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Background:Systemic lupus erythematosus (SLE) is a severe, lifelong autoimmune disease known for its multisystem organ involvement. SLE patients are known to be at risk for premature atherosclerosis at a relatively young age (1). Endothelial dysregulation is one of the pathophysiologic mechanisms that can lead to the higher risk for cardiovascular disease in SLE (2). Multiple endothelial markers with dysregulation in SLE have been described so far, of which some are associated with disease activity.Objectives:To report a systematic literature review regarding endothelial markers that are dysregulated in SLE and search for associations with disease activity.Methods:The search was performed according to the Preferred Reporting Items for Systematic review and Meta-analysis Protocols (PRISMA-P) 2015 (3). In July 2020, the search terms were used in Embase, MEDLINE, Web of Science, Google Scholar and Cochrane. Inclusion criteria were 1) published studies after the year 2000 that reported measurements of endothelial cell markers in serum and/or plasma of SLE patients (diagnosed according to ACR/SLICC criteria), 2) English language peer reviewed articles and 3) disease activity measurement (i.e. SLEDAI, BILAG, SLAM, ECLAM or PGA). Exclusion criteria were 1) case reports or editorials, 2) studies performed in animals and 3) studies with microRNA/cytokine biomarkers. There was no minimum count for study population. The screening process is shown in figure 1.Results:From 1892 hits, we identified 110 eligible articles. Table 1 shows an overview of the most frequently studied endothelial markers. These identified endothelial markers are involved in endothelial cell (EC) activation, EC apoptosis, disturbed angiogenesis, defective vascular tone control, immune dysregulation and coagulopathy. In most studies, dysregulation of the endothelial marker was associated with disease activity. The majority of the studies had a cross-sectional design, longitudinal data on endothelial markers in SLE are scarce.Conclusion:We identified multiple endothelial markers that are dysregulated in SLE and this dysregulation was often associated with disease activity in cross-sectional studies. Our future plan is to test the identified endothelial markers in (longitudinally collected) samples of (childhood onset) SLE patients, disease- and healthy controls. This will be a next step in unravelling the pathophysiology of premature atherosclerosis and cardiovascular events in SLE-patients in young adulthood.Figure 1.References:[1]Vavlukis M, Pop-Gjorceva D, Poposka L, Sandevska E, Kedev S. Myocardial Infarction in Systemic Lupus Erythematosus - the Sex Specific Risk Profile. Curr Pharm Des. 2020 Dec 9.[2]Westerweel PE, Luyten RK, Koomans HA, Derksen RH, Verhaar MC. Premature atherosclerotic cardiovascular disease in systemic lupus erythematosus. Arthritis Rheum. 2007 May;56(5):1384-96.[3]Shamseer L, Moher D, Clarke M, Ghersi D, Liberati A, Petticrew M, Shekelle P, Stewart LA; PRISMA-P Group. Preferred reporting items for systematic review and meta-analysis protocols (PRISMA-P) 2015: elaboration and explanation. BMJ. 2015 Jan 2;350:g7647.Table 1.Endothelial markerArticles(no. of studies)Significant correlation with SLEDAI(no. of studies)Studies with control groups(no. of studies)Longitudinal data(no. of studies)YesNoUnknownHealthy controlsDiseased controlsVCAM-12620152338VEGF2213542022ICAM-11811521734Thrombomodulin1710521322E-Selectin136521021MCP-18620712P-Selectin6321611IP-106510501Pentraxin-35500512vWF5410502Neopterin3210202Fas3021201Angiopoeietin-2330021-Endothelin-1312030-PAI-1311120-Adrenomedullin320120-TWEAK311112-PECAM-1311130-Disclosure of Interests:None declared

Background:Higher dosage regimes for Infliximab (IFX) have been described to be effective in partial- or non-responding adults and children with rheumatic disease and appear to be safe (1,2). To optimize IFX treatment in juvenile idiopathic arthritis (JIA) patients, therapeutic drug monitoring (TDM) might be beneficial. To support routine TDM of IFX and dose regimen optimization in JIA patients, more in-depth knowledge of the pharmacokinetic (PK) variability of IFX is needed. Ultimately, as soon as the optimal therapeutic drug ranges will be known, PK model-based simulation can be used to individualize drug dosing recommendations. Individual dosages may be adjusted by taking specific patient characteristics into account that explain inter-patient variability in pharmacokinetics (PK). Inter-patient variability can be quantified and investigated by the population approach.Objectives:Our hypothesis is that optimizing dosage and frequency of IFX administration for individual patients will improve treatment outcome. In this current study, the population PK for IFX are described for JIA patients.Methods:Data including IFX trough concentrations and anti-IFX antibodies of 27 JIA patients on IFX maintenance treatment were retrieved from electronic charts. Three population pharmacokinetic models from literature were validated for our dataset using nonlinear-mixed effects modeling program NONMEM (3,4,5). A novel population pharmacokinetic model was developed based on our study data.Results:A total of 65 obtained blood samples after a median of 32 days after the last IFX infusion (IQR 28-42) were analyzed. The three published models underpredicted the observed trough concentrations. A newly developed one compartment model best described the IFX serum concentration over time data in JIA patients (see Figure 1).Conclusion:Our study shows a novel and the first PK model for IFX in JIA patients. Our main finding was that a one- compartment model best described the IFX serum concentration over time data. Predictive performance of the known models from literature was insufficient for our patient data. Our data also show that different PK models are needed for different age categories (children or adults) and in different diseases.References:[1]Nozaki Y et al. Infliximab dose adjustment can improve the clinical and radiographic outcomes of rheumatoid arthritis patients: REVIVE study results. Biologics. 2018.[2]Tambralli A et al. High doses of infliximab in the management of juvenile idiopathic arthritis. J Rheumatol. 2013.[3]Fasanmade AA et al. Pharmacokinetic properties of infliximab in children and adults with Crohn’s disease: a retrospective analysis of data from 2 phase III clinical trials. Clin Ther. 2011.[4]Xu Z et al. Population pharmacokinetics of infliximab in patients with ankylosing spondylitis. J Clin Pharmacol. 2008.[5]Ternant D et al. Relationship between inflammation and infliximab pharmacokinetics in rheumatoid arthritis. Br J Clin Pharmacol. 2014.Table 1.Patient characteristicsN=27 patientsWeight (kg)52 [40 – 62]BSA1.6 [1.3 – 1.8]Age (years)14 [11 – 17]Male, N (%)6 (22%)CRP (mg/L)0.5 [0.2 – 0.7]WBC count6.5 [5.6 –7.5]Antibodies-to-IFX1 (4%)Dose (mg)300 [200-400]Dose (mg/kg)5.4 [4.9 -7.0]Hemoglobine (mmol/L)7.9 [7.5 -8.2]ESR (mm/h)5 [5-8]Uveitis3 (11%)Disclosure of Interests:None declared.

Background:Juvenile Idiopathic Arthritis (JIA) is the most common auto-immune disease in children and pain is a common symptom. Despite treatment advances in recent years, pain often persists when the disease is inactive. Treating JIA to target has been widely recommended1, but effectiveness in pain reduction has not been proven yet2.Objectives:To compare pain scores over two years in three treatment arms in JIA patients that were treated to target and to identify baseline characteristics predicting unfavorable pain outcomes.Methods:DMARD naïve children who participated in the BeSt for kids study3 with oligoarticular JIA, RF negative polyarticular JIA and juvenile psoriatic arthritis were included. Patient were treated to target aimed at inactive disease according to 1 of 3 different treatment groups; 1) initial sequential DMARD monotherapy 2) initial methotrexate (MTX) with prednisolone bridging or 3) initial MTX with etanercept. Pain intensity was measured using a 100 mm Visual Analogue Scale during 24 months of follow up with 3-monthly intervals. Potential differences in VAS pain scores over time between treatment arms were compared using linear mixed models with random intercept and random slope for visits clustered within patients. A similar multivariable mixed model was used to assess the ability of several baseline characteristics to predict the chance of high pain levels during follow-up.Results:92 patients were randomized into the three treatment groups. Overall, pain scores over time reduced from mean 55.3 (SD 21.7) at baseline to 19.5 (SD 25.3) after 24 months. When comparing pain over time per arm, pain scores decreased significantly over time β -1.37 (95% CI -1.726; -1.022). No significant difference was found in pain over time between treatment groups (interaction term treatment arm*time (months) β (95% CI) arm 1 0.13 (-0.36; 0.62) and arm 2 0.37 (-0.12; 0.86) compared to arm 3), Figure 1. Correction for sex and symptom duration as possible confounders yielded similar results. Multiple baseline characteristics demonstrated a significant predictive value for pain over time: VAS pain (scale 0-100) with β 0.44 (95% CI 0.25; 0.65), VAS physician (scale 0-100) with β -0.34 (-0.55; -0.06), number of active joints with β 0.77 (0.19; 1.34), Child Health Questionnaire Physical summary Score with β -0.42 (-0.72; -0.11) and Psychosocial summary Score β -0.42 (-0.77; -0.06). Symptom duration, VAS patient/parent and NSAID use were no significant predictors, Table 1.Conclusion:Treatment to target seems effective in pain reduction in non-systemic JIA patients irrespective of initial treatment strategy. Several baseline predictors for pain over time were identified, which could serve as an initial indication for non-systemic JIA-patients with a high risk of pain despite a strict treat-to-target strategy.References:[1]Ravelli A, Consolaro A, Horneff G, et al. Treating juvenile idiopathic arthritis to target: recommendations of an international task force. Ann Rheum Dis. 2018;77(6):819–828.[2]Schoemaker, C.G., Swart, J.F. & Wulffraat, N.M. Treating juvenile idiopathic arthritis to target: what is the optimal target definition to reach all goals?. Pediatr Rheumatol. 18, 34 (2020)[3]Hissink Muller P, Brinkman DMC, Schonenberg-Meinema D, et al. Treat to target (drug-free) inactive disease in DMARD-naive juvenile idiopathic arthritis: 24-month clinical outcomes of a three-armed randomised trial. Ann Rheum Dis. 2019 Jan;78(1):51-59.Table 1.Baseline Characteristicsβp-value95% Confidence IntervalVAS Pain0.450.0000.25 to 0.65VAS Physician-0.310.014-0.55 to -0.06VAS Patient/parent-0.020.873-0.21 to 0.18No. of active joints0.770.0090.19 to 1.34PhS*-0.420.008-0.72 to -0.11PsS**-0.420.022-0.77 to -0.06Symptom duration (mo.)8.090.118-2.08 to 18.26NSAID use-1.300.791-10.91 to 8.31VAS Pain, VAS physician and VAS patient/parent was measures on a 100mm scale.*PhS= Physical Summary Score of the Child Health Questionnaire Parent form 50 (scale 0-100).**PsS= Psychosocial Summary Score of the CHQ-PF50 (scale 0-100).Disclosure of Interests:None declared

Background:Even in the hands of experienced clinicians, clinical phenotyping and predicting treatment responses in Systemic Lupus Erythematosus (SLE) patients remains challenging. Therefore, the identification of biomarkers that can help physicians to divide patients into subgroups based upon aberrantly activated pathways is relevant and might guide future treatment strategies. Extensive blood transcriptional profiling has identified various gene modules that seem promising for stratification of SLE patients into subgroups (1). However, the feasibility to implement these complicated and expensive tests for use in the daily practice of routine clinical laboratories is challenging if not impossible.Objectives:The aim of this study was to develop gene signatures that stratify patients into groups with comparable disease profiles and are feasible to perform in routine clinical laboratories.Methods:To identify coordinated expression of a set of genes and reduce data complexity, genes from 4 previously described modules (Interferon M1.2, Interferon M5.12, Neutrophil- and Plasmablast (PB)(1)) were measured using real-time quantitative PCR expression on whole blood RNA samples. Subsequently, a principle component analysis was used to select 2-5 indicator genes, that represent a specific signature. Expression levels of these genes were measured in healthy donors (n=42) and samples from two independent childhood-onset SLE cohorts (n=51 and n=20). Scores higher than the mean + 2 S.D. score of healthy controls were defined as high gene signature scores. Based on their expression levels, gene signatures were divided over 14 clusters. Associated clusters were subsequently grouped into three gene fingerprints termed 1) all-signatures-low, 2) only high IFN (M1.2 and/or M5.12) and 3) high PB and/or Neutrophil. Disease activity was measured by the SELENA-SLEDAI score.Results:All four gene signatures were higher expressed in patients compared to healthy controls and showed a significant correlation with the SLEDAI. The PB signature showed the highest association with disease activity (r= 0.6512, PConclusion:Various gene signatures are associated with disease activity, which underlines the involvement of different pathophysiological mechanisms in SLE. Combining these signatures into gene fingerprints can help to stratify patients into comparable groups and guide individualized treatment choices for patients in the future.References:[1]Banchereau R, Hong S, Cantarel B, Baldwin N, Baisch J, Edens M, et al. Personalized Immunomonitoring Uncovers Molecular Networks that Stratify Lupus Patients. Cell. 2016;165(6):1548-50.Figure 1.SELENA-SLEDAI scores based on gene fingerprint distribution. Blue indicates time point one of cohort 1 (n=51); pink indicates time point two of cohort 1 (n=45); red indicates time point one of the replication cohort (n=20)Disclosure of Interests:None declared

Background:It has been suggested that a capillary scleroderma pattern in patients with systemic lupus erythematosus (SLE)-patients predisposes for clinical signs of systemic sclerosis (SSc) or overlap disease (1). However, this was previously shown not to be the case in a cross-sectional study in childhood-onset SLE (cSLE) (2).Objectives:To assess if nailfold capillary patterns in cSLE change over time and if a capillary scleroderma pattern is associated with prospective development of clinical SSc-features, higher SLE disease activity or –damage.Methods:Prospective clinical and capillaroscopy data were used from a longitudinal cohort of cSLE patients. Patients with a disease onset before the age of 18 years and diagnosis according to SLICC 2012 criteria were included. Disease activity was defined by SLEDAI score and disease damage by the SLICC damage index. Nailfold images from eight fingers (excluding thumbs) were obtained by videocapillaroscopy. A scleroderma pattern was defined according to the ‘fast track algorithm’ (3). An abnormal capillary pattern that did not match the criteria for a scleroderma pattern was defined as ‘microangiopathy’.Results:Our longitudinal study cohort consisted of n=53 cSLE patients with a median disease onset of 14 years (IQR 12.5-15.5 years) and a median SLEDAI score at diagnosis of 11 (IQR 8-15.5). Clinical follow-up data were available from 0.5-16 years after disease onset. Median disease duration at first capillaroscopy was 17 months (IQR 5.5-51.5 months) and 17/53 (32.1%) of patients had Raynaud’s phenomenon. In total, n=9 (17%) showed a scleroderma pattern (at some point in time), n=37 (70%) had microangiopathy and n=7 (13%) showed a normal capillary pattern. N=27 patients had follow up with capillaroscopy (1-7 times over 1-5 years). In most patients (23/27) we did not observe any change in capillary pattern during follow-up. Two patients showed changes from microangiopathy to a scleroderma pattern, one patient from a scleroderma pattern to microangiopathy and one patient from microangiopathy to a normal pattern. Raynaud’s phenomenon was equally distributed among patients with different capillaroscopy patterns (p=0.487), as was median SLEDAI score at diagnosis (p=0.285). Follow-up patients with a capillary scleroderma pattern did not show any clinical features for SSc over time (follow-up over 1-5 years, Table 1 below. Patients with a capillary scleroderma pattern showed significantly more disease damage (Chi-square, p=0.008), also indicated by a survival analysis for disease damage (Figure 1, p=0.042).Conclusion:Our study indicates that a capillary scleroderma pattern in cSLE correlates with disease damage but not with clinical SSc features during follow-up period.References:[1]S. Pavlov-Dolijanovic et al. Is there a difference in systemic lupus erythematosus with and without Raynaud’s phenomenon? Rheum Int 2013;33: 859–865[2]D. Schonenberg-Meinema et al. Nailfold capillary abnormalities in childhood-onset systemic lupus erythematosus. Revised manuscript after review re-submitted to Lupus in January 2021[3]V. Smith et al. Fast track algorithm. Autoimm Rev 2019 Nov;18(11): 102394Table 1.Clinical characteristics of cSLE-patients (n=9/53) with a nailfold capillary scleroderma patternButterfly rashPhotosensitive rashLupus nephritisAutoimmune cytopeniaPositive CoombsLow C3/C4SerositisDamageType of auto-antibodiesFollow-up in years1++-+++-+ANA, Anti-ds-DNA, anti-Sm, anti-RNP, anti-Ro52, anti-SS-A52++-+++-+ANA, Anti-ds-DNA, anti-Sm, anti-RNP, anti-SS-A53-+++++++ANA, Anti-ds-DNA, anti-Sm, anti-RNP, anti-SS-A104-++-++++ANA, Anti-ds-DNA, anti-Sm, anti-RNP, anti-Ro52, anti-SS-A95-+--+-+-ANA1 (lost)6-++++++-ANA, Anti-ds-DNA, anti-c1q37---+----ANA, Anti-ds-DNA, anti-Sm, anti-RNP18++-+----ANA99-+++++++ANA, Anti-ds-DNA, anti-RNP, anti-SS-A8Figure 1.Occurrence of disease damage (with survival as ‘no damage’) in cSLE patients with microangiopathy (blue) and a capillary scleroderma pattern (red)Disclosure of Interests:None declared

In juvenile idiopathic arthritis (JIA) patients there is a lack of markers that predict severe disease. Although anticitrullinated protein antibodies (ACPA) have contributed substantially to the understanding of rheumatoid arthritis (RA),1 their detection in JIA has not been equally useful as incidence rates in JIA patients are low2 and merely confined to the polyarticular immunoglobulin (Ig)M-rheumatoid factor (RF)-positive category resembling RA. Recently, anticarbamylated protein (anti-CarP) antibodies were detected in 45% of RA patients and importantly also in 16%–20% ACPA-negative patients.3–5 Within the ACPA-negative patients, anti-CarP antibodies were associated with more severe radiographic progression.3 Since most JIA patients are ACPA-negative we investigated whether anti-CarP antibodies are present in the sera of JIA patients and how they are related to ACPA and IgM-RF. JIA patients from three Dutch sources were included: the BeSt for Kids trial (NTR 1574, a treatment strategy study) (n=33), a previously described cohort6 (n=48) and the Arthritis and Biologicals in Children (ABC) register7 (n=153). Healthy controls (n=107) (mean age/range 11/(2–20)) are stem-cell graft …

Background In the BeSt for Kids (a three-armed treatment strategy study in juvenile idiopathic arthritis (JIA)) time to inactive disease, time to flare after Disease Modifying Anti Rheumatic Drug (DMARD) discontinuation, ACRpedi scores, functional ability, safety, and radiological damage are compared. Follow up will be 2 years. Here we present the 3 months clinical outcomes of initial treatments. Methods Recent onset, DMARD naive JIA patients (Rheumatoid Factor-negative polyarticular, oligoarticular or with psoriasis (ILAR-criteria), 2 /week, based on physician9s preference), 2. combination therapy: MTX 10mg/m 2 /week and 4 weeks prednisolone-bridging 0.5mg/kg/day, in 2 weeks tapered to nil, and 3. combination therapy with MTX 10mg/m 2 /week and etanercept 0.8mg/kg/wk. NSAIDs and intra-articular steroids are permitted in all patients. MTX was combined with folic acid 5mg/week. Treatment adjustments were made every 3 months after assessment by a trained, blinded examiner. Target was ACRpedi50 after 3 months and inactive disease from 6 months and onwards. Results From October 2009 to April 2014, 95 children, of which 33% boys, were enrolled: 32 in arm 1, 32 in arm 2 and 31 in arm 3. Baseline median (IQR) age was 8,6 (4,5-12,9) years. 38% were ANA positive, 12 patients had oligoarticular disease, 68 patients oligoextended/polyarticular JIA and 15 patients had JIA with psoriasis. Baseline median (IQR) ACRpedi scores: VAS physician 49 (40-58) mm, VAS patient 54 (37-70) mm, ESR 6,5 (2-14,8) mm/hr, number of active joints 8 (5-12), number of joints with limited range of motion 3 (1-5), CHAQ score 0,88 (0,63-1,5). In arm 1, 17/32 had started with MTX, the others with SSZ. One patient in arm 1 (lost to FU) and 1 in arm 3 (uveitis) dropped out before 3 months. By 3 months ACRpedi50 was reached by 10/32 (31%),12/32 (38%) and 16/30 (53%) (p=0,19) and ACRpedi70 was reached by 8/32 (25%), 6/32 (19%) and 14/30 (47%) in arms 1-3, respectively (p=0.04). Toxicity (mainly gastrointestinal complaints) was similar in the treatment arms. Three short hospital admissions (serious adverse events) were reported. In 2/32, 1/32 and 2/30 patients MTX dose was reduced or switched to subcutaneous and 3/15 patients stopped SSZ after 6 weeks because of nausea, malaise, headache. Conclusions After 3 months of initial treatment in a three-armed strategy trial, patients with recent onset JIA achieve more clinical improvement (significantly more ACRpedi70) on initial combination therapy with MTX and etanercept than on initial MTX or SSZ monotherapy. Numerically, response to initial treatment with MTX and prednisolone bridging seems more effective than monotherapy and less effective than combination with etanercept, but these differences were not statistically significant. Disclosure of Interest P. Hissink Muller Grant/research support from: Pfizer, D. Brinkman: None declared, D. Schonenberg: None declared, Y. Koopman-Keemink: None declared, J. van den Berg: None declared, P. Bekkering: None declared, M. van Rossum: None declared, L. van Suijlekom-Smit: None declared, C. Allaart: None declared, R. ten Cate: None declared

Background Currently, biological agents are not approved for the treatment of persistent oligoarticular juvenile idiopathic arthritis (oJIA). However, there are persistent oJIA patients unresponsive to the conventional treatment consisting of NSAIDs, intra-articular corticosteroids (IAS) and methotrexate (MTX), in whom biological treatment is considered. Objectives We aimed to evaluate the effectiveness and safety of TNF-blocking agents in all Dutch patients with persistent oJIA included in the Arthritis and Biologicals in Children (ABC) register until February 2011. An additional aim was to explore if persistent oJIA patients treated with TNF inhibitors resemble other non-systemic JIA patients (patients with all JIA categories except systemic JIA) included in the register. Methods The Dutch Arthritis and Biologicals in Children Register is an ongoing multicenter prospective study which, since 1999, has aimed to include Dutch children with JIA using biological agents. Response to biological treatment was evaluated using the JIA core-set disease-activity variables and the Wallace criteria for inactive disease. Results Until February 2011, sixteen persistent oJIA patients (68.8% female) had been included in the register. Median age at onset was 8.4 years (IQR 2.1-13.5), 18.8% had a history of uveitis, and 56.3% were ANA-positive. All had previously been treated with MTX, and 81.3% with IAS. Most patients started etanercept; adalimumab was started in two patients who had active arthritis and uveitis. Median follow-up after introduction of biological treatment was 13.7 months (IQR 8.3-16.7). Though patients with persistent oJIA had less affected joints, they had similarly high patient/parent assessments of pain and wellbeing as other non-systemic JIA patients treated with TNF-inhibitors. Additionally, their physician evaluated the disease activity as moderately high. After 3 months of treatment, disease activity had decreased and the disease was inactive in 63% of patients. Joint counts decreased from a median of two (IQR1-4) to no active joints (IQR 0-2); the physician global assessment of disease activity decreased from median 36 (IQR 4-65) to zero (IQR 0-30). After 15 months the disease was inactive in 90% of patients. TNF-alpha blockers were tolerated well. Conclusions TNF-blocking agents seem an effective and justifiable option in persistent oJIA when treatment with IAS and MTX has failed. On some measures of disease activity, the persistent oJIA patients currently treated with TNF-inhibitors resemble other non-systemic JIA patients from our register. Larger studies are needed to identify factors that characterize these more severely affected persistent oJIA patients, so treatment strategy for these patients can be adapted in an early stage of the disease. Disclosure of Interest J. Anink: None Declared, M. Otten: None Declared, F. Prince: None Declared, E. Hoppenreijs: None Declared, N. Wulffraat: None Declared, J. Swart: None Declared, R. ten Cate: None Declared, M. van Rossum: None Declared, J. van den Berg: None Declared, K. Dolman: None Declared, Y. Koopman-Keemink: None Declared, W. Armbrust: None Declared, S. Kamphuis: None Declared, P. van Pelt: None Declared, S. Gorter: None Declared, L. van Suijlekom-Smit Grant/Research support from: Dutch Board of Health Insurances, Pfizer International, Abbott, Consultant for: Pfizer International

Background Anti-citrullinated protein antibodies (ACPA) have a low prevalence in Juvenile Idiopathic Arthritis (JIA). Autoantibodies recognizing carbamylated protein (anti-CarP) are a promising new serological marker for ACPA negative Rheumatoid Arthritis and are associated with a more severe clinical course (Shi et al, 2011). Objectives To determine the presence of anti-CarP antibodies in sera of JIA patients and to investigate their prognostic value. Methods Samples of 249 patients with all subgroups of JIA, taken at different time points in their disease course and 107 healthy partially age matched controls were analyzed for the presence of anti-CarP antibodies as well as ACPA (commercial CCP2 ELISA). Cut-off for positivity was determined in the sera of the healthy controls as the mean plus two times standard deviation. Results The serum samples came from patients with all different subtypes of JIA (median age 12,1 years, IQR 8,1-15,7 median disease duration 2,2 years IQR 0,7-6,4) including 19 polyarticular rheumatoid factor positive patients. IgG antibodies recognizing carbamylated antigens were present in sera of 12,9% (32/249) of all JIA patients vs 2,8% (3/107) in the controls (p=0,002). Anti-CarP antibodies were detected in 58% (11/19) of the rheumatoid factor positive polyarticular JIA patients (p Conclusions Anti-CarP antibodies can be detected in sera of patients with JIA, mainly in the rheumatoid factor positive polyarticular subgroup, which is the JIA subtype that shows the most resemblance with RA in adults. Correlations between anti-CarP antibodies and disease characteristics are currently under investigation. References Shi J et al. Autoantibodies recognizing carbamylated protein are present in sera of patients with rheumatoid arthritis and predict joint damage. PNAS, October 2011;108(42):17372-7 Disclosure of Interest P. Hissink Muller Grant/Research support from: Pfizer and the Dutch League against Rheumatism, J. Anink: None Declared, J. Shi: None Declared, N. Levarht: None Declared, T. Reinards: None Declared, M. Otten: None Declared, M. van Tol: None Declared, C. Jol-van der Zijde: None Declared, C. Allaart: None Declared, E. Hoppenreijs: None Declared, Y. Koopman-Keemink: None Declared, K. Dolman: None Declared, J. van den Berg: None Declared, M. van Rossum: None Declared, L. van Suijlekom-Smit: None Declared, M. Schilham: None Declared, R. ten Cate: None Declared, R. Toes: None Declared, L. Trouw: None Declared