FRI0034 Rage Activity Influences Co-Development of Joint and Vascular Disease in RA
BackgroundRAGE is expressed by many cells in blood and joints of RA and interacts with a variety of pro-inflammatory ligands, especially HMGB1 that are enriched in inflamed joint. The RAGE-ligand interaction leads to a sustained inflammatory response. Soluble RAGE (sRAGE) lacks the transmembrane and...
Saved in:
Published in | Annals of the rheumatic diseases Vol. 75; no. Suppl 2; p. 438 |
---|---|
Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
London
BMJ Publishing Group LTD
01.06.2016
|
Online Access | Get full text |
Cover
Loading…
Abstract | BackgroundRAGE is expressed by many cells in blood and joints of RA and interacts with a variety of pro-inflammatory ligands, especially HMGB1 that are enriched in inflamed joint. The RAGE-ligand interaction leads to a sustained inflammatory response. Soluble RAGE (sRAGE) lacks the transmembrane and cytoplasmic domain of the cell surface full-length RAGE (flRAGE) and function as a decoy for RAGE ligand. Relatively little is known about factors that regulate sRAGE levels in human subjects and whether circulating levels reflect tissue RAGE expression and activity is unclear. The relationship between the up-regulation of flRAGE/HMGB1 and the level of “protective” sRAGE levels in RA is of obvious clinical interest.ObjectivesTo elucidate the balance between the expression of flRAGE on peripheral blood monocyte and dendritic cell (DC), and the plasma concentration of sRAGE and HMGB1 in patients with active RA compare to controls; To ascertain whether flRAGE expression profiles, plasma sRAGE and HMGB1 level correlated with disease activity or inflammatory markers in RA patients.Methods40 consecutive patients attending the rheumatology clinic at Prince of Wales Hospital, who fulfilled the 2010 ACR/RULAR classification criteria with active RA (28 joint disease activity score 28–4 [CRP] (DAS28)>3.2) and 40 age- and sex-matched healthy volunteers were recruited for this cross-sectional study. The expression profile of cellular transmembrane RAGE on peripheral blood monocyte (ILT3+CD123–), total DC (ILT3+CD14–CD16–), myeloid DC (ILT3+CD14–CD16–CD123–) and plasmacytoid DC (ILT3+CD14–CD16–CD123+), plasma levels of HMGB1 and soluble RAGE in all RA patients and healthy controls were measured at baseline using flow cytometry and ELISA. In RA patients, associations with disease activity and severity variables were analyzed by simple and multiple linear regressions.ResultsProtein expression of flRAGE on peripheral blood monocytes (ILT3+CD123–), total DCs (ILT3+CD14–CD16–) and myeloid DCs (ILT3+CD14–CD16–CD123–) were significant increased in RA patients with active disese compared with control subjects (all p<0.01) (no enough cells for flRAGE detection on plasmacytoid ILT3+CD14–CD16–CD123+DCs). Also, the flRAGE was more common in patients with cardiac affection. There was no statistically significant difference of the plasma level of HMGB1 from active RA patients as compared healthy controls (p>0.05). The plasma sRAGE level was significantly lower in patients compared to healthy controls (p<0.001), which correlated negatively with serum levels of CRP, ESR, DAS28 and high-density lipoprotein (HDL) (all p<0.05). Linear regrssion analysis detected CRP as significant predictors for sRAGE level.ConclusionsAutoimmunity-mediated inflammation might induce aberrant expression and activation of flRAGE while decreasing the plasma level of sRAGE in RA patients, subsequently leading to the augmented inflammatory response. Moreover, membrance flRAGE and sRAGE were associated not just with RA inflammation and autoantibody protein, but also with classical vascular risk factors for end-organ damage. These data suggest that RAGE activity influences co-development of joint and vascular disease in RA patients.Disclosure of InterestNone declared |
---|---|
AbstractList | BackgroundRAGE is expressed by many cells in blood and joints of RA and interacts with a variety of pro-inflammatory ligands, especially HMGB1 that are enriched in inflamed joint. The RAGE-ligand interaction leads to a sustained inflammatory response. Soluble RAGE (sRAGE) lacks the transmembrane and cytoplasmic domain of the cell surface full-length RAGE (flRAGE) and function as a decoy for RAGE ligand. Relatively little is known about factors that regulate sRAGE levels in human subjects and whether circulating levels reflect tissue RAGE expression and activity is unclear. The relationship between the up-regulation of flRAGE/HMGB1 and the level of “protective” sRAGE levels in RA is of obvious clinical interest.ObjectivesTo elucidate the balance between the expression of flRAGE on peripheral blood monocyte and dendritic cell (DC), and the plasma concentration of sRAGE and HMGB1 in patients with active RA compare to controls; To ascertain whether flRAGE expression profiles, plasma sRAGE and HMGB1 level correlated with disease activity or inflammatory markers in RA patients.Methods40 consecutive patients attending the rheumatology clinic at Prince of Wales Hospital, who fulfilled the 2010 ACR/RULAR classification criteria with active RA (28 joint disease activity score 28–4 [CRP] (DAS28)>3.2) and 40 age- and sex-matched healthy volunteers were recruited for this cross-sectional study. The expression profile of cellular transmembrane RAGE on peripheral blood monocyte (ILT3+CD123–), total DC (ILT3+CD14–CD16–), myeloid DC (ILT3+CD14–CD16–CD123–) and plasmacytoid DC (ILT3+CD14–CD16–CD123+), plasma levels of HMGB1 and soluble RAGE in all RA patients and healthy controls were measured at baseline using flow cytometry and ELISA. In RA patients, associations with disease activity and severity variables were analyzed by simple and multiple linear regressions.ResultsProtein expression of flRAGE on peripheral blood monocytes (ILT3+CD123–), total DCs (ILT3+CD14–CD16–) and myeloid DCs (ILT3+CD14–CD16–CD123–) were significant increased in RA patients with active disese compared with control subjects (all p<0.01) (no enough cells for flRAGE detection on plasmacytoid ILT3+CD14–CD16–CD123+DCs). Also, the flRAGE was more common in patients with cardiac affection. There was no statistically significant difference of the plasma level of HMGB1 from active RA patients as compared healthy controls (p>0.05). The plasma sRAGE level was significantly lower in patients compared to healthy controls (p<0.001), which correlated negatively with serum levels of CRP, ESR, DAS28 and high-density lipoprotein (HDL) (all p<0.05). Linear regrssion analysis detected CRP as significant predictors for sRAGE level.ConclusionsAutoimmunity-mediated inflammation might induce aberrant expression and activation of flRAGE while decreasing the plasma level of sRAGE in RA patients, subsequently leading to the augmented inflammatory response. Moreover, membrance flRAGE and sRAGE were associated not just with RA inflammation and autoantibody protein, but also with classical vascular risk factors for end-organ damage. These data suggest that RAGE activity influences co-development of joint and vascular disease in RA patients.Disclosure of InterestNone declared Background RAGE is expressed by many cells in blood and joints of RA and interacts with a variety of pro-inflammatory ligands, especially HMGB1 that are enriched in inflamed joint. The RAGE-ligand interaction leads to a sustained inflammatory response. Soluble RAGE (sRAGE) lacks the transmembrane and cytoplasmic domain of the cell surface full-length RAGE (flRAGE) and function as a decoy for RAGE ligand. Relatively little is known about factors that regulate sRAGE levels in human subjects and whether circulating levels reflect tissue RAGE expression and activity is unclear. The relationship between the up-regulation of flRAGE/HMGB1 and the level of "protective" sRAGE levels in RA is of obvious clinical interest. Objectives To elucidate the balance between the expression of flRAGE on peripheral blood monocyte and dendritic cell (DC), and the plasma concentration of sRAGE and HMGB1 in patients with active RA compare to controls; To ascertain whether flRAGE expression profiles, plasma sRAGE and HMGB1 level correlated with disease activity or inflammatory markers in RA patients. Methods 40 consecutive patients attending the rheumatology clinic at Prince of Wales Hospital, who fulfilled the 2010 ACR/RULAR classification criteria with active RA (28 joint disease activity score 28-4 [CRP] (DAS28)>3.2) and 40 age- and sex-matched healthy volunteers were recruited for this cross-sectional study. The expression profile of cellular transmembrane RAGE on peripheral blood monocyte (ILT3+ CD123- ), total DC (ILT3+ CD14- CD16- ), myeloid DC (ILT3+ CD14- CD16- CD123- ) and plasmacytoid DC (ILT3+ CD14- CD16- CD123+ ), plasma levels of HMGB1 and soluble RAGE in all RA patients and healthy controls were measured at baseline using flow cytometry and ELISA. In RA patients, associations with disease activity and severity variables were analyzed by simple and multiple linear regressions. Results Protein expression of flRAGE on peripheral blood monocytes (ILT3+ CD123- ), total DCs (ILT3+ CD14- CD16- ) and myeloid DCs (ILT3+ CD14- CD16- CD123- ) were significant increased in RA patients with active disese compared with control subjects (all p<0.01) (no enough cells for flRAGE detection on plasmacytoid ILT3+ CD14- CD16- CD123+ DCs). Also, the flRAGE was more common in patients with cardiac affection. There was no statistically significant difference of the plasma level of HMGB1 from active RA patients as compared healthy controls (p>0.05). The plasma sRAGE level was significantly lower in patients compared to healthy controls (p<0.001), which correlated negatively with serum levels of CRP, ESR, DAS28 and high-density lipoprotein (HDL) (all p<0.05). Linear regrssion analysis detected CRP as significant predictors for sRAGE level. Conclusions Autoimmunity-mediated inflammation might induce aberrant expression and activation of flRAGE while decreasing the plasma level of sRAGE in RA patients, subsequently leading to the augmented inflammatory response. Moreover, membrance flRAGE and sRAGE were associated not just with RA inflammation and autoantibody protein, but also with classical vascular risk factors for end-organ damage. These data suggest that RAGE activity influences co-development of joint and vascular disease in RA patients. Disclosure of Interest None declared |
Author | Li, E.K. Tam, L.-S. Wong, C.-K. Yu, S. |
Author_xml | – sequence: 1 givenname: S. surname: Yu fullname: Yu, S. organization: Rheumatology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou – sequence: 2 givenname: C.-K. surname: Wong fullname: Wong, C.-K. organization: Chemical Pathology – sequence: 3 givenname: E.K. surname: Li fullname: Li, E.K. organization: Medicine & Therapeutics, The Chinese University of Hong Kong, Hong Kong, China – sequence: 4 givenname: L.-S. surname: Tam fullname: Tam, L.-S. organization: Medicine & Therapeutics, The Chinese University of Hong Kong, Hong Kong, China |
BookMark | eNqVkL1OwzAUhS1UJErhHSx1TrGd1LHFVLX8FFVCqoDVcpxrSJXYJW4qdWPhRXkSHMrAynT_zrlH-s7RwHkHCI0pmVCa8ivtXPsGXVNWIWGE8gS6WrcTKll-goY04yKuORmgISEkTTLJ8zN0HsImjkRQMUTPt-tlPGVfH59r_Qp4ZnbVvtod8NLZugNnIOC5Txawh9pvG3A77C1-8FVstCvxiw6mz8SLKoAOgCuH17MLdGp1HeDyt45izs3T_D5ZPd4t57NVUlCWy8RKoCCJEXYqcsJSK6ZTrk1urcgYmLRgOWfSllTbjBcFE7qIo0gZNVroEtIRGh__blv_3kHYqY3vWhcjFZWECpLzTEbV9VFlWh9CC1Zt26rR7UFRonqO6g9H1XNUPxxVzzG6-dFdNJt_Gb8Bt5uATA |
CODEN | ARDIAO |
ContentType | Journal Article |
Copyright | 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 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 |
Copyright_xml | – notice: 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 – notice: 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 |
DBID | AAYXX CITATION 3V. 7X7 7XB 88E 88I 8AF 8FE 8FH 8FI 8FJ 8FK ABUWG AFKRA AZQEC BBNVY BENPR BHPHI BTHHO CCPQU DWQXO FYUFA GHDGH GNUQQ HCIFZ K9- K9. LK8 M0R M0S M1P M2P M7P PQEST PQQKQ PQUKI Q9U |
DOI | 10.1136/annrheumdis-2016-eular.1927 |
DatabaseName | CrossRef ProQuest Central (Corporate) Health & Medical Complete (ProQuest Database) ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) Science Database (Alumni Edition) STEM Database ProQuest SciTech Collection ProQuest Natural Science Collection Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials Biological Science Collection AUTh Library subscriptions: ProQuest Central ProQuest Natural Science Collection BMJ Journals ProQuest One Community College ProQuest Central Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student SciTech Premium Collection (Proquest) (PQ_SDU_P3) Consumer Health Database ProQuest Health & Medical Complete (Alumni) Biological Sciences Family Health Database (Proquest) Health & Medical Collection (Alumni Edition) PML(ProQuest Medical Library) Science Database (ProQuest) Biological Science Database ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central Basic |
DatabaseTitle | CrossRef ProQuest Central Student ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest AP Science ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest Natural Science Collection ProQuest Family Health (Alumni Edition) ProQuest Central Health Research Premium Collection Health and Medicine Complete (Alumni Edition) Natural Science Collection ProQuest Central Korea Biological Science Collection ProQuest Medical Library (Alumni) ProQuest Science Journals (Alumni Edition) ProQuest Biological Science Collection ProQuest Central Basic ProQuest Science Journals ProQuest Family Health ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) Biological Science Database ProQuest SciTech Collection ProQuest Hospital Collection (Alumni) ProQuest Health & Medical Complete ProQuest Medical Library ProQuest One Academic UKI Edition BMJ Journals ProQuest One Academic ProQuest Central (Alumni) |
DatabaseTitleList | ProQuest Central Student |
Database_xml | – sequence: 1 dbid: BENPR name: AUTh Library subscriptions: ProQuest Central url: https://www.proquest.com/central sourceTypes: Aggregation Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine |
EISSN | 1468-2060 |
EndPage | 438 |
ExternalDocumentID | 4322510201 10_1136_annrheumdis_2016_eular_1927 |
GroupedDBID | --- .55 .GJ .VT 0R~ 23M 2WC 39C 3O- 3V. 4.4 40O 53G 5GY 5RE 5VS 6J9 7X7 7~S 88E 88I 8AF 8FE 8FH 8FI 8FJ 8R4 8R5 AAHLL AAKAS AAOJX AAWJN AAWTL ABAAH ABJNI ABKDF ABMQD ABOCM ABTFR ABUWG ABVAJ ACGFO ACGFS ACGOD ACGTL ACHTP ACMFJ ACOFX ACPRK ACTZY ADBBV ADCEG ADFRT ADUGQ ADZCM AEKJL AENEX AFKRA AFWFF AHMBA AHNKE AHQMW AJYBZ AKKEP ALIPV ALMA_UNASSIGNED_HOLDINGS ASPBG AVWKF AZFZN AZQEC BAWUL BBNVY BENPR BHPHI BKNYI BLJBA BOMFT BPHCQ BTFSW BTHHO BVXVI C1A C45 CAG CCPQU COF CS3 CXRWF DIK DWQXO E3Z EBS EJD F5P FRP FYUFA GNUQQ H13 HAJ HCIFZ HMCUK HYE HZ~ IAO IEA IGG IHR INH INR IOF J5H K9- KQ8 L7B LK8 M0R M1P M2P M7P N9A NTWIH NXWIF O9- OK1 OVD P2P PQQKQ PROAC PSQYO Q2X R53 RHF RHI RMJ RPM RV8 RWL RXW TAE TEORI TR2 UAW UKHRP UYXKK V24 VM9 VVN W2D W8F WH7 WOQ X6Y X7M YFH YOC YQY ZGI ZXP AAYXX CITATION ITC 7XB 8FK K9. PQEST PQUKI Q9U |
ID | FETCH-LOGICAL-b1279-f9e1e90c8f587023f8556ac7ff842ec3b27629fd1af46bb28ab29f8321ca8ade3 |
IEDL.DBID | BENPR |
ISSN | 0003-4967 |
IngestDate | Thu Oct 10 22:13:07 EDT 2024 Thu Sep 26 18:52:51 EDT 2024 Wed Aug 21 03:29:18 EDT 2024 |
IsPeerReviewed | true |
IsScholarly | true |
Issue | Suppl 2 |
Language | English |
LinkModel | DirectLink |
MergedId | FETCHMERGED-LOGICAL-b1279-f9e1e90c8f587023f8556ac7ff842ec3b27629fd1af46bb28ab29f8321ca8ade3 |
PQID | 1901807649 |
PQPubID | 2041045 |
PageCount | 1 |
ParticipantIDs | proquest_journals_1901807649 crossref_primary_10_1136_annrheumdis_2016_eular_1927 bmj_primary_10_1136_annrheumdis_2016_eular_1927 |
PublicationCentury | 2000 |
PublicationDate | 20160600 2016-06-00 20160601 |
PublicationDateYYYYMMDD | 2016-06-01 |
PublicationDate_xml | – month: 06 year: 2016 text: 20160600 |
PublicationDecade | 2010 |
PublicationPlace | London |
PublicationPlace_xml | – name: London |
PublicationTitle | Annals of the rheumatic diseases |
PublicationYear | 2016 |
Publisher | BMJ Publishing Group LTD |
Publisher_xml | – name: BMJ Publishing Group LTD |
SSID | ssj0000818 |
Score | 2.2332623 |
Snippet | BackgroundRAGE is expressed by many cells in blood and joints of RA and interacts with a variety of pro-inflammatory ligands, especially HMGB1 that are... Background RAGE is expressed by many cells in blood and joints of RA and interacts with a variety of pro-inflammatory ligands, especially HMGB1 that are... |
SourceID | proquest crossref bmj |
SourceType | Aggregation Database Publisher |
StartPage | 438 |
Title | FRI0034 Rage Activity Influences Co-Development of Joint and Vascular Disease in RA |
URI | http://dx.doi.org/10.1136/annrheumdis-2016-eular.1927 https://www.proquest.com/docview/1901807649 |
Volume | 75 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1LTwIxEG4EEuLF-IwokiZ6XaG73W73ZBAhQAIxKIbbps-ICbvI4__bLt0gFxNv22x6-dp-M52ZzgfAA20ZKxpK4RGbH8SKEo9HthEkD1s6jIxLju3j5NGY9Kd4OAtnLuC2dmWVBSfmRC0zYWPkTWu4qLl04_hp-e1Z1SibXXUSGiVQ8RG2adrKc3f8OtlzMUW00MzDMYmq4N7pmFiZl9Wn2i7kfG22CiKesnWfj8bjsZaKL74OLdUhUefWp3cKTpzbCNu7dT4DRyo9B9WRS4xfgLfeZGCbwMCJ4QfYFjtNCDgoJEjWsJN5vwqEYKbhMJubD5ZK-OHKUeHLLl0D5ymctC_BtNd97_Q9p5fgceRHsadjhVTcElSH5hT6gaZhSJiItKbYVyLgvmG-WEvENCac-5RxM7RSRYJRJlVwBcpplqprACXTkgSchcLMVQFjgiAZaYIYQkIKVgNNg1Cy3HXESPKbRJC_bi4wTSymSY5pYjGtAVyg-b9p9QL5xJ2udbLfCzd__74Fx_nS5lGTOihvVlt1Z5yIDW-AUjSLGm6__ABPQscj |
link.rule.ids | 315,786,790,12083,21416,27955,27956,31752,33777,43343,43838,74100,74657 |
linkProvider | ProQuest |
linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV3JTsMwEB1BKwEXxCqWApbgGlpncZwTKqVVC7RCZVFvkVdRpCbQ5f-xU0fQCxK3WJEvz_ab8cx4HsAVbRgrGknhEZsfDBUlHo9tI0geNXQUG5c8tI-T-wPSfQ3vR9HIBdxmrqyy5MSCqGUubIy8bg0XNZfuMLn5_PKsapTNrjoJjXWo2pabtALV2_bgafjDxRTTUjMvTEi8AZdOx8TKvEzf1WIixzOzVTDxlK37vDYej7VUfPKxaqlWibqwPp0d2HZuI2ou13kX1lS2Bxt9lxjfh-fOsGebwKCh4QfUFEtNCNQrJUhmqJV7vwqEUK7RfT42HyyT6M2Vo6K7ZboGjTM0bB7Aa6f90up6Ti_B49iPE08nCqukIaiOzCn0A02jiDARa01DX4mA-4b5Ei0x0yHh3KeMm6GVKhKMMqmCQ6hkeaaOAEmmJQk4i4SZqwLGBMEy1gQzjIUU7BjqBqH0c9kRIy1uEkHxurnENLWYpgWmqcX0GMISzf9Nq5XIp-50zdKfvXDy9-8L2Oy-9B_Tx97g4RS2imUuIig1qMynC3VmHIo5P3e75hsvY8ky |
linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1bT8IwFG4UE-KL8RpR1Cb6OqG7dN2TIeACKMTgJbwtvUZM2JDB_7fduiAvJr6tWfry9fSc056v5wPgjrR1FA0Ed7CpD_qSYIeFphEkC9oqCHVK7pvHyaMx7r_7w2kwtfyn3NIqK59YOGqRcXNH3jKBi-hDtx-1lKVFvPTih8W3YxSkTKXVymnsgj0dJdtGxiGchhuvTBCp1PP8CId1cGsVTYzgy_JTrudilmujQdiRhgF6r3MfE7PY_Gs7Zm277CIOxYfgwCaQsFOu-BHYkekxqI9sifwEvMaTgWkHAyfaU8AOL9Uh4KASI8lhN3N-UYVgpuAwm-kPmgr4YYmpsFcWbuAshZPOKXiPH9-6fccqJzgMuWHkqEgiGbU5UYHej66nSBBgykOliO9K7jFX-8BICUSVjxlzCWV6aESLOCVUSO8M1NIslecACqoE9hgNuJ4rPUo5RiJUGFGEuOC0AVoaoWRR9sZIijOFV7xzrjBNDKZJgWliMG0Av0Lzf9OaFfKJ3Wd5srGKi79_34C6NpfkeTB-ugT7xSoXVylNUFst1_JKZxYrdl2YzA_Uz8vv |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=FRI0034%E2%80%85Rage+Activity+Influences+Co-Development+of+Joint+and+Vascular+Disease+in+RA&rft.jtitle=Annals+of+the+rheumatic+diseases&rft.au=Yu%2C+S.&rft.au=Wong%2C+C.-K.&rft.au=Li%2C+E.K.&rft.au=Tam%2C+L.-S.&rft.date=2016-06-01&rft.issn=0003-4967&rft.eissn=1468-2060&rft.volume=75&rft.issue=Suppl+2&rft.spage=438&rft.epage=438&rft_id=info:doi/10.1136%2Fannrheumdis-2016-eular.1927&rft.externalDBID=n%2Fa&rft.externalDocID=10_1136_annrheumdis_2016_eular_1927 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0003-4967&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0003-4967&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0003-4967&client=summon |