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  • Brink, M, et al. (författare)
  • PULMONARY FIBROSIS IN EARLY RHEUMATOID ARTHRITIS IN RELATION TO GENETIC LOCI AND INDIVIDUAL ACPA SPECIFICITIES
  • 2022
  • Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 81, s. 203-204
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Pulmonary manifestations in rheumatoid arthritis (RA) are common comorbidities but the underlying mechanisms are largely unknown. We found in a previous study 3 SNPs associated with pulmonary fibrosis (PF); rs35705950 (MUC5B), rs111521887 (TOLLIP), and rs2609255 (FAM13A) besides age, rheumatoid factor positivity and methotrexate treatment.ObjectivesTo evaluate for the added value of a multiplex of anti-citrullinated peptide antibodies (ACPA) for the development of pulmonary fibrosis (PF) in an inception cohort of RA patients.MethodsA total of 1184 patients with early RA were consecutively included and followed prospectively from the date of diagnosis (index date) until death or until 31 December 2016. The diagnosis of PF was based on high resolution tomography. The presence of 21 ACPA fine specificities were analysed in plasma sampled at index date, using a custom-made microarray chip (Thermo Fisher Scientific, Uppsala, Sweden). Data on both ACPA and genetic data was available for 841 RA patients, of whom 50 developed PF. Associations were analysed using logistic regression analysis and presented as the odds ratio (OR) with the 95% confidence interval (CI). Models were adjusted for sex, age, DAS28 and presence of RF at RA diagnosis, smoking ever, and HLA-SE and in a second step for the three SNPs (.rs35705950, rs111521887 and rs2609255), respectively.ResultsIn unadjusted analyses eight ACPA reactivities were found associated with PF development (p< 0.05-0.001). The number of ACPA reactivities was related to PF development, both in crude and adjusted models (p<0.05 for both). In models concomitantly adjusted for the three SNPs (rs35705950, rs111521887 and rs2609255) respectively, in addition to mentioned adjustments the number of ACPA reactivities (p<0.05 for all three nmodels), Vim60-75 (p<0.05, in all three models), Fibβ62–78 (72) (p<0.001-p<0.05) and F4-CIT-R (p<0.01-p<0.05) were all found significantly associated to PF development irrespective of the SNPs.ConclusionThe development of PF in an inception cohort of RA patients was associated both with risk genes and, independently of the risk genes, the presence of certain ACPA, and the number of ACPA reactivities.References[1]Jönsson E, et al. Pulmonary fibrosis in relation to genetic loci in an inception cohort of patients with early rheumatoid arthritis from northern Sweden. Rheumatology (Oxford). 2021 May 16:keab441. doi: 10.1093/rheumatology/keab441.AcknowledgementsI have no acknowledgements to declare. The staff and patients at the departments of rheumatology in northern Sweden.Disclosure of InterestsNone declared
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  • Elbagir, S, et al. (författare)
  • ANTI-PHOSPHATIDYLSERINE/PROTHROMBIN ANTIBODIES AND VASCULAR EVENTS ASSOCIATE POSITIVELY WITH HLA-DRB1*13 AND NEGATIVELY WITH HLA-DRB1*03 IN SLE
  • 2022
  • Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 81, s. 658-659
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Anti-phosphatidylserine/prothrombin antibodies (anti-PS/PT) associate with thrombotic events (1). HLA-DRB1 alleles contribute to the occurrence of conventional antiphospholipid antibodies (aPL), including anti-beta2glycoprotein-I (beta2GPI) and anti-cardiolipin (CL) (2).ObjectivesWe investigated associations between anti-PS/PT and HLA-DRB1 alleles and thrombosis in patients with SLE. Conventional aPL were included for comparison.MethodsWe included 341 consecutive Swedish SLE patients, with information on general cardiovascular risk factors, including blood lipids, lupus anticoagulant (LAC) and thrombotic events. Anti-PS/PT, anti-beta2GPI and anti-CL of IgA/G/M isotypes were quantified in parallel using particle-based multi-analyte technology. The 99th percentiles among 162 age- and sex-matched populations controls were used as cutoffs. HLA-DRB1 typing was performed using sequence-specific primer PCR.ResultsAnti-PS/PT antibodies associated positively with HLA-DRB1*13 (odds ratio [OR] 2.7, P=0.002), whereas anti-beta2GPI and anti-CL antibodies associated primarily with HLA-DRB1*04 (OR 2.5, P=0.0005; Table 1). These associations remained after adjustment for other significant HLA-DRB1 alleles identified in Table 1 (Figure 1a and b) also for LAC (Figure 1c), and also after adjustment for age and gender (not shown). HLA-DRB1*13, but not DRB1*04, remained as an independent risk factor for thrombosis after adjustment for significant HLA alleles (Figure 1d), and also after adjustment for cardiovascular risk factors in stepwise regression (not shown). Mediation analysis showed that 31.3% of the HLA-DRB1*13-related risk for thrombosis was mediated by anti-PS/PT positivity. HLA-DRB1*03, on the other hand, associated negatively with thrombotic events (Figure 1d) as well as with all aPL (Figure 1a-c). HLA-DRB1*03 had thrombo-protective effect in aPL positive patients (Figure 1d). Additionally, HLA-DRB1*03 positivity was associated with a favourable lipid profile regarding high-density lipoprotein (median 1.4 vs. 1.2 mmol/L, p=0.02) and triglycerides (median 0.9 vs 1.1 mmol/L, p=0.04); whereas no other HLA-DRB1 alleles showed any associations to lipid levels.Table 1.Frequency of individual HLA DRB1 and associations with antibody phenotypes. Odds ratios (OR) and confidence intervals (CI) for being antibody positive given a specific HLA allele and corresponding p values were calculated using Chi2 tests, with significant associations underlined.HLA DRB1HLA-DRB1 n (%) total patientsAnti-PS/PT positive (any isotype) n=48OR (95%CI); PAnti-β2GPI or anti-CL positive (any isotype) n=96OR (95%CI); P*0141 (12.9%)4 (8.3%)0.6 (0.2-1.7); 0.311 (11.4%)0.8 (0.4-1.7); 0.6*03147 (46.5%)13 (27.1%)0.4 (0.2-0.7); 0.00433 (34.4%)0.5 (0.3-0.8); 0.006*0494 (29.7%)18 (37.5%)1.6 (0.8-2.9); 0.241 (42.7%)2.5 (1.5-4.1); 0.0005*0728 (8.9%)6 (12.5%)1.5 (0.6-4); 0.49 (9.4%)1 (0.4-2.4); 0.9*0828 (8.9%)6 (12.5%)1.6 (0.6-4.3); 0.39 (9.4%)1.2 (0.5-2.7); 0.7*099 (2.8%)1 (2.1%)0.7 (0.1-5.5); 0.72 (2.1%)0.6 (0.1-3.0); 0.5*107 (2.2%)0 (0)NA2 (2.1%)0.9 (0.2-4.6); 0.9*1127 (8.5%)6 (12.5%)1.6 (0.6-4.3); 0.38 (8.3%)0.9 (0.4-2.2); 0.8*127 (2.2%)0 (0)NA1 (1%)0.4 (0.05-3.7); 0.4*1379 (25%)21 (43.7%)2.7 (1.4-5.2); 0.00233 (34.3%)2 (1.2-3.4%); 0.01*146 (1.9%)2 (4.2%)3.7 (0.6-23); 0.12 (2.1%)1.4 (0.2-8.9); 0.8*15118 (37.3%)12 (48%)0.5 (0.2-0.9); 0.04527 (28.1%)0.5 (0.3-0.9); 0.01*168 (2.5%)1 (2.1%)0.8 (0.09-6.4); 0.84 (4.2%)2.2 (0.5-9.2); 0.2ConclusionHLA-DRB1*13 confers risk for both anti-PS/PT and thrombotic events in SLE. The association between HLA-DRB1*13 and thrombosis is largely, but not entirely, mediated through anti-PS/PT. Due to the negative association of HLA-DRB1*03 with aPL and the positive association with favourable lipid levels, HLA-DRB1*03 seems to identify a subgroup of SLE patients with reduced vascular risk.References[1]Elbagir S et al. Lupus 2021;30(8):1289.[2]Lundström E et al. Ann Rheum Dis 2013;72:1018.Disclosure of InterestsSahwa Elbagir: None declared, Lina M. Diaz-Gallo: None declared, Giorgia Grosso: None declared, Agneta Zickert: None declared, Iva Gunnarsson: None declared, Michael Mahler Employee of: Dr Mahler is employee of Werfen., Elisabet Svenungsson Speakers bureau: Dr Svennungson has obtained speaker’s fees from Janssen., Grant/research support from: Dr Svennungson has obtained research grant from Merck., Johan Rönnelid Speakers bureau: Dr Rönnelid has given paid lectures for Thermo Fisher Scientific., Consultant of: Dr Rönnelid has been a member of the Scientific Advisory Board for Thermo Fisher Scientific.
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  • Gronwall, C, et al. (författare)
  • THE RELATIONSHIP BETWEEN DIFFERENT IGG AND IGA ANTI-MODIFIED PROTEIN AUTOANTIBODIES IN RHEUMATOID ARTHRITIS
  • 2021
  • Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 80, s. 206-207
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Seropositive rheumatoid arthritis (RA) is characterized by the presence of rheumatoid factor (RF) and anti-citrullinated protein autoantibodies (ACPA) with different fine-specificities. Yet, other serum anti-modified protein autoantibodies (AMPA), e.g. anti-carbamylated (Carb), anti-acetylated (KAc), and anti-malondialdehyde acetaldehyde (MAA) modified protein antibodies, have been described. By using RA patient single-cell derived monoclonal antibodies we have previously shown that individual ACPA clones recognize small distinct citrulline-containing epitopes giving them extensive multireactivity when these epitopes are found in many peptides and proteins. Moreover, certain CCP2+ multireactive ACPA clones bind also to cabamylated and acetylated autoantigens [1].Objectives:To provide a comprehensive evaluation of serum IgG and IgA autoreactivity to different post-translational modifications in RA.Methods:We analyzed 30 different IgG and IgA AMPA reactivities to modified antigens by ELISA and autoantigen arrays, in N=1985 newly diagnosed RA patients and population controls. The study utilized both previously established (i.e IgG and IgA CCP2; IgG ACPA fine-specificities; IgG anti-Carb fibrinogen and Carb FCS; IgG and IgA Cit/Carb/KAc/Orn(Ac)-vimentin), and novel assays (e.g. IgG anti-MAA and IgG anti-acetylated histones). Association with patient characteristics such as smoking and disease activity were explored. The newly developed assays were also evaluated in SLE disease controls and CCP2+ RA-risk individuals without arthritis.Results:Carb and KAc reactivities by different assays were primarily seen in patients also positive for citrulline-reactivity. Modified vimentin (mod-Vim) peptides were used for direct comparison of different AMPA reactivities, revealing that IgA AMPA recognizing mod-Vim was mainly detected in subsets of patients with high IgG anti-Cit-Vim levels and a history of smoking. IgG acetylation reactivity was mainly detected in a subset of patients with Cit and Carb reactivity. Anti-acetylated histone 2B reactivity was RA-specific and associated with high anti-CCP2 IgG levels, multiple ACPA fine-specificities, and smoking. This reactivity was also found to be present in CCP2+ RA-risk individuals without arthritis. Our data further demonstrate that IgG autoreactivity to MAA was increased in RA compared to controls with highest levels in CCP2+ RA, but was not RA-specific, and showed low correlation with other AMPA. Anti-MAA was instead associated with disease activity and was not significantly increased in CCP2+ individuals at risk of RA. Notably, RA patients could be subdivided into four different subsets based on their AMPA IgG and IgA reactivity profiles.Conclusion:We conclude that autoantibodies exhibiting different patterns of ACPA fine-specificities as well as Carb and KAc reactivity are present in RA and may be derived from multireactive B-cell clones. Anti-Carb and anti-KAc could be considered reactivities within the “Cit-umbrella” similar to ACPA fine-specificities, while MAA is distinctly different.References:[1]Sahlström P, Hansson M, Steen J, Amara K, Titcombe PJ, Forsström B, Stålesen R, Israelsson L, Piccoli L, Lundberg K, Klareskog L, Mueller DL, Catrina AI, Skriner K, Malmström V, Grönwall C. Different Hierarchies of Anti-Modified Protein Autoantibody Reactivities in Rheumatoid Arthritis. Arthritis Rheumatol. 2020 Oct;72(10):1643-1657. PMID: 32501655Caroline Grönwall: None declared, Lisa Liljefors: None declared, Holger Bang Employee of: Employee at ORGENTEC Diagnostika GmbH, Aase Hensvold: None declared, Monika Hansson: None declared, Linda Mathsson-Alm Employee of: Employee at Thermo Fisher Scientific, Lena Israelsson: None declared, Anna Svärd: None declared, Cyril CLAVEL: None declared, Elisabet Svenungsson: None declared, Iva Gunnarsson: None declared, Guy Serre: None declared, Saedis Saevarsdottir: None declared, Alf Kastbom: None declared, Lars Alfredsson: None declared, Vivianne Malmström: None declared, Johan Rönnelid: None declared, Anca Catrina: None declared, Karin Lundberg: None declared, Lars Klareskog: None declared
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  • Mathsson-Alm, L, et al. (författare)
  • THE NORA PROJECT - PREDICTION OF THERAPY RESPONSE IN RHEUMATOID ARTHRITIS
  • 2021
  • Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 80, s. 1090-1090
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Personalized medicine in Rheumatoid arthritis (RA) especially regarding therapy response is still in early stages. The Nordic RA (NORA) project is aiming to improve the prediction of therapy outcome by combining established serologic marker with new markers, genetic information and patient-derived data.Objectives:As an initial step in the project the aim was to select clinically characterized patient cohorts and evaluate if changes or patterns in serological markers could predict therapy response and/or disease progress.Methods:The ARCTIC (Aiming for Remission in rheumatoid arthritis: a randomised trial examining the benefit of ultrasound in a Clinical TIght Control regimen) study [1] was designed to compare two tight control treatment strategies for early Rheumatoid arthritis and was used as a first cohort. Plasma samples (n=1622) from 224 RA patients from the ARCTIC study were included and taken at baseline and 3, 4, 6, 8, 10, 12, 14, 16, 20, and 24 months from trial start, and analyzed for the presence of EliATM RF (IgM, IgA, IgG), anti-CCP (IgG, IgA) and anti-RA33 (IgM, IgA, IgG) autoantibodies, as well as Calprotectin using the EliA instrument platform (Phadia AB, Uppsala, Sweden). In addition, a custom-made multiplex chip (Thermo Fisher Scientific, Sweden) [2] was used for measurement of anti-IgG antibodies against RA-specific antigens (citrullinated, acetylated and carbamylated), and established CTD-markers (Connective Tissue Disease), e.g. Ro52/60 and dsDNA. The citrullinated peptides on the multiplex chip were both multiple as well as single citrullinated at different positions within the peptide sequence. Additionally, we included an ELISA to measure antibodies against native human collagen II [3].Results:The different single assays in the baseline samples varied between 7 – 80% positive test results, e.g. anti-CCP IgG 80%. For some patients we could see changes in levels for anti-CCP, RF and anti-RA33 in the follow up samples, which varied from negative to more than 3-10xULN (Upper Limit of Normal). For anti-CCP IgG we found 9 patients (4%), who changed from negative to positive (patient 1-5) or from positive to negative (patient 6-8), while patient 9 had a peak at visit 6 (=12 months) and declined afterwards (figure 1). In addition, the above mentioned 9 patients showed clear changes in signal strength for the markers included on the multiplex chip and followed a similar pattern as the anti-CCP IgG signal. Different antibody patterns against single citrullinated peptides were observed and number of ACPA-positive peptides correlated with IgG anti-CCP levels.Figure 1.Anti-CCP IgG value normalised to cutoff (blue line) for patient 1 to 9. The heatmap visualizes the change over time in anti-CCP IgG signal with dark blue showing negative results and orange/red showing results >5xULN.Anti-Collagen II antibodies (anti-CII) were detected in 15% of the baseline samples and in most cases declined over time. Two patients showed low baseline anti-CII levels that increased in the follow up samples. The changes in serological markers and the different reactivity patterns could possibly correlate with clinical outcome and define subgroups of patients with different response to therapy.Results could be repeated in RA patients from the NOR-VEAC [4] cohort. At baseline 73% of the 106 RA patients had a positive anti-CCP IgG result and 11 patients (10%) showed a significant change of anti-CCP IgG level over time.Conclusion:Different response patterns and changes in serological antibody levels over the first 24 months after RA diagnosis could possibly reveal subgroups of patients with different prognosis and response to treatment. Further evaluations in additional treatment cohorts and correlation with clinical data are ongoing.References:[1]Haavardsholm et al., BMJ 2016;354:i4205.[2]Hansson et al. Arthritis Research & Therapy 2012, 14:R201.[3]Manivel et al Ann Rheum Dis. 2017 Sep;76(9):1529-1536.[4]Mjaavatten et al., Arthritis Research & Therapy 2009, 11:R146.Acknowledgements:The NORA project is a NordForsk funded project.Disclosure of Interests:Linda Mathsson-Alm Employee of: Employee of Thermo Fisher Scientific, Isabel Gehring Employee of: Employee of Thermo Fisher Scientific, Maryam Poorafshar Employee of: Employee of Thermo Fisher Scientific, Johan Rönnelid: None declared, Johan Askling Grant/research support from: Research grants from Abbvie, Astra-Zeneca, BMS, Eli Lilly, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi, and UCB, mainly in the context of safety monitoring (ARTIS), Espen Haavardsholm: None declared, Hilde Berner Hammer: None declared
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  • Nurul-Aain, AF, et al. (författare)
  • ASSOCIATIONS BETWEEN HLA-DRB1 SHARED EPITOPES ALLELES AND ANTI-RA33 ANTIBODIES IN DIFFERENT SUBSETS OF RHEUMATOID ARTHRITIS IN MALAYSIAN POPULATION
  • 2021
  • Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 80, s. 408-408
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • The mechanisms affecting anti-RA33 antibody’s involvement in RA pathogenesis is still unclear. Refining our understanding of anti-RA33’s role in RA in relation to known RA-associated genes and serological elements is needed.Objectives:We investigated the relationship between RA-associated HLA-DRB1 epitope (SE) allele and presence of anti-RA33 antibodies in different serological subsets of rheumatoid arthritis in a Malaysian population.Methods:Serum samples from 550 RA cases comprising seronegative (negative for anti-CCP2, IgG and IgM, n=250), seropositive (triple-autoantibody positive, n=150), singular anti-CCP2 positive (n=100), and double RF positive RA (n=50) were chosen from the Malaysian Epidemiological Investigations of RA (MyEIRA) case-control study. Three hundred MyEIRA population controls were used for comparison. All serum samples were assayed using a commercial anti-RA33 ELISA kit. All genetic samples were genotyped for four-digit HLA-DRB1 alleles using the PCR-SSO method on Luminex platform.Results:The proportions of anti-RA33 positive was 20.9% in all RA cases (i.e. 34% in RF only positive RA; 25% in seropositive RA; 18% in seronegative RA and 18% in anti-CCP2 only positive RA). The HLA-DRB1 shared epitope alleles were significantly associated with anti-RA33 positive in the seropositive RA subgroup (OR=6.9, 95% CI 1.4-34.8; p=0.02). We observed significant association between anti-RA33 negative and HLA-DRB1 SE alleles among the seropositive RA patients (OR=4.5, 95% CI 2.8-7.2; p<0.001) and among CCP only positive RA (OR=4.4; 95% CI 2.6-7.4; p<0.01). No association was observed between anti-RA33 status and HLA-DRB1 SE alleles in seronegative RA and RF only positive RA.Conclusion:The HLA-DRB1 SE alleles increased the risk of seropositive and CCP only positive RA independent of anti-RA33 positivity.References:[1]Boeters, Debbie M et al. “The 2010 ACR/EULAR criteria are not sufficiently accurate in the early identification of autoantibody-negative rheumatoid arthritis: Results from the Leiden-EAC and ESPOIR cohorts.” Seminars in arthritis and rheumatism vol. 47,2 (2017): 170-174.[2]de Brito Rocha, Sara et al. “Clinical and pathophysiologic relevance of autoantibodies in rheumatoid arthritis.” Advances in rheumatology (London, England) vol. 59,1 2. 17 Jan. 2019.Acknowledgements:The authors would like to thank the Director General of Health, Ministry of Health Malaysia for supporting this study. The authors are also indebted to participants for their kind participation. This study was financially supported by the Ministry of Health, Malaysia (JPP-IMR 08-012).Disclosure of Interests:None declared
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  • Sabrina, MRNA, et al. (författare)
  • CHANGES OF RF ISOTYPE PROFILE IN PATIENTS WITH RHEUSMATOID ARTHRITIS: DATA FROM 10 YEARS FOLLOW-UP STUDY
  • 2021
  • Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 80, s. 459-460
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Presence of autoantibodies such as anti-cyclic citrullinated peptide (anti-CCP2) and rheumatoid factor (RF) is of considerable diagnostic and prognostic value in patients with rheumatoid arthritis (RA). Limited data are available for autoantibody profile changes over time in patients with RA.Objectives:Thus, we compared the presence of anti-CCP2 and different RF isotypes in individual RA patients at baseline and during 10 years follow-up.Methods:A total of 320 RA patients from the Malaysian Epidemiological Investigation of Rheumatoid Arthritis (MyEIRA) case-control study was included in this study. The presence of anti-CCP2, IgM RF, IgG RF, and IgA RF at baseline and at later time point (±10 years) were determined using enzyme-linked immunosorbent assays, with identical techniques in paired samples. Seropositive RA is defined by the presence of at least one autoantibody, whilst seronegative RA is defined by the absence of all investigated autoantibodies.Results:The proportion of seropositive RA were higher for the follow-up samples (n=263, 82.2%) as compared to the baseline samples (n=251, 78.4%). Among the baseline samples, 105 (41.8%) were positive for anti-CCP2 and all RF isotypes. Of these individuals, 85 (81.0%) remained positive for all antibodies at the follow-up, while 20 (19.0%) lost one or more RF isotypes (4 IgM RF, 19 IgG RF and 13 IgA RF). Interestingly, 14 (5.6%) RA patients who were seropositive at baseline became totally seronegative after follow-up. Among the 69 patients seronegative at baseline, 26 (37.7%) acquired one or more autoantibodies at follow-up (14 IgM RF, 2 IgG RF, 9 IgA RF and 8 anti-CCP2) (Figure 1).Conclusion:Anti-CCP2 present at baseline usually remained at follow-up. Among Malaysian RA patients, changes in status were mainly found for RF of all isotypes.References:[1]Barra, Lillian et al. “Lack of seroconversion of rheumatoid factor and anti-cyclic citrullinated peptide in patients with early inflammatory arthritis: a systematic literature review.” Rheumatology (Oxford, England) vol. 50,2 (2011): 311-6.[2]van Delft, Myrthe A M, and Tom W J Huizinga. “An overview of autoantibodies in rheumatoid arthritis.” Journal of autoimmunity vol. 110 (2020): 102392.Figure 1.Comparison of serum autoantibody profile in rheumatoid arthritis patients during baseline enrolment and 10 years follow-up.Acknowledgements:The authors would like to thank the Director General of Health, Ministry of Health Malaysia for supporting this study. The authors are also indebted to participants for their kind participation. This study was financially supported by the Ministry of Health, Malaysia (JPP-IMR 08-012; 18-051).Disclosure of Interests:None declared
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