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BackgroundSystemic sclerosis (SSc) belongs to the group of connective tissue diseases and is associated with the occurrence of disease-specific autoantibodies. Although it is still controversial whether these antibodies contribute to pathogenesis, there are new insights into the development of these specific antibodies and their possible pathophysiological properties. Interestingly, they are associated with specific clinical manifestations, but for some rarer antibodies this association is not fully clarified. The aim of this study is a comprehensive analysis of the serum autoantibody status in patients with SSc followed by correlation analyses of autoantibodies with the clinical course of the disease.MethodsSerum from SSc patients was analyzed using a line blot (EUROLINE, EUROIMMUN AG) for SSc-related autoantibodies. Autoantibodies to centromere, Topo-1, antimitochondrial antibodies (AMA) M2 subunit, angiotensin II type 1 receptors (AT1R) and endothelin-1 type-A-receptors (ETAR) were also determined by ELISA. We formed immunological clusters and used principal components analysis (PCA) to assign specific clinical characteristics to these clusters.ResultsA total of 372 SSc patients were included. 95.3% of the patients were antinuclear antibody positive and in 333 patients at least one SSc specific antibody could be detected. Four immunological clusters could be found by PCA. Centromere, Topo-1 and RP3 all formed own clusters, which are associated with distinct clinical phenotypes. We found that patients with an inverted phenotype, such as limited cutaneous SSc patients within the Topo-1 cluster show an increased risk for ILD compared to ACA positive patients. Anti-AT1R and anti-ETAR autoantibodies were measured in 176 SSc patients; no association with SSc disease manifestation was found. SSc patients with AMA-M2 antibodies showed an increased risk of cardiovascular events.ConclusionIn our in large cluster analysis, which included an extended autoantibody profile, we were able to show that serologic status of SSc patients provides important clues to disease manifestation, co-morbidities and complications. Line blot was a reliable technique to detect autoantibodies in SSc and detected rarer autoantibodies in 42% of our patients.

Most patients with Post COVID Syndrome (PCS) present with a plethora of symptoms without clear evidence of organ dysfunction. A subset of them fulfills diagnostic criteria of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Symptom severity of ME/CFS correlates with natural regulatory autoantibody (AAB) levels targeting several G-protein coupled receptors (GPCR). In this exploratory study, we analyzed serum AAB levels against vaso- and immunoregulatory receptors, mostly GPCRs, in 80 PCS patients following mild-to-moderate COVID-19, with 40 of them fulfilling diagnostic criteria of ME/CFS. Healthy seronegative (n=38) and asymptomatic post COVID-19 controls (n=40) were also included in the study as control groups. We found lower levels for various AABs in PCS compared to at least one control group, accompanied by alterations in the correlations among AABs. Classification using random forest indicated AABs targeting ADRB2, STAB1, and ADRA2A as the strongest classifiers (AABs stratifying patients according to disease outcomes) of post COVID-19 outcomes. Several AABs correlated with symptom severity in PCS groups. Remarkably, severity of fatigue and vasomotor symptoms were associated with ADRB2 AAB levels in PCS/ME/CFS patients. Our study identified dysregulation of AAB against various receptors involved in the autonomous nervous system (ANS), vaso-, and immunoregulation and their correlation with symptom severity, pointing to their role in the pathogenesis of PCS.

BackgroundInhibition of interleukin (IL)-1 represents a promising treatment option in adult-onset Still's disease (AOSD).ObjectiveTo investigate the efficacy and safety of canakinumab in patients with AOSD and active joint involvement by means of a multicentre, double-blind, randomised, placebo-controlled trial.MethodsPatients with AOSD and active joint involvement (tender and swollen joint counts of ≥4 each) were treated with canakinumab (4 mg/kg, maximum 300 mg subcutaneous every 4 weeks) or placebo. The primary endpoint was the proportion of patients with a clinically relevant reduction in disease activity at week 12 as determined by the change in disease activity score (ΔDAS28>1.2).ResultsAt enrolment, patients had high active disease with a mean DAS28(ESR) of 5.4 in the canakinumab and 5.3 in the placebo group, respectively. In the intention-to-treat analysis, 12 patients (67%) in the canakinumab group and 7 patients (41%) in the placebo group fulfilled the primary outcome criterion (p=0.18). In the per-protocol analysis, significantly higher American College of Rheumatology (ACR) 30% (61% vs 20%, p=0.033), ACR 50% (50% vs 6.7%, p=0.009) and ACR 70% (28% vs 0%, p=0.049) response rates were observed in the canakinumab group compared with the placebo group. Two patients in the canakinumab group experienced a serious adverse event.ConclusionAlthough the study was terminated prematurely and the primary endpoint was not achieved, treatment with canakinumab led to an improvement of several outcome measures in AOSD. The overall safety findings were consistent with the known profile of canakinumab. Thus, our data support indication for IL-1 inhibition with canakinumab in AOSD.

Background: The current subclassification of systemic sclerosis into cutaneous subtypes does not fully capture the heterogeneity of the disease. We aimed to compare the performances of stratification into LeRoy's cutaneous subtypes versus stratification by autoantibody status in systemic sclerosis. Methods: For this cohort study, we assessed people with systemic sclerosis in the multicentre international European Scleroderma Trials and Research (EUSTAR) database. Individuals positive for systemic-sclerosis autoantibodies of two specificities were excluded, and remaining individuals were classified by cutaneous subtype, according to their systemic sclerosis-specific autoantibodies, or both. We assessed the performance of each model to predict overall survival, progression-free survival, disease progression, and different organ involvement. The three models were compared by use of the area under the curve (AUC) of the receiver operating characteristic and the net reclassification improvement (NRI). Missing data were imputed. Findings: We assessed the database on July 26, 2019. Of 16 939 patients assessed for eligibility, 10 711 patients were included: 1647 (15·4%) of 10 709 were male, 9062 (84·6%) were female, mean age was 54·4 (SD 13·8) years, and mean disease duration was 7·9 (SD 8·2) years. Information regarding cutaneous subtype was available for 10 176 participants and antibody data were available for 9643 participants. In the prognostic analysis, there was no difference in AUC for overall survival (0·82, 95% CI 0·81–0·84 for cutaneous only vs 0·84, 0·82–0·85 for antibody only vs 0·84, 0·83–0·86 for combined) or for progression-free survival (0·70, 0·69–0·71 vs 0·71, 0·70–0·72 vs 0·71, 0·70–0·72). However, at 4 years the NRI showed substantial improvement for the antibody-only model compared with the cutaneous-only model in prediction of overall survival (0·57, 0·46–0·71 for antibody only vs 0·29, 0·19–0·39 for cutaneous only) and disease progression (0·36, 0·29–0·46 vs 0·21, 0·14–0·28). The antibody-only model did better than the cutaneous-only model in predicting renal crisis (AUC 0·72, 0·70–0·74 for antibody only vs 0·66, 0·64–0·69 for cutaneous only) and lung fibrosis leading to restrictive lung function (AUC 0·76, 0·75–0·77 vs 0·71, 0·70–0·72). The combined model improved the prediction of digital ulcers and elevated systolic pulmonary artery pressure, but did poorly for cardiac involvement. Interpretation: The autoantibody-only model outperforms cutaneous-only subsetting for risk stratifying people with systemic sclerosis in the EUSTAR cohort. Physicians should be aware of these findings at the time of decision making for patient management. Funding: World Scleroderma Foundation.

ObjectivesHand osteoarthritis (OA) is a condition characterised by cartilage degradation and frequently erosive changes. Analgesics and non-steroidal anti-inflammatory drugs are used for symptomatic relief but are often poorly tolerated or contraindicated. Previous publications suggest hydroxychloroquine (HCQ) as a possible treatment for hand OA. The OA-TREAT study aimed to investigate the efficacy and safety of HCQ in patients with inflammatory and erosive hand OA (EOA).MethodsOA-TREAT was an investigator-initiated, multicentre, randomised, double-blind, placebo (PBO)-controlled trial. Patients with inflammatory and EOA, according to the ACR criteria, with radiographically erosive disease were randomised 1:1 to HCQ 200–400 mg/day or PBO for 52 weeks (W52). Both groups received stable standard therapy. The primary endpoint was Australian Canadian Hand Osteoarthritis Index (AUSCAN) for pain and hand disability at W52.Results75 patients were randomised to HCQ and 78 to PBO. At W52, mean AUSCAN pain was 26.7 in HCQ and 26.5 in PBO patients (p=0.92). Hand disability measured by AUSCAN function (mean) was 48.1 in HCQ and 51.3 in PBO patients (p=0.36). Changes in radiographic scores did not differ significantly (p>0.05) between treatment groups. There were 7 serious adverse events in the HCQ and 15 in the PBO group.ConclusionsOA-TREAT is the first large randomised PBO controlled trial focusing on EOA. HCQ was no more effective than PBO for changes in pain, function and radiographic scores in the 52-week period. Overall safety findings were consistent with the known profile of HCQ.

Background:Hand osteoarthritis (OA) is a very common condition with cartilage degradation and frequently erosive bone changes. It may be very painful and can greatly affect everyday activities. Common analgesics and NSAIDs are used for symptomatic relief but are often poorly tolerated or contraindicated especially in elderly patients. There is no effective and proven disease modifying therapy available. Previous publications and anecdotal reports suggest hydroxychloroquine (HCQ) as a possible treatment, and some physicians use HCQ off-label for the treatment of OAObjectives:To investigate the efficacy and safety of HCQ in patients with inflammatoryanderosive hand OA in a randomized, double-blind, placebo controlled, multi-centre, investigator-initiated trialMethods:Patients with inflammatory and erosive hand OA, according to the ACR criteria, with radiographically proven erosive disease were randomized 1:1 to HCQ 200-400mg per day or matching placebo (PBO) for 52 weeks. Both groups received standard therapy (stable NSAIDs). The primary endpoint was AUSCAN for pain and hand disability at week 52 (W52). A secondary endpoint was radiographic progression from baseline (BL) to W52. A multiple endpoint test and analysis of covariance was used to compare changes between groups. All analyses were conducted on an intention-to-treat baseResults:Of 156 patients 3 were excluded and 75 were randomized to HCQ and 78 to PBO. Mean age was 52.4 (SD 8.1) in the HCQ and 50.2 (SD 6.6) years in the PBO group. 68 (90.7%) of the patients were female in the HCQ and 60 (76.9%) in the PBO group. Disease duration was 9.5 (SD 7.5) in HCQ and 10.8 (SD 8.8) years in PBO group. CRP and ESR were normal in both groups. BL pain (AUSCAN) was 31.1 (SD 8.2) and 30.7 (SD 8.9), BL function (AUSCAN) was 58.5 (SD 15.5) in HCQ and 57.8 (SD 17.1) in PBO patients. Table 1 shows clinical and functional parameters at W52. Only morning stiffness was significantly reduced in the HCQ group (p=0.001). Changes in radiographic scores did not differ significantly (p>0.05) between treatment groups. There were 7 SAE in the HCQ and 15 in the PBO group. No new safety issues were detectedTable 1.Results of the covariance analysis (ANCOVA)-adjusted mean values and 95%-confidence intervals for primary and secondary outcomes at W52, as well as a p-value for group comparisonOutcomeAdj. Mean HCQ95%-CI HCQAdj. Mean PBO95%-CI PBOP-value HCQ x PBOAUSCAN Function48.14353.351.346.6560.36AUSCAN Pain26.723.929.426.523.929.10.92tender joint6.44.87.97.15.48.70.49swollen joint21.32.72.11.42.70.93ESR (mm/h)8.26.99.611.710.113.5HAQ0.90.810.80.70.90.46Phys. Global3.22.83.63.533.90.39Pat. Global4.53.95.15.24.65.80.14SF36 mental48.846.65150.848.752.80.22SF36 physical39.83841.639.938.241.60.95Morning Stiffness (min)30.22436.316.310.322.30.001Modif. Kallmann Score53.652.155.152.851.454.20.24The associated BL value or, if available, a mean value from BL and screening was included in the ANCOVA model as a covariate.Conclusion:The OATREAT trial examined the clinical and radiological efficacy and safety of HCQ as a treatment option for inflammatory and erosive OA over 52 weeks. OATREAT is the first large randomized PBO controlled trial focusing on erosive hand OA. HCQ was no more effective than PBO for changes in pain, function and radiographic scores in the 52-week period. Overall safety findings were consistent with the known profile of HCQ. Thus, our data failed to show that HCQ is effective in patients with inflammatory, erosive hand OADisclosure of Interests:Claudia Kedor Consultant of: Advisory Board for Novartis Pharma GmbH, Jacqueline Detert: None declared, Rolf Rau: None declared, Siegfried Wassenberg: None declared, Joachim Listing: None declared, Pascal Klaus Employee of: Pfizer Pharma GmbH, Tanja Braun: None declared, Walter Hermann: None declared, Stefan Weiner: None declared, Martin Bohl-Bühler: None declared, Frank Buttgereit Grant/research support from: Amgen, BMS, Celgene, Generic Assays, GSK, Hexal, Horizon, Lilly, medac, Mundipharma, Novartis, Pfizer, Roche, and Sanofi., Gerd Rüdiger Burmester Consultant of: AbbVie Inc, Eli Lilly, Gilead, Janssen, Merck, Roche, Pfizer, and UCB Pharma, Speakers bureau: AbbVie Inc, Eli Lilly, Gilead, Janssen, Merck, Roche, Pfizer, and UCB Pharma

Muraviov and Muraviova are asking for further1 elucidation of the chosen endpoints and a more detailed characterisation of the included patients in our study of canakinumab for the treatment of patients with adult-onset Still’s disease (AOSD) with articular involvement.2 As mentioned in our previous communication, at the time of Canakinumab for treatment of adult ONset StIll’s Disease to achiEve Reduction of arthritic manifestation (CONSIDER) trial conception in 2012, there were no approved drugs and no validated scores available for AOSD. On the other hand, accumulating evidence suggested that inhibition of Interleukin-1 (IL1) could be beneficial for the patients.2–5 Thus, our aim was to investigate the effects of canakinumab in a controlled setting to provide convincing data, which could even be useful for regulatory …

We would like to thank Ruscitti et al 1 for their interest in our recent publication, in which we presented the results of the Canakinumab for treatment of adult onset Still‘s disease to achieve reduction ofarthritic manifestation (CONSIDER) trial. In this study, we investigated the efficacy of canakinumab for the treatment of patients with adult-onset Still’s disease (AOSD) with articular involvement (tender and swollen joint counts≥4 each) by means of a multicentre, double-blind, randomised, placebo-controlled trial.2 Patients were randomised to receive either canakinumab 4 mg/kg body weight (maximum 300 mg) every 4 weeks or placebo. According to the study goal, the primary endpoint was defined as the proportion of patients with a clinically relevant reduction in Disease Activity Score (DAS 28 >1.2) at week 12. Since no controlled studies existed in this indication at that time of the study initiation, we were not able to base our statistical considerations on known facts of response rates to placebo or any immunosuppressive regimen. After careful consideration, our sample size calculation indicated that it requires a total of n=68 randomised patients to show a significant difference between the groups. …

Background:Inhibition of interleukin-1 (IL-1) represents a promising treatment option in adult-onset Still’s disease (AOSD). Canakinumab is approved for treatment of systemic juvenile idiopathic arthritis and has a marked impact on systemic as well as articular activity of the disease.Objectives:To investigate the efficacy and safety of canakinumab in patients with AOSD and active joint involvement by means of a multi-centre, double-blinded, randomized, placebo controlled trial over a period of 24 weeks with the option of a long-term extension.Methods:Patients with AOSD and active joint involvement (tender and swollen joint count ≥4 each) were stratified by pre-treatment status with biologic DMARDs to canakinumab (4 mg/kg, maximum 300 mg s.c. q4w) or placebo. After approval of canakinumab for AOSD by the European Medicines Agency, recruitment was stopped prematurely with enrollment of 35 out of 68 planned patients. The primary endpoint was the proportion of patients with a clinically-relevant reduction in disease activity at week 12 as determined by the change in disease activity score (ΔDAS28 >1.2).Results:At enrollment, patients had high active disease with a mean DAS28(ESR) of 5.4 in the canakinumab group (n=18, [CI 43.1; 85.2]) and 5·3 in the placebo group (n=17, [CI 20.1; 65.0]). In the intention-to-treat analysis, 12 (67%) canakinumab and 7 (41%) placebo patients fulfilled the primary outcome criterion (p=0.18). Figure 2 shows the DAS28-ESR disease activity by treatment groups and visits with imputation. In the per-protocol analysis, significantly higher ACR30 (61% vs. 33% p=0.033), ACR50 (50% vs. 6.7% p= 0.009) and ACR70 (28% vs. 0% p=0.049) response rates were observed in the canakinumab group compared with placebo (Figure 1). Two patients in the canakinumab group experienced an SAE.Figure 1.Response rates (PP)Figure 2.DAS28-ESR disease activity by treatment groups and visits with imputationConclusion:Although the study was terminated prematurely and the primary endpoint was not achieved, treatment with canakinumab led to an improvement of several outcome measures in AOSD. The overall safety findings were consistent with the known profile of canakinumab. Thus, our data support indication for IL-1 inhibition with canakinumab in AOSD.References:[1]Nirmala N et al. Gene-expression analysis of AOSD and SJIA is consistent with a continuum of a single disease entity. Pediatr Rheumatol Online J. 2015P-values are shown above each pair of bars; P-values in red are significant ACR, American College of Rheumatology; CRP, C-reactive protein; DAS, disease activity score; EULAR, European League Against Rheumatism; PP, per-protocolDisclosure of Interests:Claudia Kedor Consultant of: Advisory Board for Novartis Pharma GmbH, Joachim Listing: None declared, Jan Zernicke: None declared, Anja Weiß: None declared, Frank Behrens Grant/research support from: Abbvie, Pfizer, Roche, Chugai, Janssen, Consultant of: Abbvie, Pfizer, Roche, Chugai, UCB, BMS, Celgene, MSD, Novartis, Biotest, Janssen, Genzyme, Lilly; Boehringer; Sandoz, Speakers bureau: Abbvie, Pfizer, Roche, Chugai, UCB, BMS, Celgene, MSD, Novartis, Biotest, Janssen, Genzyme, Lilly; Boehringer; Sandoz, Norbert Blank Grant/research support from: Novartis, Sobi, Consultant of: Novartis, Sobi, Lilly, Pfizer, Abbvie, BMS, MSD, Actelion, UCB, Boehringer-Ingelheim, Roche, Jörg Henes Grant/research support from: Novartis, Roche-Chugai, Consultant of: Novartis, Roche, Celgene, Pfizer, Abbvie, Sanofi, Boehringer-Ingelheim,, Jörn Kekow Speakers bureau: BMS, MSD, Pfizer, Roche, Andrea Rubbert-Roth Consultant of: Abbvie, BMS, Chugai, Pfizer, Roche, Janssen, Lilly, Sanofi, Amgen, Novartis, Hendrik Schulze-Koops Grant/research support from: Pfizer Inc, Eva Seipelt: None declared, Christof Specker Consultant of: Abbvie, Boehringer Ingelheim, Chugai, Lilly, Novartis, Sobi, UCB, Celgene, Janssen-Cilag, MSD, Pfizer, Roche, UCB, Toshiba, Eugen Feist Consultant of: Novartis, Roche, Sobi, Lilly, Pfizer, Abbvie, BMS, MSD, Sanofi, Speakers bureau: Novartis, Roche, Sobi, Lilly, Pfizer, Abbvie, BMS, MSD, Sanofi

Background:Abatacept (CTLA4-Ig) is a biological DMARD (bDMARD) for treatment of rheumatoid arthritis (RA) and selectively modulates the co-stimulatory signal by CD28: CD80/CD86 interaction required for T cell activation. CD28 mediated signaling regulates many T cell functions including cytokine production. The role of proteasome was approved in many autoimmune diseases, and the effect of Abatacept on modifying cytokines including interferon-γ that alters proteasome proteolytic activities was shown in RA.Objectives:To characterize the effect of Abatacept on the expression and proteolytic activity of the immunoproteasome.Methods:Effects of Abatacept on the proteasome system were investigated in 39 patients with rheumatoid arthritis over a period of 24 weeks. Using real time PCR, transcript expression levels of constitutive and corresponding immunoproteasome catalytic subunits were investigated at baseline (T0), week 16 (T16) and week 24 (T24) in sorted blood cells. Proteasomal activity and induction of apoptosis after proteasome inhibition were also evaluated in cellular subsets.Results:Upon treatment with Abatacept, remission or low disease activity according to DAS28 was achieved in 55 % of patients at T16 and in 70 % at T24. By Two- (time and type of response) way ANOVA, a significant reduction of proteasome immunosubunit β1i expression was shown only in CD4+ and CD8+ T cells of prolonged responders at both T16 and T24 (P= 0.0390 andP= 0.0198, respectively). One-way ANOVA analysis for each response group separately confirmed the results and showed significant reduction at T24;P= 0.0396 difference between T0 and T24,P= 0.0260 between T16 and T24 in CD4+ T cells of the same group. Abatacept did not influence chymotrypsin like activity of proteasome, which is carried out by the subunit β5i and had no effect on induction of apoptosis under exposure to a proteasome inhibitor in-vitro.Conclusion:Treatment with Abatacept showed a clear effect on the expression of the proteasome immunosubunit β1i. This phenomenon was only seen in CD4+ and CD8+ T cells of prolonged responding patients with RA suggesting an association between persistent induction of β1i and failure to the T cell directed therapy with Abatacept.References:[1]Keating, G.M., Abatacept: A Review of its Use in the Management of Rheumatoid Arthritis. Drugs, 2013. 73(10): p. 1095-1119.[2]Ferrington, D.A. and D.S. Gregerson, Immunoproteasomes: Structure, Function, and Antigen Presentation. Progress in molecular biology and translational science, 2012. 109: p. 75-112.[3]Marti, L., et al., Alterations in Cytokine Profile and Dendritic Cells Subsets in Peripheral Blood of Rheumatoid Arthritis Patients before and after Biologic Therapy. Annals of the New York Academy of Sciences, 2009. 1173: p. 334-42.Disclosure of Interests:Khetam Ghannam: None declared, Lorena Martinez Gamboa: None declared, Claudia Kedor Consultant of: Advisory Board for Novartis Pharma GmbH, Lydia Spengler: None declared, Gerd Rüdiger Burmester Consultant of: AbbVie Inc, Eli Lilly, Gilead, Janssen, Merck, Roche, Pfizer, and UCB Pharma, Speakers bureau: AbbVie Inc, Eli Lilly, Gilead, Janssen, Merck, Roche, Pfizer, and UCB Pharma, Eugen Feist Consultant of: Novartis, Roche, Sobi, Lilly, Pfizer, Abbvie, BMS, MSD, Sanofi, Speakers bureau: Novartis, Roche, Sobi, Lilly, Pfizer, Abbvie, BMS, MSD, Sanofi

Objective.Regulatory T cells are characterized by expression of the transcription factor FoxP3 and are thought to be involved in the pathogenesis of autoimmune diseases. We determined the frequency and phenotypic characteristics of CD4+FoxP3+ T cells in the blood and synovial fluid (SF) of patients with inflammatory joint diseases.Methods.SF from 10 patients with ankylosing spondylitis (AS), 20 patients with other spondyloarthritides or with peripheral arthritis (pSpA), and 12 patients with rheumatoid arthritis (RA), and peripheral blood (PB) from 22 patients with AS, 19 with pSpA, 15 with RA, and 12 healthy controls were stained for CD4, FoxP3, CD25, and CD127 and different effector cytokines and then analyzed by flow cytometry. Methylation pattern of the Treg-specific demethylated region (TSDR) was determined after bisulfite treatment by quantitative polymerase chain reaction.Results.In all groups of patients we observed higher frequencies of Foxp3+ cells/CD4+ T cells within SF compared to PB. The frequency of synovial Foxp3+ cells/CD4+ T cells was significantly higher in patients with pSpA (18.79% ± 6.41%) compared to patients with AS (9.69% ± 4.11%) and patients with RA (5.95% ± 2.21%). CD4+FoxP3+ T cells were CD25+ and CD127− and lacked effector cytokine production in any of the different patient groups. The majority of the CD4+CD25+CD127− T cells showed demethylation of the TSDR within the Foxp3 locus, confirming its regulatory phenotype.Conclusion.Our data show accumulation of Foxp3+ T cells within inflamed joints. These Foxp3+ T cells are mainly of stable T regulatory phenotype. The high frequency of Foxp3+ T cells in pSpA might contribute to the spontaneous resolution and remitting course of arthritis in pSpA as compared to the more persistent joint inflammation in RA.

Background Physical exercises and physiotherapy are of high importance for maintenance of joint function in patients with rheumatoid arthritis (RA). However, many RA patients complain about problems to receive prescriptions for or lack of access to physical therapy. Recent reports have shown positive effects of the Wii™ game console (Nintendo®) on physical and psychosocial conditions of patients with other underlying diseases. In fact, a home-based animated physical exercise program could be cost-effective, freely available and adjustable to the individual situation. Objectives To investigate practicability and effects of an animated home-based exercise program for RA patients treated with biologic DMARDs. Methods This study was conducted as an investigator initiated, not manufacturer supported, single-center, cross-over trial with two treatment arms over 24 weeks. Eligibility criteria included patients with RA with low disease activity according to DAS28 under biological DMARD therapy. After detailed instruction, 10 patients started with a conventional home-based physical exercise program and 10 patients with the animated exercise program by using the Wii™ game console for 12 weeks. Afterwards, patients were crossed over to the other treatment arm for another period of 12 weeks. A multi-methodical approach was used for this study: A qualitative analysis of the interview-data was performed by interpretation and inter-individual comparison of given answers. Measurements for muscle strength (isometric measurement) and 6-minute walk test (6-MWT) were compared from Baseline to week 12 and week 24. Statistical computing was performed with SPSS using the 9Analysis of Covariance9 (ANCOVA), adjusted for baseline status. Results We evaluated data from 20 patients (17 females) with a mean age of 55,5 (±9) years. More than 14 hours of interview data were transcribed and analyzed. By using a special software for coding patients response, categories were identified indicating practicability and easy accessibility. Of note, mainly fore foot disabilities were described as limiting factors for performing some exercises of the program. Many patients stated a positive influence by the game console on their perseverance to doing exercises. Over the observation period, both groups showed a clear benefit from the exercise programs and the analysis of test results showed no significant differences between both treatment arms after 12 weeks: Muscle strength improved by mean of 11 N (increase of 13% from baseline) with a non-significant difference of 3 N between both groups (p=0,64). The mean 6-MWT distance was increased by 50 meters (increase of 9% from baseline) without a relevant difference between both groups (p=0,73). Results from week 24 suggested that beginning with the home based physical exercise program followed by a subsequent Wii™ game console program was the most effective program. Conclusions This study showed that an animated home-based exercise program by using a Wii™ game console was beneficial for RA-Patients. Compared to standard physical home exercises, similar effects in both treatment groups were observed indicating that such an animated and well received program might be an alternative or additional option for RA-patients depending on their own preferences. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.2305