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Recurrent FUO (fever of unknown origin) is a rare subtype of FUO for which diagnostic procedures are ill-defined and outcome data are lacking. We performed a retrospective multicentre study of patients with recurrent FUO between 1995 and 2018. By multivariate analysis, we identified epidemiological, clinical and prognostic variables independently associated with final diagnosis and mortality. Of 170 patients, 74 (44%) had a final diagnosis. Being ≥ 65 years of age (OR = 5.2; p < 0.001), contributory history (OR = 10.4; p < 0.001), and abnormal clinical examination (OR = 4.0; p = 0.015) independently increased the likelihood of reaching a diagnosis, whereas lymph node and/or spleen enlargement decreased it (OR = 0.2; p = 0.004). The overall prognosis was good; 58% of patients recovered (70% of those with a diagnosis). Twelve (7%) patients died; patients without a diagnosis had a fatality rate of 2%. Being ≥ 65 years of age (OR = 41.3; p < 0.001) and presence of skin signs (OR = 9.5; p = 0.005) significantly increased the risk of death. This study extends the known yield of recurrent FUO and highlights the importance of repeated complete clinical examinations to discover potential diagnostic clues during follow-up. Moreover, their overall prognosis is excellent.

Background: Anti-filaggrin antibodies (AFA) are among the most specific antibodies for rheumatoid arthritis, so procedures for their detection should be included in early biological diagnoses. AFA can be detected by indirect immunofluorescence (anti-keratin antibodies, AKA) or by new enzyme immunoassays (EIA). Their comparative performance needs to be established. Objective: To compare these technical procedures to optimise the serological diagnosis of rheumatoid arthritis. Methods: Results obtained using AKA and EIA were compared in 271 sera from 140 patients with rheumatoid arthritis at various stages, 98 patients with other autoimmune diseases, and 33 healthy subjects. EIA were successively undertaken with citrullinated linear filaggrin peptide (home made EIA) or cyclic citrullinated peptide (CCP2, commercial kits). Rheumatoid factor (RF) was assessed by EIA in all patients. Results: Anti-CCP2 kits showed the best sensitivity and specificity (65% and 96%, respectively). Among the 140 patients with rheumatoid arthritis, those with very recent disease (less than six months’ duration, n = 21) were studied as a separate group. In this group, the sensitivity of anti-CCP2 kits decreased to ~50%. Nevertheless this assay remained the most accurate when compared with AKA or home made EIA using linear filaggrin peptides. The combination of anti-CCP2 and RF only slightly increased the sensitivity of the diagnosis of very early rheumatoid arthritis. Conclusions: Kits using citrullinated cyclic peptides (CCP2) were more suitable than either AKA or EIA using linear filaggrin peptides for the diagnosis of early rheumatoid disease.

Objectives The objective of this report is to investigate the feasibility of collecting patient-reported outcomes (PROs) via e-questionnaires delivered to patients with chronic inflammatory diseases (CIDs). Methods Consecutive outpatients with a confirmed diagnosis of systemic lupus erythematosus, primary Sjögren’s syndrome or inflammatory bowel disease were followed at two medical departments. Patients received monthly e-mails containing the SF36, Hospital Anxiety and Depression scale and an analogue symptom scale over a six-month period. Participation rate, socio-demographic characteristics and patients’ satisfaction were analysed. Results A total of 128 patients were included (79% female; mean age: 42 ± 12 years). Eighty-two per cent of questionnaires were returned. The monthly participation rate ranged from 89% to 77%, with a six-month attrition rate of 13%. The mean completion rate of questionnaires was 98%. Factors significantly associated with increased answer rate were: married/couple status, greater number of children at home and previous participation in online surveys. The main reasons for non-response were: ‘too busy to participate’ (35%) and ‘away from home Internet access’ (31%). Overall, 68% of the participants found the study convenient and 96% agreed to continue at a monthly or bimonthly frequency. Conclusion Online home self-assessment of PROs was feasible in the setting of CIDs. Patients were satisfied and willing to continue the survey. The Internet allows immediate and sophisticated presentation of PROs to clinicians. Future studies are warranted to determine how PRO monitoring may contribute to routine care in CIDs and other diseases.

BackgroundGiant cell arteritis (GCA) is the most common systemic vasculitis that triggers acute arterial occlusion and can even lead to death over the age of 50 [1]. While mechanism underlying GCA are predominantly derived from inflammatory response, none of the anti-inflammatory drugs currently used limit efficiently patient’s disease course. It was previously shown that histopathological lesions involve the three layers of the artery wall called adventitia, media, and intima. Activation of adventitial dendritic cells is the initial trigger of the vascular remodeling in GCA leading to intimal hyperplasia but the early molecular mechanism that activates those cells remains unknown. Our hypothesis is that each layer of the artery, perivascular tissue included, shows a unique transcriptomic signature which could define and explain the different molecular events in the inflammatory and vascular remodeling processes in GCA. For that, whole tissue spatial transcriptomics analysis offers advanced opportunities in elucidating functional mechanisms of pathologic tissues with complex organization such as GCA especially in human temporal artery, the most frequently affected artery in GCA.ObjectivesUncover the key coding genes to define new biomarkers or pathways associated with GCA by performing the first in situ spatial profiling characterization of molecular actors involved in temporal arteries from GCA patients in comparison to normal arteries.MethodsFrom human formalin-fixed paraffin-embedded temporal artery biopsy samples (GCA n=9; controls n=7), we performed a whole transcriptome analysis by using NanoString GeoMx Digital Spatial Profiler (DSP) [2]. A total of 59 individual regions of interest (ROIs) were created within each of the 4 layers for each individual artery. After ROIs collection and library construction, samples were sequenced on the Illumina NovaSeq 6000 platform and reads were digitally quantified and normalized using GeoMx DSP Data Analysis software. Differential expressed genes (DEGs) (fold change >2 or <-2, p-adjusted <0.05) were compared for each layer, to build a spatial and pharmacogenomic network in disease course.ResultsOverall, we found that most of the transcriptome studied (12076 genes) was upregulated in GCA arteries. Precisely, 350, 340, 142 and 5 DEGs were found in intima, media, adventitia, and perivascular tissue respectively. Enrichment analysis highlighted that inflammation/immune-related functions and vascular remodeling were significantly limited to intima and media layers. Upregulated immune-related functions concerned macrophage differentiation & T cell, B cell, complement activations. Regarding vascular remodeling pathways, we found an upregulation of: (i) collagen metabolic process and fibroblast proliferation concerning the 3 artery layers, (ii) angiogenesis & epithelial cell migration in intima and media layers, (iii) smooth muscle cell proliferation & ossification in intima layer. Our pharmacogenomic network analysis identified genes that could potentially be targeted by immunosuppressive drugs currently approved or new immunotherapies.ConclusionOur findings provide the first in situ spatial profiling characterization of molecular actors involved in GCA which is essential for the discovery of potential new therapeutic targets to cure this disease. The differential spatial upregulation of genes involved in inflammatory process and vascular remodeling suggests a differential chronological involvement of each layer of the artery.References[1]Weyand CM, Goronzy JJ. Clinical practice. Giant-cell arteritis and polymyalgia rheumatica. N Engl J Med. 2014 371:50-7.[2]Merritt CR, Ong GT, Church SE, Barker K, Danaher P, Geiss G, et al. Multiplex digital spatial profiling of proteins and RNA in fixed tissue. Nat Biotechnol. 2020 38:586-599.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

Background:Sjögren’s disease (SjD) is a heterogenous autoimmune disease, with a wide range of symptoms, from dryness, fatigue, pain, to systemic manifestations, and an increased risk of lymphoma. Recently, three clusters of patients with SjD have been described based on unsupervised clustering analysis according to symptoms, clinical signs and biologic parameters: 1/ BA-LS (B-cell active with low symptoms); 2/ HSA (High systemic activity); 3/ LSA-HS (Low systemic activity with high symptoms). These findings suggest potential heterogeneity in pathophysiological mechanisms.Objectives:To investigate this hypothesis, we examined whether these three clusters were associated with distinct biomarkers.Methods:This study involved SjD patients meeting AECG criteria from the ASSESS cohort. The following biomarkers were measured in sera at the time of inclusion: for IFN pathways—IFN-alpha 2, IFN gamma, CXCL-10; for B cell activation—CXCL-13, BAFF, B2-microglobulin, FLT-3; for T cell activation—IL-7, CCL-19, TNF-RII. Additionally, the IFN signature was assessed using transcriptomic analysis. Kruskal-Wallis rank sum test was used to compare different clusters for continuous variables. Additionally, the risk of lymphoma and of new immunosuppressive drugs prescriptions were compared according to the IFN signature.Results:This analysis included 395 (94% female, median age 53 [43-63] years) patients from the ASSESS cohorts. The three clusters displayed differences in the IFN pathways (IFN signature), primarily driven by type I IFN (IFN-a2 level) elevated only in BA-LS and HSA clusters and not in the LSA-HS cluster (p=0.001). IFN gamma and CXCL-10 were not different between the 3 clusters.The same clusters that exhibit high level of type 1 IFN also had higher CXCL-13 levels (p=0.0032) reflecting B-cell activation, higher IL-7 (p=0.0042) and TNFRII (p<0.001) levels reflecting T-cell activation. Higher levels of FLT-3 were found in the HSA cluster. BAFF level was not different between the 3 clusters.Lastly, there were a trend indicating an increased risk of lymphoma in patients with positive IFN signature (HR 2.53; 95%CI 0.67–9.55), and an increased risk of immunosuppressant prescription during follow-up (HR 2.81; 95%CI 1.26-6.29).Conclusion:The two clusters BA-LS and HSA have a very distinct cytokine signature than the patients with LSA-HS. These two active clusters share a high type 1 IFN level, and elevated markers of both B-cell and T-cell activation. Patients from the BA-LS cluster being younger, it is likely that this cluster represent an earlier disease stage than HSA cluster. In order to go towards personalized medicine, work is in progress for deciphering patients in these two active clusters exhibiting one predominant pathways among type 1 IFN, B-cell and T-cell activation.REFERENCES:[1] Nguyen Y, Nocturne G, Henry J. Identification of distinct phenotypes of Sjögren disease by cluster analysis based on clinical and biological manifestations: data from the cross-sectional Paris-Saclay and the prospective ASSESS cohorts. Lancet Rheumatology 2024.Acknowledgements:The authors are indebted to all patients for their participation, and to all physicians who included patients in the Paris-Saclay and ASSESS cohorts. The Assessment of Systemic Signs and Evolution in Sjögren’s Syndrome (ASSESS) national multicenter prospective cohort was formed in 2006 with a French Ministry of Health grant (Programme Hospitalier de Recherche Clinique 2005 P060228). The ASSESS cohort is promoted by the French Society of Rheumatology and receives research grants from the French Society of Rheumatology.Disclosure of Interests:Yann Nguyen: None declared, Xavier Mariette Xavier Mariette received consulting fees from Astra Zeneca, Bristol Myer Squib, Galapagos, GSK, Novartis and Pfizer, Maxime Beydon: None declared, Divi Cornec: None declared, Jacques-Olivier Pers: None declared, Jacques MorelJacques Morel received honoraria from Abbvie, Boehringer Ingelheim, Biogen, Lilly, Mylan, Pfizer, Sanofi, Bristol Myers Squib, Fresenius Kabi, Galapagos, Medac, Novartis, Roche Chugai;,Jacques Morel received grants from Bristol Myers Squib, Fresenius Kabi, Lilly, Novartis, Pfizer, and Roche-Chugaï;, Aleth PERDRIGER: None declared, Emmanuelle Dernis Emmanuelle Dernis received consulting fees from BMS, Celgène, Lilly, MSD, Novartis, UCB; honoria for lectures from Abbvie, BMS, Janssen, Lilly, Medac, MSD, Novartis, Roche-Chugaï, Sanofi, UCB, Celgène, Amgen, Galapagos;, Valerie Devauchelle-Pensec: None declared, Damien Sene: None declared, Philippe Dieudé Philippe Dieudé received consulting fees from Pfizer, Roche Chugai, Bristol Myers Squibb, Abbvie, MSD., Philippe Dieudé received grants from Novartis, Marion Couderc: None declared, Anne-Laure Fauchais: None declared, Claire Larroche: None declared, Olivier Vittecoq: None declared, Carine Salliot Carine Salliot received Honoria from Novartis, Roche Chugaï, Eric Hachulla: None declared, Véronique Le Guern: None declared, Jacques-Eric Gottenberg Jacques-Eric Gottenberg consulting fees from Abbvie, Astra Zeneca, Sanofi, Lilly, Galapagos, Gilead, Roche Chugai, Pfizer, Bristol Myer Squib, MSD., Jacques-Eric Gottenberg received grants from Pfizer, Abbvie, Lilly, Raphaèle Seror Raphaèle Seror received consulting fees from GSK, Bristol Myer Squib, Boerhinger and Janssen; honoraria from GSK, Bristol Myer Squib, Boehringer, Amgen, Pfizer and Roche; travel fees from Amgen and GSK;, Gaetane Nocturne: None declared.

B-cell chronic lymphocytic leukemia (B-CLL) cells are resistant to apoptosis, and consequently accumulate to the detriment of normal B cells and patient immunity. Because current therapies fail to eradicate these apoptosis-resistant cells, it is essential to identify alternative survival pathways as novel targets for anticancer therapies. Overexpression of cell-surface G protein-coupled receptors drives cell transformation, and thus plays a critical role in malignancies. In this study, we identified neurotensin receptor 2 (NTSR2) as an essential driver of apoptosis resistance in B-CLL. NTSR2 was highly expressed in B-CLL cells, whereas expression of its natural ligand, neurotensin (NTS), was minimal in both B-CLL cells and patient plasma. Surprisingly, NTSR2 remained in a constitutively active phosphorylated state, caused not by a mutation-induced gain-of-function but rather by an interaction with the oncogenic tyrosine kinase receptor TrkB. Functional and biochemical characterization revealed that the NTSR2–TrkB interaction acts as a conditional oncogenic driver requiring the TrkB ligand brain-derived neurotrophic factor (BDNF), which unlike NTS is highly expressed in B-CLL cells. Together, NTSR2, TrkB and BDNF induce autocrine and/or paracrine survival pathways that are independent of mutation status and indolent or progressive disease course. The NTSR2–TrkB interaction activates survival signaling pathways, including the Src and AKT kinase pathways, as well as expression of the anti-apoptotic proteins Bcl-2 and Bcl-xL. When NTSR2 was downregulated, TrkB failed to protect B-CLL cells from a drastic decrease in viability via typical apoptotic cell death, reflected by DNA fragmentation and Annexin V presentation. Together, our findings demonstrate that the NTSR2–TrkB interaction plays a crucial role in B-CLL cell survival, suggesting that inhibition of NTSR2 represents a promising targeted strategy for treating B-CLL malignancy.

BackgroundPrimary Sjögren syndrome (pSS) is a systemic autoimmune disease that may complicate with pulmonary manifestations in up to 16% of patients [1], including interstitial lung disease (SS-ILD) and airway disease (SS-AD).ObjectivesTo assess the associated factors with SS-ILD and SS-AD.Secondary objectives: to describe these manifestations and to investigate their prognosis.MethodsWe performed a retrospective multicentric study involving 9 French centers. We included pSS patients fulfilling the ACR/EULAR 2016 criteria and having a pulmonary disease associated with pSS evidenced by at least one clinician and one computed tomography (CT) report. We collected clinical and biological data at the visit giving access to the most exhaustive collection, pulmonary function test (PFT) and CT scans of the patients. CT scans were reviewed by a radiologist specialist in thoracic diseases. SS-ILD were considered progressive if there were at least a 10% decrease of the forced vital capacity (FVC) between 2 consecutive measurements. SS-ILD and SS-AD were compared to pSS controls with no history of pulmonary involvement, matched on age and disease duration with a 2/1 ratio.ResultsWe included 56 SS-ILD, 31 SS-AD and 174 pSS controls. Comparison of SS-ILD, SS-AD and pSS controls is shown in Table 1. We found that SS-ILD and SS-AD had higher disease activity (ESSDAI) and B cell biological markers at visit time. Incident lymphomas were more prevalent in SS-ILD.SS-ILD were mostly nonspecific interstitial pneumonia (NSIP, n=16, 36%), usual or probable usual interstitial pneumonia (UIP, n=8, 18%), indeterminate for UIP (n=8, 18%) and lymphoid interstitial pneumonia (LIP, n=4, 9%). Fibrosis features were observed in 43% of cases. 44% of SS-ILD were progressive, independently of pSS characteristics and CT pattern, despite any significant evolution of PFT parameters of overall SS-ILD within 7 years follow-up (Figure 1A).We indirectly assessed the impact of the first line of systemic treatments in SS-ILD comparing PFT evolution of treated (43%) and untreated patients. We found that treated SS-ILD tended to have reduce PFT deterioration than non-treated patients with a 6 years follow-up [especially FVC and total lung capacity (TLC)], with a trend to improved FVC and forced expiratory volume (FEV1) with cyclophosphamide and rituximab (Figure 1C-D).SS-AD were mostly diffuse, associating bronchiolitis and bronchiectasis in 60% of cases. Here again, we did not find a significant worsening of PFT parameters with 9 years follow-up in SS-AD (Figure 1B), despite CT abnormalities worsening in 41% of cases at 6 years.Table 1.Comparison between SS-ILD, SS-AD and pSS controlSS-ILD, n=56pSS control, n=112SS-AD, n=31pSS control, n=62Clinical feature:Age, mean56565656Women49 (87)103 (92)30 (97)58 (93)Death7 (13)7 (6)2 (7)3 (5)Muscular7 (13)*3 (3)3(10)3 (5)Splenomegaly5 (9)*1 (1)2 (6)2 (3)ESSDAI, mean16*410*4ESSDAI (pulmonary excluded), mean9*47*4Incident lymphoma5 (9)*01(3)0Biology:Anti-SSA41 (76)*66 (59)21 (70)38 (65)Anti-RNP11 (22)*2 (2)01 (2)Gammaglobulinemia, mean23*181918Beta2-microglobulinemia, mean3*23*2Data are n (%) unless otherwise indicated. Stars indicate significant comparisons to pSS control. Mann-Whitney and Fisher’s exact test were used. *: p<0.05.Figure 1.PFT evolution of SS-ILD and SS-ADComparison of baseline and last follow-up PFT of SS-ILD (A) and SS-AD (B). Delta between last follow-up and baseline PFT of treated compared to untreated SS-ILD (C). Delta between post-therapeutical and pre-therapeutical PFT for cyclophosphamide and rituximab (D). Wilcoxon test was used. *: p<0.05.ConclusionSS-ILD are usually fibrosing and progressive manifestations of pSS, associated with disease activity, incident lymphoma and B cell biological markers. Despite the absence of randomized trials in SS-ILD, our results suggest an effect of the therapeutics. SS-AD are also associated with the disease activity and seems to progress slowly.Reference[1]Ramos-Casals et al., Rheumatology. 2015;54(12):2230‑8.AcknowledgementsThe authors would like to thank all the investigators of the ASSESS cohort for their contribution to this study.Disclosure of InterestsNone Declared.

BackgroundGlucocorticoids (GC) remain the mainstay of treatment for patients with GCA. However, relapses and recurrences (events) occurred in 34% to 74.5% of the patients.1–3 Most studies compared mainly patients with disease relapses/recurrences to whom without any.ObjectivesTo compare patients who had multiple events to those who presented only one in order to identify characteristics and predictive factors of multiple events in patient with GCAMethodsFrom 1976 to 2016, we collected prospectively clinical, laboratory, and pathological data, and the treatments and outcomes, of consecutive patients who were diagnosed to have GCA based ACR classification criteria. We compared these data in patients who had more than one event (group 1), either a relapse or a recurrence, to those who had only one (group 2). Relapse was defined as occurrence of clinical symptoms and/or inflammatory parameters, attributable to GCA, which required increased medication during follow-up i.e. under GC therapy while new disease activity after a period of remission was defined as a recurrence.ResultsWe included 494 patients for whom data was collected. Forty-seven patients were excluded from our cohort due to lack of data. Among the 447 patients, 228 (51%) presented at least one event. Mean age of this population was 73,3±7 years with female predominance (70%). The median follow-up was 75±55 months. Among these patients 139 (61%) had only one event while 89 (39%) presented more than one. The total number of events was 477 of which 89 recurrences. Events occurred during the first year of treatment in 74% of patients. The majority of these events occurred with a mean prednisone dose of 12.8±9 mg/day (median dose 10 mg/d). In univariate analysis, significant differences between both groups is illustrated in table 1. Multivariate analysis showed that ear pain and an elevated ESR were predictive factors of multiple events (OR: 2,45 and 1,93; p=0,04 and p=0,03 respectively). We also found that this risk is lower in patients over 80 years-old (OR: 0,35, p=0,008)Abstract SAT0536 – Table 1CharacteristicGroup 1 (>1; n=89)Group 2 (=1; n=139)P Age (years)72,6775,340.011Cough (%)20,710,90.042Ear pain (%)19,59,40.029PMR (%)11,34,30.041Duration of CS (m)53,726,30.0001Complications of CS(%)28,4160.024Steroid sparing treatment(%)30,717,80.024Remission(%)35,662,10.0001Death(%)23,836,40.046ConclusionsPatients with more than 1 event represent 7% to 46% of patients with event1–3 which is consistent with our study (39%). The event occured most often during the first year of GC therapy in our cohort (74% of patients) while it affects 24% to 50% of patients in other series for the same period.1–3 This difference could be explained by the heterogeneity of GC protocols. We did not found any positive correlation with hypertension, diabetes, and deep vein thrombosis that seemed to be more frequent in patients with multiple events.2 In our study, this group of patients appeared younger and presented more oftently with cough, ear pain, and polymyalgia rheumatica that preceded GCA. Logically, in these patients, corticosteroid therapy was longer and the use of GC-sparing agent was more common. Although getting remission was more difficult in these patients, the long-term prognosis is not poor.References[1] Restuccia, et al. Medicine2016.[2] Labarca, et al. Rheumatology2015.[3] Kermani, et al. J Rheumatol2015.Disclosure of InterestNone declared

The aim of this study is to determine prevalence, clinical significance of antiphospholipidantibodies (aPL) including anticardiolipin antibodies (aCL), anti-b2GP1 and lupus anticoagulant (LA) in a cohort of 74 patients with primary Sjögren’s syndrome (pSS) according to revised European criteria. aPL were found in 25 (34%) patients; IgG in 23 (12 had low titres, six moderate titres and five high titres) and IgM in five (three and two had respectively moderate and high titres). Eight (11%) patients were found to have LA; anti-b2GP1 antibodies were detected only in three (4%) patients. Only two patients with LA, aPL and b2GP1 had recurrent venous thrombosis. One patient with moderate titres of aPL exhibited recurrent spontaneous foetal losses. Peripheral neuropathies without cryoglobulinemia were more frequent in the aPL group. Other systemic involvements of pSS were the same in both groups with or without aPL. Patients with aPL have more concurrentimmunological diseases such as thyroiditis and primary biliary cirrhosis and a higher prevalence of hypergammaglobulinemia (P < 0.05). Even if aPL prevalence reached 30% in pSS, titres were usually low, with a close correlation with hypergammaglobulinemia but not with antiphospholipid syndrome, which is related to positivity of both LA and aPL.

BackgroundPrimary Sjogren’s syndrome (pSS) is a chronic inflammatory disorder characterised by diminished lacrimal and salivary gland functions. Joint involvement is reported in 20% to 60% of pSS patients, and among them one third of patients present synovitis. There is a lack of data concerning therapeutic management during pSS-associated synovitis.ObjectivesTo describe the characteristics and the outcome of pSS associated arthritis and to compare the efficacy of different therapeutic regimen.MethodsWe conducted a retrospective study using Club Rhumatisme and Inflammation (CRI) and French Internal Medicine Society (SNFMI) networks. All patients with a diagnosis of primary Sjögren’s Syndrome (pSS) and at least one clinical and/or echographic synovitis were included. Patients with synovitis (cases) were compared to pSS patients without synovitis (controls).Results57 patients (93% women) were included with a median age of 54 years.45–63 Patients with synovitis had more frequently lymph node enlargement (12.3% vs. 1.8%, p=0.007) and a higher ESSDAI score (86–12 vs. 2,1–4 p<0.0001). There was no difference concerning CRP levels, rheumatoid factor and CCP-antibodies positivity. Among 57 patients with synovitis, 101 lines of various treatments have been used during the follow-up of 40 [22.5–77] months. First line treatment consisted in steroids alone (3.5%), steroids in association (79%) with hydroxychloroquine (HCQ) (49%), methotrexate (MTX) (35%), rituximab (RTX) (5.3%) or other immunosuppressive drugs (7%). The number of complete/partial joint responses significantly increased considering the number of overall lines of treatment for MTX, HCQ and RTX: 52% for the first line, 76% for the second line and 83% for the third line (p<0.05), and data were similar considering each drug separately. There was no difference of efficacy between HCQ, MTX, and RTX concerning tender and swollen joint count, CRP level, ESSDAI score and steroids sparing effect at the end of each drug regimen. We performed a propensity score based analysis to determine whether HCQ, MTX, or RTX treatment was associated with better joint outcome. No difference could be shown for the joint response between three treatment regimen (MTX vs. HCQ, OR 1.55 [0.18–13.55], p=0.69; MTX vs. RTX, OR 5.08 [0.49–52.17], p=0.17; HCQ vs. RTX OR 3.28 [0.28–38.02], p=0.34). All 3 treatments (HCQ, MTX, and RTX) were associated with a significant reduction of ESSDAI score and a significant steroids-sparing effect.ConclusionspSS articular manifestations may include synovitis which could mimic rheumatoid arthritis but differ by the absence of structural damage. Even if the use of HCQ, MTX, and RTX seem to be effective for joint involvement, the best regimen remains to be determined.Disclosure of InterestNone declared