A5.09 Mri-detected osteitis is not associated with the presence or level of ACPA alone, but with the combined presence of ACPA and RF
Background and objectivesIn patients with rheumatoid arthritis (RA) bone marrow oedema (BME) as observed by magnetic resonance imaging (MRI) represents osteitis with infiltration of leucocytes and an increased number of osteoclasts. Both BME and anti-citrullinated protein antibodies (ACPAs) are pred...
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Veröffentlicht in: | Annals of the rheumatic diseases 2016-02, Vol.75 (Suppl 1), p.A44-A45 |
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description | Background and objectivesIn patients with rheumatoid arthritis (RA) bone marrow oedema (BME) as observed by magnetic resonance imaging (MRI) represents osteitis with infiltration of leucocytes and an increased number of osteoclasts. Both BME and anti-citrullinated protein antibodies (ACPAs) are predictors of radiographic progression in RA and recent data indicate that ACPA can directly activate osteoclasts. These findings together lead to the hypothesis that ACPA is associated with BME; indeed, two small studies observed an association between BME and ACPA. Thus far the association of ACPA with other forms of MRI-detected inflammation (synovitis and tenosynovitis) has not been thoroughly explored. Furthermore, it is unknown if the association with MRI-detected inflammation is only present for ACPA or also for other RA-related auto-antibodies. This study addressed these questions.Materials and methodsA total of 589 early arthritis patients, included in the Leiden Early Arthritis Clinic cohort, underwent contrast-enhanced 1.5T MRI of the unilateral wrist, metacarpophalangeal and metatarsophalangeal joints at baseline. BME, synovitis and tenosynovitis were scored according to the RAMRIS-method. ACPA, rheumatoid factor (RF) and anti-carbamylated protein (antiCarP) antibodies were determined at baseline.ResultsBME, synovitis and tenosynovitis were concomitantly present on MRI. In univariable analyses, ACPA-positive patients had higher BME-scores than ACPA-negative patients (median scores 4.5 vs. 2.0, p < 0.001), but not more synovitis and tenosynovitis.Besides ACPA, also RF (median scores 3.75 vs 2.0, p < 0.001) and anti-CarP antibodies (median scores 3.5 vs 2.5, p = 0.012) were associated with higher BME-scores in univariable analyses. To explore the association of the different antibodies with BME the BME-scores of patients with different auto-antibody combinations were compared. ACPA+RF-antiCarP- patients did not have higher BME-scores than ACPA-RF-antiCarP- patients, however ACPA+RF+antiCarP- and ACPA+RF+antiCarP+ patients had higher BME-scores (median 5.0 and 4.5 vs. 2.0 respectively, p < 0.001 and p < 0.001). ACPA and RF levels were not associated with BME-scores.ConclusionsThe presence and the level of ACPA alone were not associated with BME-scores. However, the combined presence of ACPA and RF did associate with more BME. This suggests an additive role of RF to ACPA in mediating osteitis. |
doi_str_mv | 10.1136/annrheumdis-2016-209124.107 |
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Both BME and anti-citrullinated protein antibodies (ACPAs) are predictors of radiographic progression in RA and recent data indicate that ACPA can directly activate osteoclasts. These findings together lead to the hypothesis that ACPA is associated with BME; indeed, two small studies observed an association between BME and ACPA. Thus far the association of ACPA with other forms of MRI-detected inflammation (synovitis and tenosynovitis) has not been thoroughly explored. Furthermore, it is unknown if the association with MRI-detected inflammation is only present for ACPA or also for other RA-related auto-antibodies. This study addressed these questions.Materials and methodsA total of 589 early arthritis patients, included in the Leiden Early Arthritis Clinic cohort, underwent contrast-enhanced 1.5T MRI of the unilateral wrist, metacarpophalangeal and metatarsophalangeal joints at baseline. BME, synovitis and tenosynovitis were scored according to the RAMRIS-method. ACPA, rheumatoid factor (RF) and anti-carbamylated protein (antiCarP) antibodies were determined at baseline.ResultsBME, synovitis and tenosynovitis were concomitantly present on MRI. In univariable analyses, ACPA-positive patients had higher BME-scores than ACPA-negative patients (median scores 4.5 vs. 2.0, p < 0.001), but not more synovitis and tenosynovitis.Besides ACPA, also RF (median scores 3.75 vs 2.0, p < 0.001) and anti-CarP antibodies (median scores 3.5 vs 2.5, p = 0.012) were associated with higher BME-scores in univariable analyses. To explore the association of the different antibodies with BME the BME-scores of patients with different auto-antibody combinations were compared. ACPA+RF-antiCarP- patients did not have higher BME-scores than ACPA-RF-antiCarP- patients, however ACPA+RF+antiCarP- and ACPA+RF+antiCarP+ patients had higher BME-scores (median 5.0 and 4.5 vs. 2.0 respectively, p < 0.001 and p < 0.001). ACPA and RF levels were not associated with BME-scores.ConclusionsThe presence and the level of ACPA alone were not associated with BME-scores. However, the combined presence of ACPA and RF did associate with more BME. This suggests an additive role of RF to ACPA in mediating osteitis.</description><identifier>ISSN: 0003-4967</identifier><identifier>EISSN: 1468-2060</identifier><identifier>DOI: 10.1136/annrheumdis-2016-209124.107</identifier><identifier>CODEN: ARDIAO</identifier><language>eng</language><publisher>Kidlington: Elsevier Limited</publisher><ispartof>Annals of the rheumatic diseases, 2016-02, Vol.75 (Suppl 1), p.A44-A45</ispartof><rights>2016, 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</rights><rights>Copyright: 2016 (c) 2016, 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</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://ard.bmj.com/content/75/Suppl_1/A44.3.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://ard.bmj.com/content/75/Suppl_1/A44.3.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,776,780,3183,23550,27901,27902,77342,77373</link.rule.ids></links><search><creatorcontrib>Boeters, DM</creatorcontrib><creatorcontrib>Nieuwenhuis, WP</creatorcontrib><creatorcontrib>Verheul, MK</creatorcontrib><creatorcontrib>Newsum, EC</creatorcontrib><creatorcontrib>Toes, REM</creatorcontrib><creatorcontrib>Trouw, LA</creatorcontrib><creatorcontrib>van der Helm-van Mil, AHM</creatorcontrib><title>A5.09 Mri-detected osteitis is not associated with the presence or level of ACPA alone, but with the combined presence of ACPA and RF</title><title>Annals of the rheumatic diseases</title><description>Background and objectivesIn patients with rheumatoid arthritis (RA) bone marrow oedema (BME) as observed by magnetic resonance imaging (MRI) represents osteitis with infiltration of leucocytes and an increased number of osteoclasts. Both BME and anti-citrullinated protein antibodies (ACPAs) are predictors of radiographic progression in RA and recent data indicate that ACPA can directly activate osteoclasts. These findings together lead to the hypothesis that ACPA is associated with BME; indeed, two small studies observed an association between BME and ACPA. Thus far the association of ACPA with other forms of MRI-detected inflammation (synovitis and tenosynovitis) has not been thoroughly explored. Furthermore, it is unknown if the association with MRI-detected inflammation is only present for ACPA or also for other RA-related auto-antibodies. This study addressed these questions.Materials and methodsA total of 589 early arthritis patients, included in the Leiden Early Arthritis Clinic cohort, underwent contrast-enhanced 1.5T MRI of the unilateral wrist, metacarpophalangeal and metatarsophalangeal joints at baseline. BME, synovitis and tenosynovitis were scored according to the RAMRIS-method. ACPA, rheumatoid factor (RF) and anti-carbamylated protein (antiCarP) antibodies were determined at baseline.ResultsBME, synovitis and tenosynovitis were concomitantly present on MRI. In univariable analyses, ACPA-positive patients had higher BME-scores than ACPA-negative patients (median scores 4.5 vs. 2.0, p < 0.001), but not more synovitis and tenosynovitis.Besides ACPA, also RF (median scores 3.75 vs 2.0, p < 0.001) and anti-CarP antibodies (median scores 3.5 vs 2.5, p = 0.012) were associated with higher BME-scores in univariable analyses. To explore the association of the different antibodies with BME the BME-scores of patients with different auto-antibody combinations were compared. ACPA+RF-antiCarP- patients did not have higher BME-scores than ACPA-RF-antiCarP- patients, however ACPA+RF+antiCarP- and ACPA+RF+antiCarP+ patients had higher BME-scores (median 5.0 and 4.5 vs. 2.0 respectively, p < 0.001 and p < 0.001). ACPA and RF levels were not associated with BME-scores.ConclusionsThe presence and the level of ACPA alone were not associated with BME-scores. However, the combined presence of ACPA and RF did associate with more BME. This suggests an additive role of RF to ACPA in mediating osteitis.</description><issn>0003-4967</issn><issn>1468-2060</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNqVkE1LAzEQhoMoWKv_IdCrWyfd3WSDp1L8gooiel7yMUu3tJuapIo3L-L_9JeYUqVehTAhM-8zgYeQAYMhYzk_U13nZ7he2jZkI2A8FclGxZCB2CM9VvAqdTjskx4A5FkhuTgkRyHM0xMqVvXI57gcgvx6_7j1bWYxooloqQsR29gGmk7nIlUhONOqzei1jTMaZ0hXHgN2BqnzdIEvuKCuoePJ_ZiqhevwlOp13KWNW-q2S_wO-013lj5cHpODRi0CnvzcffJ0efE4uc6md1c3k_E002wkeFY0oLgWCKCEsVICNoW0Aktt8tzgyFq0DZRSlJXgIJTQhlstKuBKWakh75PBdu_Ku-c1hljP3dp36cuayWRQyrLkKXW-TRnvQvDY1CvfLpV_qxnUG_P1H_P1xny9NZ_mItF8S-vl_F_gNzlZjSM</recordid><startdate>201602</startdate><enddate>201602</enddate><creator>Boeters, DM</creator><creator>Nieuwenhuis, WP</creator><creator>Verheul, MK</creator><creator>Newsum, EC</creator><creator>Toes, REM</creator><creator>Trouw, LA</creator><creator>van der Helm-van Mil, AHM</creator><general>Elsevier Limited</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope></search><sort><creationdate>201602</creationdate><title>A5.09 Mri-detected osteitis is not associated with the presence or level of ACPA alone, but with the combined presence of ACPA and RF</title><author>Boeters, DM ; Nieuwenhuis, WP ; Verheul, MK ; Newsum, EC ; Toes, REM ; Trouw, LA ; van der Helm-van Mil, AHM</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b1276-4f0a6b7e00a7cd990ef49d7e5bc33ce2ddedf0597587607a7bc6db7806aad9b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Boeters, DM</creatorcontrib><creatorcontrib>Nieuwenhuis, WP</creatorcontrib><creatorcontrib>Verheul, MK</creatorcontrib><creatorcontrib>Newsum, EC</creatorcontrib><creatorcontrib>Toes, REM</creatorcontrib><creatorcontrib>Trouw, LA</creatorcontrib><creatorcontrib>van der Helm-van Mil, AHM</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest - Health & Medical Complete保健、医学与药学数据库</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest Biological Science Journals</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><jtitle>Annals of the rheumatic diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Boeters, DM</au><au>Nieuwenhuis, WP</au><au>Verheul, MK</au><au>Newsum, EC</au><au>Toes, REM</au><au>Trouw, LA</au><au>van der Helm-van Mil, AHM</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A5.09 Mri-detected osteitis is not associated with the presence or level of ACPA alone, but with the combined presence of ACPA and RF</atitle><jtitle>Annals of the rheumatic diseases</jtitle><date>2016-02</date><risdate>2016</risdate><volume>75</volume><issue>Suppl 1</issue><spage>A44</spage><epage>A45</epage><pages>A44-A45</pages><issn>0003-4967</issn><eissn>1468-2060</eissn><coden>ARDIAO</coden><abstract>Background and objectivesIn patients with rheumatoid arthritis (RA) bone marrow oedema (BME) as observed by magnetic resonance imaging (MRI) represents osteitis with infiltration of leucocytes and an increased number of osteoclasts. Both BME and anti-citrullinated protein antibodies (ACPAs) are predictors of radiographic progression in RA and recent data indicate that ACPA can directly activate osteoclasts. These findings together lead to the hypothesis that ACPA is associated with BME; indeed, two small studies observed an association between BME and ACPA. Thus far the association of ACPA with other forms of MRI-detected inflammation (synovitis and tenosynovitis) has not been thoroughly explored. Furthermore, it is unknown if the association with MRI-detected inflammation is only present for ACPA or also for other RA-related auto-antibodies. This study addressed these questions.Materials and methodsA total of 589 early arthritis patients, included in the Leiden Early Arthritis Clinic cohort, underwent contrast-enhanced 1.5T MRI of the unilateral wrist, metacarpophalangeal and metatarsophalangeal joints at baseline. BME, synovitis and tenosynovitis were scored according to the RAMRIS-method. ACPA, rheumatoid factor (RF) and anti-carbamylated protein (antiCarP) antibodies were determined at baseline.ResultsBME, synovitis and tenosynovitis were concomitantly present on MRI. In univariable analyses, ACPA-positive patients had higher BME-scores than ACPA-negative patients (median scores 4.5 vs. 2.0, p < 0.001), but not more synovitis and tenosynovitis.Besides ACPA, also RF (median scores 3.75 vs 2.0, p < 0.001) and anti-CarP antibodies (median scores 3.5 vs 2.5, p = 0.012) were associated with higher BME-scores in univariable analyses. To explore the association of the different antibodies with BME the BME-scores of patients with different auto-antibody combinations were compared. ACPA+RF-antiCarP- patients did not have higher BME-scores than ACPA-RF-antiCarP- patients, however ACPA+RF+antiCarP- and ACPA+RF+antiCarP+ patients had higher BME-scores (median 5.0 and 4.5 vs. 2.0 respectively, p < 0.001 and p < 0.001). ACPA and RF levels were not associated with BME-scores.ConclusionsThe presence and the level of ACPA alone were not associated with BME-scores. However, the combined presence of ACPA and RF did associate with more BME. This suggests an additive role of RF to ACPA in mediating osteitis.</abstract><cop>Kidlington</cop><pub>Elsevier Limited</pub><doi>10.1136/annrheumdis-2016-209124.107</doi></addata></record> |
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title | A5.09 Mri-detected osteitis is not associated with the presence or level of ACPA alone, but with the combined presence of ACPA and RF |
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