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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

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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

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DOI: 10.1136/annrheumdis-2012-eular.1906

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<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>
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<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>
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<author>
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<author>
<persName>
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<author>
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<surname>Pødenphant</surname>
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<affiliation>Gentofte Hospital, Gentofte, Denmark</affiliation>
</author>
<author>
<persName>
<forename type="first">K.</forename>
<surname>Stengaard-Pedersen</surname>
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<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>
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<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>
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<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>
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<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>
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