported a factor 300 difference in the synovial fluid M-ficolin concentration between rheumatoid arthritis (RA) and osteoarthritis, suggesting a pathogenic role of M-ficolin1. Objectives To assess M-ficolin in DMARD naïve early RA patients, investigate correlations between M-ficolin and disease activity markers, and analyze the predictive value of M-ficolin. Methods 180 DMARD naïve RA patients with disease duration <6 months were included in a randomized double blind placebo-controlled trial (OPERA) of methotrexate, intraarticular glucucorticoids + either adalimumab (ADA) or placebo (PLA). A sandwich-type time-resolved immunofluorometric assay using monoclonal antibodies was used for quantification of M-ficolin in the OPERA cohort, 101 healthy adults and 51 chronic RA patients in remission. Concentrations are reported as medians. Spearman test, Students T-test and one-way analysis of variance were used. Logistic regression analyses were performed and adjusted for CRP, treatment group (ADA/PLA), x-ray erosions, anti-CCP, IgM-RF, neutrophils and monocytes. Results The highest M-ficolin levels were measured in the OPERA cohort at baseline (2.84μg/l, CI 2.63-3.09), and during treatment the level decreased 24% (CI 18-31%, p<0.001) at year one (2.31μg/l, CI 2.14-2.50). The healthy adults had significantly lower concentrations (1.88μg/l, CI 1.72-2.06) than the OPERA cohort at baseline (p<0.001) and year one (p<0.001), and the chronic RA patients (2.17μg/l, CI 1.94-2.42) (p=0.03). At baseline M-ficolin correlated to DAS28 (rho=0.29, p<0.001) and the four variables constituting DAS28 (0.001< p≤0.04). At year one M-ficolin correlated to DAS28 (rho=0.36, p<0.001) and 3 of the 4 variables constituting DAS28 (0.001< p≤0.05), except tender joint count 28 (p=0.23). Furthermore M-ficolin correlated to HAQ at debut (rho=0.25, p=0.003) and year one (rho=0.23, p<0.001). Logistic regression analysis determined M-ficolin as the strongest predictor of DAS28<2.6 at year one (coefficient=1.42, p=0.0001) followed by treatment group (PLA/ADA) (coefficient=1.23, p=0.001) and erosions on baseline x-ray (coefficient=-1.19, p=0.02), but M-ficolin was the only variable that predicted DAS28<3.2 at year one (coefficient=0.89, p=0.02). Low baseline M-ficolin level was the only variable associated with low disease activity at year one, and this was further analyzed by comparing the group with the 25% lowest baseline M-ficolin levels with the remaining 75% of patients (cutoff 2.00 μg/l). This resulted in a sensitivity of 29%, a specificity of 96%, and a positive predictive value of 98% in determining a DAS28 score <3.2 at year one. Conclusions The elevated baseline M-ficolin levels in early RA correlated consistently to disease activity markers, most notably DAS28 and HAQ, thus reflecting essential parts of the disease activity. Low M-ficolin levels at baseline predicts a positive predictive value of 98% of a DAS28<3.2 after one year irrespective of treatment and well-known prognostic factors. References Ammitzbøll CG, et al. Rheumatol Int 2011. Disclosure of Interest None Declared</abstract>
<relatedItem type="host">
<titleInfo>
<title>Annals of the Rheumatic Diseases</title>
</titleInfo>
<titleInfo type="abbreviated">
<title>Ann Rheum Dis</title>
</titleInfo>
<identifier type="ISSN">0003-4967</identifier>
<identifier type="eISSN">1468-2060</identifier>
<identifier type="JournalID">ard</identifier>
<identifier type="JournalID-hwp">annrheumdis</identifier>
<identifier type="JournalID-nlm-ta">Ann Rheum Dis</identifier>
<part>
<date>2013</date>
<detail type="title">
<title>Annual European Congress of Rheumatology EULAR abstracts 2012, 6 – 9 June 2012, Berlin, Germany</title>
</detail>
<detail type="volume">
<caption>vol.</caption>
<number>71</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>Suppl 3</number>
</detail>
<extent unit="pages">
<start>131</start>
</extent>
</part>
</relatedItem>
<identifier type="istex">3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B</identifier>
<identifier type="DOI">10.1136/annrheumdis-2012-eular.1906</identifier>
<identifier type="href">annrheumdis-71-131-1.pdf</identifier>
<identifier type="ArticleID">annrheumdis-2012-eular.1906</identifier>
<accessCondition type="use and reproduction" contentType="Copyright">© 2013, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</accessCondition>
<recordInfo>
<recordContentSource>BMJ</recordContentSource>
</recordInfo>
</mods>
</metadata>
<serie></serie>
</istex>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Musique/explor/OperaV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000905 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 000905 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Musique
   |area=    OperaV1
   |flux=    Istex
   |étape=   Corpus
   |type=    RBID
   |clé=     ISTEX:3B9E2DAA9E3DC5A3AF9DA0F22453DE8EA715735B
   |texte=   OP0223 M-ficolin, an activator of the complement system, predicts DAS28 remission in early DMARD naïve rheumatoid arthritis
}}

Wicri

This area was generated with Dilib version V0.6.21.
Data generation: Thu Apr 14 14:59:05 2016. Site generation: Thu Oct 8 06:48:41 2020