SAT0011 What is Undifferentiated Arthritis (UA) in 2013, and can Progression to Rheumatoid Arthritis (RA) be Predicted?
Background In applying 2010 criteria to patients with early inflammatory arthritis, the weighting of serology in the criteria is such that the majority of ACPA positive arthritis patients are classified as RA. A significant proportion of patients with UA have persistent disease1,2. Differences betwe...
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| Veröffentlicht in: | Annals of the rheumatic diseases 2013-06, Vol.72 (Suppl 3), p.A582 |
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| creator | Horton, S. C. Wakefield, R. J. Tan, A. L. Freeston, J. E. Buch, M. H. Emery, P. |
| description | Background In applying 2010 criteria to patients with early inflammatory arthritis, the weighting of serology in the criteria is such that the majority of ACPA positive arthritis patients are classified as RA. A significant proportion of patients with UA have persistent disease1,2. Differences between ACPA negative(-) and ACPA positive(+) patients suggest their disease pathogenesis is divergent. Objectives Compare UA and ACPA- RA, and determine clinical and/or ultrasound (US) features predictive of progression to RA. Methods DMARD-naïve patients with UA or RA (2010 criteria) with outcomes available at 6 months were selected from the Leeds Early inflammatory arthritis cohort (recruitment since 2010). Steroid within the preceding 4 weeks was an exclusion. Patients with UA were categorised as palindromic, oligo- or polyarthritis according to intermittent or persistent joint tenderness and/or swelling and involvement of |
| doi_str_mv | 10.1136/annrheumdis-2013-eular.1737 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_1777912466</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4008721221</sourcerecordid><originalsourceid>FETCH-LOGICAL-b1656-884007f76a2aa5dbb0482ae8c575953847080692d7f8d43c07b2b9e70c4a9b5e3</originalsourceid><addsrcrecordid>eNqVkMtKAzEUhoMoWC_vEOhGwdGTuSQZXEgp3qCotNaCm5CZydjUNqNJCrpz44v6JGasiC5dhZPz_ec_50eoS-CQkIQeSWPsVC0XlXZRDCSJ1HIu7SFhCVtDHZJSHr4prKMOACRRmlO2ibacm4USOOEd9Drq3QIQ8vH2PplKj7XDY1PpulZWGa-lVxXuWT-12ofW3ri3j7XBrdcBlqbCpTT4xjYPVjmnG4N9g4ftRtI3-o9yGJSFCqyqdBmmnuygjVrOndr9frfR-Oz0tn8RDa7PL_u9QVQQmtGI8xSA1YzKWMqsKgpIeSwVLzOW5VnCUwYcaB5XrOZVmpTAirjIFYMylXmRqWQbdVdzn2zzvFTOi1mztCZYCsIYy0mcUhqo4xVV2sY5q2rxZPVC2ldBQLRZi19Zi_Z-8ZW1aLMO6mil1s6rlx-ptI-Chn4mru76YpLEbHR_F4t-4OmKLxazfxl9Ajm5mAg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1777912466</pqid></control><display><type>article</type><title>SAT0011 What is Undifferentiated Arthritis (UA) in 2013, and can Progression to Rheumatoid Arthritis (RA) be Predicted?</title><source>BMJ Journals - NESLi2</source><creator>Horton, S. C. ; Wakefield, R. J. ; Tan, A. L. ; Freeston, J. E. ; Buch, M. H. ; Emery, P.</creator><creatorcontrib>Horton, S. C. ; Wakefield, R. J. ; Tan, A. L. ; Freeston, J. E. ; Buch, M. H. ; Emery, P.</creatorcontrib><description>Background In applying 2010 criteria to patients with early inflammatory arthritis, the weighting of serology in the criteria is such that the majority of ACPA positive arthritis patients are classified as RA. A significant proportion of patients with UA have persistent disease1,2. Differences between ACPA negative(-) and ACPA positive(+) patients suggest their disease pathogenesis is divergent. Objectives Compare UA and ACPA- RA, and determine clinical and/or ultrasound (US) features predictive of progression to RA. Methods DMARD-naïve patients with UA or RA (2010 criteria) with outcomes available at 6 months were selected from the Leeds Early inflammatory arthritis cohort (recruitment since 2010). Steroid within the preceding 4 weeks was an exclusion. Patients with UA were categorised as palindromic, oligo- or polyarthritis according to intermittent or persistent joint tenderness and/or swelling and involvement of <4 or ≥4 joints respectively. Results ACPA negativity was observed in 33/37 UA patients and 35/108 RA patients. Baseline characteristics are shown in the table: n(%) or median(IQR), unless otherwise stated. Symptom duration was longer in UA patients, potentially due to a trend towards lower disease activity and lower HAQ in this group. At 6 months, 70% and 89% of patients with UA and ACPA- RA respectively were receiving any DMARD (p=0.08). There were no statistically significant differences (UA vs ACPA- RA) in; median(IQR) DAS44 1.7(1.3-2.4) vs 2.2(1.7-2.7), improvement in DAS44 from baseline 0.7(-0.1-1.3) vs 0.8(0.1-1.7) or HAQ 0.4(0.1-0.8) vs 0.8(0.3-1.0). In patients with UA, 7(19%), 19(51%) and 11(30%) were categorised as palindromic, oligo- and polyarthritis respectively at baseline. Over 6 months, 5/19(26%) of patients with oligoarthritis progressed to polyarthritis, only 1 of these patients(5%) fulfilled 2010 criteria when applied cumulatively. Whereas 3/7(43%) palindromic and 4/11(36%) polyarthritis patients progressed to RA (p=0.02 for comparison between oligoarthritis and palindromic/polyarthritis combined). Of palindromic UA 2 patients had subclinical synovitis on US, both of whom progressed to RA (1 patient was ACPA+). Baseline US findings were not significantly associated with progression to RA or need for DMARD over 6 months amongst oligoarthritis or UA patients overall. Conclusions Clinically important levels of disease activity and disability exist in patients with UA. Differences in clinical phenotype of patients with UA may be predictive of disease progression. References Krabben A, et al. ARD 2012;71(2):238-41. van der Helm-van Mil A, Huizinga TW. ARD 2012;71:1596-8. Disclosure of Interest S. Horton: None Declared, R. Wakefield: None Declared, A. L. Tan: None Declared, J. Freeston: None Declared, M. Buch Consultant for: Abbot, Pfizer, Roche, Chugai, BMS, UCB, P. Emery Consultant for: Abbot, Pfizer, Roche, Chugai, BMS, UCB, MSD</description><identifier>ISSN: 0003-4967</identifier><identifier>EISSN: 1468-2060</identifier><identifier>DOI: 10.1136/annrheumdis-2013-eular.1737</identifier><identifier>CODEN: ARDIAO</identifier><language>eng</language><publisher>Kidlington: BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><ispartof>Annals of the rheumatic diseases, 2013-06, Vol.72 (Suppl 3), p.A582</ispartof><rights>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</rights><rights>Copyright: 2013 (c) 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</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/72/Suppl_3/A582.2.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://ard.bmj.com/content/72/Suppl_3/A582.2.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,776,780,3183,23550,27901,27902,77343,77374</link.rule.ids></links><search><creatorcontrib>Horton, S. C.</creatorcontrib><creatorcontrib>Wakefield, R. J.</creatorcontrib><creatorcontrib>Tan, A. L.</creatorcontrib><creatorcontrib>Freeston, J. E.</creatorcontrib><creatorcontrib>Buch, M. H.</creatorcontrib><creatorcontrib>Emery, P.</creatorcontrib><title>SAT0011 What is Undifferentiated Arthritis (UA) in 2013, and can Progression to Rheumatoid Arthritis (RA) be Predicted?</title><title>Annals of the rheumatic diseases</title><addtitle>Ann Rheum Dis</addtitle><description>Background In applying 2010 criteria to patients with early inflammatory arthritis, the weighting of serology in the criteria is such that the majority of ACPA positive arthritis patients are classified as RA. A significant proportion of patients with UA have persistent disease1,2. Differences between ACPA negative(-) and ACPA positive(+) patients suggest their disease pathogenesis is divergent. Objectives Compare UA and ACPA- RA, and determine clinical and/or ultrasound (US) features predictive of progression to RA. Methods DMARD-naïve patients with UA or RA (2010 criteria) with outcomes available at 6 months were selected from the Leeds Early inflammatory arthritis cohort (recruitment since 2010). Steroid within the preceding 4 weeks was an exclusion. Patients with UA were categorised as palindromic, oligo- or polyarthritis according to intermittent or persistent joint tenderness and/or swelling and involvement of <4 or ≥4 joints respectively. Results ACPA negativity was observed in 33/37 UA patients and 35/108 RA patients. Baseline characteristics are shown in the table: n(%) or median(IQR), unless otherwise stated. Symptom duration was longer in UA patients, potentially due to a trend towards lower disease activity and lower HAQ in this group. At 6 months, 70% and 89% of patients with UA and ACPA- RA respectively were receiving any DMARD (p=0.08). There were no statistically significant differences (UA vs ACPA- RA) in; median(IQR) DAS44 1.7(1.3-2.4) vs 2.2(1.7-2.7), improvement in DAS44 from baseline 0.7(-0.1-1.3) vs 0.8(0.1-1.7) or HAQ 0.4(0.1-0.8) vs 0.8(0.3-1.0). In patients with UA, 7(19%), 19(51%) and 11(30%) were categorised as palindromic, oligo- and polyarthritis respectively at baseline. Over 6 months, 5/19(26%) of patients with oligoarthritis progressed to polyarthritis, only 1 of these patients(5%) fulfilled 2010 criteria when applied cumulatively. Whereas 3/7(43%) palindromic and 4/11(36%) polyarthritis patients progressed to RA (p=0.02 for comparison between oligoarthritis and palindromic/polyarthritis combined). Of palindromic UA 2 patients had subclinical synovitis on US, both of whom progressed to RA (1 patient was ACPA+). Baseline US findings were not significantly associated with progression to RA or need for DMARD over 6 months amongst oligoarthritis or UA patients overall. Conclusions Clinically important levels of disease activity and disability exist in patients with UA. Differences in clinical phenotype of patients with UA may be predictive of disease progression. References Krabben A, et al. ARD 2012;71(2):238-41. van der Helm-van Mil A, Huizinga TW. ARD 2012;71:1596-8. Disclosure of Interest S. Horton: None Declared, R. Wakefield: None Declared, A. L. Tan: None Declared, J. Freeston: None Declared, M. Buch Consultant for: Abbot, Pfizer, Roche, Chugai, BMS, UCB, P. Emery Consultant for: Abbot, Pfizer, Roche, Chugai, BMS, UCB, MSD</description><issn>0003-4967</issn><issn>1468-2060</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNqVkMtKAzEUhoMoWC_vEOhGwdGTuSQZXEgp3qCotNaCm5CZydjUNqNJCrpz44v6JGasiC5dhZPz_ec_50eoS-CQkIQeSWPsVC0XlXZRDCSJ1HIu7SFhCVtDHZJSHr4prKMOACRRmlO2ibacm4USOOEd9Drq3QIQ8vH2PplKj7XDY1PpulZWGa-lVxXuWT-12ofW3ri3j7XBrdcBlqbCpTT4xjYPVjmnG4N9g4ftRtI3-o9yGJSFCqyqdBmmnuygjVrOndr9frfR-Oz0tn8RDa7PL_u9QVQQmtGI8xSA1YzKWMqsKgpIeSwVLzOW5VnCUwYcaB5XrOZVmpTAirjIFYMylXmRqWQbdVdzn2zzvFTOi1mztCZYCsIYy0mcUhqo4xVV2sY5q2rxZPVC2ldBQLRZi19Zi_Z-8ZW1aLMO6mil1s6rlx-ptI-Chn4mru76YpLEbHR_F4t-4OmKLxazfxl9Ajm5mAg</recordid><startdate>201306</startdate><enddate>201306</enddate><creator>Horton, S. C.</creator><creator>Wakefield, R. J.</creator><creator>Tan, A. L.</creator><creator>Freeston, J. E.</creator><creator>Buch, M. H.</creator><creator>Emery, P.</creator><general>BMJ Publishing Group Ltd and European League Against Rheumatism</general><general>Elsevier Limited</general><scope>BSCLL</scope><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>201306</creationdate><title>SAT0011 What is Undifferentiated Arthritis (UA) in 2013, and can Progression to Rheumatoid Arthritis (RA) be Predicted?</title><author>Horton, S. C. ; Wakefield, R. J. ; Tan, A. L. ; Freeston, J. E. ; Buch, M. H. ; Emery, P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b1656-884007f76a2aa5dbb0482ae8c575953847080692d7f8d43c07b2b9e70c4a9b5e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Horton, S. C.</creatorcontrib><creatorcontrib>Wakefield, R. J.</creatorcontrib><creatorcontrib>Tan, A. L.</creatorcontrib><creatorcontrib>Freeston, J. E.</creatorcontrib><creatorcontrib>Buch, M. H.</creatorcontrib><creatorcontrib>Emery, P.</creatorcontrib><collection>Istex</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</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 Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</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>Horton, S. C.</au><au>Wakefield, R. J.</au><au>Tan, A. L.</au><au>Freeston, J. E.</au><au>Buch, M. H.</au><au>Emery, P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SAT0011 What is Undifferentiated Arthritis (UA) in 2013, and can Progression to Rheumatoid Arthritis (RA) be Predicted?</atitle><jtitle>Annals of the rheumatic diseases</jtitle><addtitle>Ann Rheum Dis</addtitle><date>2013-06</date><risdate>2013</risdate><volume>72</volume><issue>Suppl 3</issue><spage>A582</spage><pages>A582-</pages><issn>0003-4967</issn><eissn>1468-2060</eissn><coden>ARDIAO</coden><abstract>Background In applying 2010 criteria to patients with early inflammatory arthritis, the weighting of serology in the criteria is such that the majority of ACPA positive arthritis patients are classified as RA. A significant proportion of patients with UA have persistent disease1,2. Differences between ACPA negative(-) and ACPA positive(+) patients suggest their disease pathogenesis is divergent. Objectives Compare UA and ACPA- RA, and determine clinical and/or ultrasound (US) features predictive of progression to RA. Methods DMARD-naïve patients with UA or RA (2010 criteria) with outcomes available at 6 months were selected from the Leeds Early inflammatory arthritis cohort (recruitment since 2010). Steroid within the preceding 4 weeks was an exclusion. Patients with UA were categorised as palindromic, oligo- or polyarthritis according to intermittent or persistent joint tenderness and/or swelling and involvement of <4 or ≥4 joints respectively. Results ACPA negativity was observed in 33/37 UA patients and 35/108 RA patients. Baseline characteristics are shown in the table: n(%) or median(IQR), unless otherwise stated. Symptom duration was longer in UA patients, potentially due to a trend towards lower disease activity and lower HAQ in this group. At 6 months, 70% and 89% of patients with UA and ACPA- RA respectively were receiving any DMARD (p=0.08). There were no statistically significant differences (UA vs ACPA- RA) in; median(IQR) DAS44 1.7(1.3-2.4) vs 2.2(1.7-2.7), improvement in DAS44 from baseline 0.7(-0.1-1.3) vs 0.8(0.1-1.7) or HAQ 0.4(0.1-0.8) vs 0.8(0.3-1.0). In patients with UA, 7(19%), 19(51%) and 11(30%) were categorised as palindromic, oligo- and polyarthritis respectively at baseline. Over 6 months, 5/19(26%) of patients with oligoarthritis progressed to polyarthritis, only 1 of these patients(5%) fulfilled 2010 criteria when applied cumulatively. Whereas 3/7(43%) palindromic and 4/11(36%) polyarthritis patients progressed to RA (p=0.02 for comparison between oligoarthritis and palindromic/polyarthritis combined). Of palindromic UA 2 patients had subclinical synovitis on US, both of whom progressed to RA (1 patient was ACPA+). Baseline US findings were not significantly associated with progression to RA or need for DMARD over 6 months amongst oligoarthritis or UA patients overall. Conclusions Clinically important levels of disease activity and disability exist in patients with UA. Differences in clinical phenotype of patients with UA may be predictive of disease progression. References Krabben A, et al. ARD 2012;71(2):238-41. van der Helm-van Mil A, Huizinga TW. ARD 2012;71:1596-8. Disclosure of Interest S. Horton: None Declared, R. Wakefield: None Declared, A. L. Tan: None Declared, J. Freeston: None Declared, M. Buch Consultant for: Abbot, Pfizer, Roche, Chugai, BMS, UCB, P. Emery Consultant for: Abbot, Pfizer, Roche, Chugai, BMS, UCB, MSD</abstract><cop>Kidlington</cop><pub>BMJ Publishing Group Ltd and European League Against Rheumatism</pub><doi>10.1136/annrheumdis-2013-eular.1737</doi></addata></record> |
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| title | SAT0011 What is Undifferentiated Arthritis (UA) in 2013, and can Progression to Rheumatoid Arthritis (RA) be Predicted? |
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