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Background:Giant cell arteritis (GCA) may be divided into cranial, and extracranial GCA. Tocilizumab (TCZ) has shown efficacy and safety in GCA and other large-vessel vasculitis (LVV) (1-5).Objectives:To compare the efficacy of TCZ in cranial and extracranial GCA.Methods:Multicenter observational study of 312 patients with GCA treated with TCZ. They were divided into 3 groups a) only cranial (cGCA), b) only extracranial (ecGCA), c) mixed affection (mixGCA). GCA was diagnosed by a) ACR criteria, and/or b) positive temporal artery biopsy, and/or c) LVV by imaging. Remission and sustained remission was defined according to EULAR definitions (1). In ecGCA and mixGCA we also studied the improvement (complete or partial) by imaging techniques.Results:We studied 312 patients (218 females; mean age, 73.4±9.6 years). TABLE shows the main features of the 3 groups. Remission at month 6 was higher in cGCA, as well as the sustained remission at month12 (FIGURE). At 18 and 24months, were similar in the 3 groups. Improvement by imaging techniques was partial/complete at 6,12,18 and 24 months, in 50%/0%,71%/0%, 61%/15% and 67%/17% respectively, in ecGCA, and in 75%/0%,53%/18%, 64%/12% and 50%/28% in mixGCA.Table 1.Main features of 312 patients at TCZ onset.Cranial GCA(n=152)Extracranial GCA(n=49)Mixed GCA(n=111)Cranial vs Extracranial GCApAge at TCZ onset, years, mean± SD76.0±8.265.4±12.273.5±8.10.000*Sex, female/male, n (% female)105/47 (69)33/16 (67)80/31 (72)0.960Time from diagnosis to TCZ onset (months, median [IQR]6 [2-21]7 [2-20]9 [3-25]0.765Biopsy-proven GCA, n (%)87/128 (68)0 (0)50/87 (57)0.000*Systemic manifestations at TCZ onset109 (72)32 (65)84 (76)0.501Fever, n (%)18 (12)1 (2)8 (7)0.048*Constitutional syndrome, n (%)52 (34)16 (33)47 (42)0.933PmR, n (%)88 (58)29 (59)71 (64)0.999Ischemic manifestations at TCZ onset117 (77)0 (0)70 (63)0.000*Visual involvement, n (%)31 (20)0 (0)16 (14)0.000*Headache, n (%)103 (85)0 (0)63 (57)0.000*Jaw claudication, n (%)39 (26)0 (0)21 (19)0.000*Acute phase reactantsESR, mm/1st hour, median [IQR]28 [9-53]24 [10-43]28 [15-48]0.462CRP, mg/dL, median [IQR]1.2 [0.3-3.4]0.7 [0.4-1.8]1.6 [0.4-3.8]0.153Prednisone dose at TCZ onset, mean ± SD26.2±17.615.4±14.220.1±14.90.000*TCZmono/TCZcombo, n (% TCZ mono)116/36 (76)26/23 (53)69/42 (62)0.003*Follow-up (months), mean ± SD27.3±21.132.7±23.327.9±22.00.143Figure 1.Remission and sustained remission of cGCA, ecGCA and mixGCA according to EULAR (1). In the first 3 months we only could assess cGCA because in ecGCA and mixGCA a control imaging was not performedConclusion:TCZ seems to be effective in all phenotypes but it is faster in cGCA in reaching remission. However, improvement by imaging techniques was partial and very rarely complete in ecGCA and mixGCA.References:[1]Hellmich B, et al. Ann Rheum Dis. 2020; 79: 19-30.[2]Stone JH, et al. N Engl J Med. 2017; 377: 317-28.[3]Calderón-Goercke M, et al. Semin Arthritis Rheum 2019; 49:126-35. https://doi.org/10.1016/j.semarthrit.2019.01.003.[4]Prieto Peña D et al. Clin Exp Rheumatol 2020 Nov 27. PMID: 33253103.[5]Loricera J, et al. Clin Exp Rheumatol 2016; 34:S44-53. PMID: 27050507Disclosure of Interests:Lara Sanchez-Bilbao: None declared, Javier Loricera: None declared, Vicente Aldasoro: None declared, Juan Pablo Valdivieso-Achá: None declared, Ignacio Villa-Blanco: None declared, Olga Maiz: None declared, Rafael Melero: None declared, Clara Moriano: None declared, Julio Sánchez: None declared, Eugenio de Miguel: None declared, Eva Perez-Pampín: None declared, Juan Ramón De Dios: None declared, Juan Carlos Nieto González: None declared, Eva Galíndez-Agirregoikoa: None declared, Patricia Moya: None declared, Francisca Sivera: None declared, José Luis Andréu Sánchez: None declared, Valvanera Pinillos: None declared, Andrea García-Valle: None declared, Paloma Vela-Casasempere: None declared, Noelia Alvarez-Rivas: None declared, Marcelino Revenga: None declared, Sara Manrique Arija: None declared, Carlos Fernández-López: None declared, Enrique Raya: None declared, Cristina Hidalgo: None declared, Ruth López-González: None declared, Cristina Campos Fernández: None declared, Antonio Juan-Mas: None declared, Beatriz Arca: None declared, Iñigo Rua-Figueroa: None declared, María Dolors Boquet: None declared, Antonio García: None declared, Adela Gallego: None declared, Eva Salgado-Pérez: None declared, Miguel A González-Gay Speakers bureau: Abbvie, Pfizer, Roche, Sanofi, Lilly, Celgene and MSD, Grant/research support from: Abbvie, MSD, Jansen and Roche, Ricardo Blanco Speakers bureau: Abbvie, Lilly, Pfizer, Roche, Bristol-Myers, Janssen, UCB Pharma and MSD, Grant/research support from: Abbvie, MSD and Roche

Background:Esperanza was a multicenter national health program developed to facilitate an early diagnosis of patients with Spondyloarthritis (SpA) in Spain.Objectives:To compare the clinical evolution of patients with axial SpA (axSpA) and peripheral SpA (pSpA) included in this program.Methods:Patients from the Esperanza cohort fulfilling ASAS criteria for axSpA or pSpA and completed the 6-year follow-up were included. Patients were classified according to the predominant symptom. In case of having axSpA and pSpA, they were classified as axSpA. Clinical features, disease activity and treatment aspects at baseline and 6-year visit were evaluated.Results:From 775 patients recruited at baseline, 6-year follow-up data from 178 (83.5%) fulfilling ASAS criteria at the final visit were available: 133 (74.7%) for axSpA and 45 for pSpA (25.3%). 118 (66.3%) were males (50.6% with axSpA and 62.2%, pSpA, p=0.4). Patients with axSpA had more frequently positive HLA-B27 (90.5%) vs. (9.5%), pConclusion:The early diagnosis of recent-onset SpA achieves a significant improvement in clinical features, disease activity and quality of life in patients with axSpA and pSpA after 6 years of follow-up. Although previous publications revealed a low radiographic progression in this cohort1, the worsening of BASMI must aware clinicians of possible evolutive structural damage.Reference:[1]Fernández-Carballido et al. RMD Open. 2020 Sep;6(2):e001345Acknowledgements:The Spanish Foundation of Rheumatology received funding from Pfizer (formerly Wyeth) to develop the Esperanza Program. Later, the Program has been supported by restricted grants from the Instituto de Salud Carlos III and Fondos FEDER (FIS PI13/02034 and PI17/01840) and AbbVie.Disclosure of Interests:Carolina Tornero: None declared, Victoria Navarro-Compán: None declared, Beatriz Joven-Ibáñez: None declared, RAQUEL ALMODOVAR: None declared, Xavier Juanola-Roura: None declared, Cristina Fernández-Carballido: None declared, Juan Carlos Quevedo-Abeledo: None declared, Jose Rosas: None declared, Azucena Hernández: None declared, Carlos A. Montilla-Morales: None declared, Jose Ramón Maneiro: None declared, A. Juan-Mas: None declared, Jose Antonio Pinto Tasende: None declared, Mireia Moreno: None declared, Jesus Sanz: None declared, Teresa Ruiz Jimeno: None declared, Manuel Moreno: None declared, María Lourdes Ladehesa Pineda: None declared, Eugenio de Miguel Speakers bureau: AbbVie, Novartis, Pfizer, MSD, BMS, UCB, Roche, Grunental, Janssen, Sanofi., Paid instructor for: Janssen, Novartis, Roche, Consultant of: AbbVie, Novartis, Pfizer, Galapagos, Grant/research support from: Abbvie, Novartis, Pfizer.

Background:Interstitial Lung Disease (ILD) is an extra-articular complication of rheumatoid arthritis (RA) that is associated with increased morbidity and mortality. Conventional disease-modifying drugs (DMARDs) such as methotrexate (MTX) have been implicated in the development and exacerbation of a pre-existing ILD.Objectives:The aim of our study was to check the influence of combined MTX treatment in patients with RA-ILD treated with abatacept (ABA).Methods:National multicentre retrospective registry of 263 patients with RA-ILD treated with ABA. RA was diagnosed according to the ACR classification criteria of 1987 or by the EULAR/ACR criteria of 2010. ILD was diagnosed by high resolution computed tomography (HRCT). In this study we have done a subanalysis of the 46 patients treated with ABA in combination with MTX (ABA+MTX) vs. 217 patients treated with ABA in monotherapy or in combination with other synthetic DMARDs. Efficacy was evaluated according to the following parameters: a) Dyspnoea (MMRC) considering variations ≥ 1; b) Lung function test (LFT) considering variations ≥ 10% in FVC and a variation of DLCO ≥ 10%; c) Imaging test (HRCT) d) DAS28 score e) prednisone dose. Variables were collected at the beginning of the study and at months 3, 6, 12 and then every 12 months until a maximum of 60 months.Results:263 patients with ILD associated with RA were included in the study with mean age 64.64±10 years. RF or CCPA were positive in 235 (89.4%) and 233 (88.6%) cases, respectively, with a mean follow-up of 22.7±19.7 months. Baseline characteristics of both groups are shown in table 1, while data obtained during evolution of this complication are presented in Figure 1.Conclusion:Despite the baseline differences of both groups, the good evolution in the ABA+MTX subgroup suggests that this therapeutic strategy can be a safe combination for patients with RA-ILD.ABA with MTX (n=46)ABA w/t MTX (n=217)PSex (F/M)28/18122/950.625Age (years)65.11±10.216.2±9.80.202RF/CCPA + (%)91.3/91.389.8/90.10.810Smoking or past smoking (%)47.855.10.417Follow-up (months)22.73±18.0022.3±20.850.916DAS28 at baseline4.08±1.514.61±1.470.056DAS28 at last visit3.00±1.463.13±1.310.642Prednisone at baseline, median (IQR) (mg)5 (5-7.5)7.75 (5-15)0.008*Prednisone at the end of study, median (IQR) (mg)5 (1-5)5 (5-7.5)0.032*DLCO at baseline (%)66.85±19.0465.43±18.210.823DLCO at the end of study (%)66.05±20.9565.17±19.720.831FVC at baseline (%)90.06±17.7785.40±21.560.164FVC at the end of study (%)90.58±15,4584.21±21.490.038*Disclosure of Interests:Carlos Fernández-Díaz Speakers bureau: Brystol Meyers Squibb, Santos Castañeda: None declared, Rafael Melero: None declared, J. Loricera: None declared, Francisco Ortiz-Sanjuán: None declared, A. Juan-Mas: None declared, Carmen Carrasco-Cubero Speakers bureau: Janssen, MSD, AbbVie, Novartis, Bristol Myers Squibb, and Celgene, S, Rodriguéz-Muguruza: None declared, S. Rodrigez -Garcia: None declared, R. Castellanos-Moreira: None declared, RAQUEL ALMODOVAR Speakers bureau: Abbvie, Celgene, Janssen, Lilly, Novartis, Pfizer., CLARA AGUILERA CROS: None declared, Ignacio Villa-Blanco Consultant of: UCB, Speakers bureau: Novartis, MSD, Lilly, Sergi Ordoñez: None declared, Susana Romero-Yuste: None declared, C. Ojeda-Garcia: None declared, Manuel Moreno: None declared, Gemma Bonilla: None declared, I. Hernández-Rodriguez: None declared, Mireia Lopez Corbeto: None declared, José Luis Andréu Sánchez: None declared, Trinidad Pérez Sandoval: None declared, Alejandra López Robles: None declared, Patricia Carreira Grant/research support from: Actelion, Roche, MSD, Consultant of: GlaxoSmithKline, VivaCell Biotechnology, Emerald Health Pharmaceuticals, Boehringer Ingelheim, Roche, Speakers bureau: Actelion, GlaxoSmithKline, Roche, Natalia Mena-Vázquez: None declared, C. Peralta-Ginés: None declared, ANA URRUTICOECHEA-ARANA: None declared, Luis Marcelino Arboleya Rodríguez: None declared, J. Narváez: None declared, DESEADA PALMA SANCHEZ: None declared, Olga Maiz-Alonso: None declared, J. Fernández-Leroy: None declared, I. Cabezas-Rodriguez: None declared, Ivan Castellví Consultant of: Boehringer Ingelheim, Actelion, Kern Pharma, Speakers bureau: Boehringer Ingelheim, Actelion, Bristol-Myers Squibb, Roche, A. Ruibal-Escribano: None declared, JR De Dios-Jiménez Aberásturi: None declared, Paloma Vela-Casasempere: None declared, C. González-Montagut Gómez: None declared, J M Blanco: None declared, Noelia Alvarez-Rivas: None declared, N. Del-Val: None declared, M. Rodíguez-Gómez: None declared, Eva Salgado-Pérez: None declared, Carlos Fernández-López: None declared, E.C. Cervantes Pérez: None declared, A. Devicente-DelMas: None declared, Blanca Garcia-Magallon Consultant of: MSD, Speakers bureau: Pfizer, Amgen, Celgene, MSD, Cristina Hidalgo: None declared, Sabela Fernández: None declared, Edilia García-Fernández: None declared, R. López-Sánchez: None declared, S. Castro: None declared, P. Morales-Garrido: None declared, Andrea García-Valle: None declared, Rosa Expósito: None declared, L. Exposito-Perez: None declared, Lorena Pérez Albaladejo: None declared, Ángel García-Aparicio: None declared, Ricardo Blanco Grant/research support from: AbbVie, MSD, and Roche, Speakers bureau: AbbVie, Pfizer, Roche, Bristol-Myers, Janssen, and MSD, Miguel A González-Gay Grant/research support from: Pfizer, Abbvie, MSD, Speakers bureau: Pfizer, Abbvie, MSD

Background:Interstitial Lung Disease (ILD) is a severe complication of Rheumatoid Arthritis (RA). Several conventional disease-modifying anti-rheumatic drugs (cDMARDs) and biologic (b) DMARDs may induce or impaired ILD-RA. Abatacept (ABA) may be useful in ILD-RA (1).Objectives:To assess the efficacy and safety of ABA in a large series of ILD-RA for a long-term follow-up.Methods:Multicenter open-level study of ILD-RA treated with at least 1 dose of ABA. ILD was diagnosed by high-resolution computed tomography (HRTC). We study these outcomes: a) 1-point change Modied Medical Research Council (MMRC); b) forced vital capacity (FVC) and/or DLCO improvement or decline ≥10%; c) change in HRCT, d) change in DAS28. e) Prednisone dose. Values were collected at 0, 3, 6, 12 and then every 12 months.Results:We studied 263 patients (150 women/113 men) (mean age;64.6±10 years), with ILD-RA. At ABA-onset they were smokers or exsmoker (53.8%), positive APCC (88.6%), median [IQR] duration of ILD of 12 [3-41.25] months, mean DLCO (65.7±18.3) and FVC (85.9±21.8).The ILD-pattern were usual interstitial pneumonia (UIP) (40.3%), non-specific interstitial pneumonia (NSIP) (31.9%) and others (27.8%).ABA was prescribed at standard subcutaneous (125 mg/w) in 196 (74.5%) or intravenously (10 mg/kg/4 w) in 67 (25.5%); in monotherapy (n=111) or combined with cDMARDs (n=152); especially leflunomide (n=55), MTX (n=46), or antimarials (n=21).After a mean follow-up of 22.7±19.7 months most outcomes remain stable (Figure). Moreover, DAS28 improved from 4.5±1.5 to 3.1±1.3; prednisone dose reduced from a median 7.5 [5-10] to 5 mg [5-7.5] and retention rate was 76.4%. The main adverse effects were serious infections (n=28), neoplasia (n=3), serious infusion reaction (n=1) and myocardial infarction (n=1).Conclusion:ABA seems effective and relatively safe in ILD-RA.References:[1]Fernández-Díaz C et al. Semin Arthritis Rheum. 2018; 48:22-27Disclosure of Interests:Carlos Fernández-Díaz Speakers bureau: Brystol Meyers Squibb, Santos Castañeda: None declared, Rafael Melero: None declared, J. Loricera: None declared, Francisco Ortiz-Sanjuán: None declared, A. Juan-Mas: None declared, Carmen Carrasco-Cubero Speakers bureau: Janssen, MSD, AbbVie, Novartis, Bristol Myers Squibb, and Celgene, S, Rodriguéz-Muguruza: None declared, S. Rodrigez -Garcia: None declared, R. Castellanos-Moreira: None declared, RAQUEL ALMODOVAR Speakers bureau: Abbvie, Celgene, Janssen, Lilly, Novartis, Pfizer.CLARA AGUILERA CROS: None declared, Ignacio Villa-Blanco Consultant of: UCB, Speakers bureau: Novartis, MSD, Lilly, Sergi Ordoñez: None declared, Susana Romero-Yuste: None declared, C. Ojeda-Garcia: None declared, Manuel Moreno: None declared, Gemma Bonilla: None declared, I. Hernández-Rodriguez: None declared, Mireia Lopez Corbeto: None declared, José Luis Andréu Sánchez: None declared, Trinidad Pérez Sandoval: None declared, Alejandra López Robles: None declared, Patricia Carreira Grant/research support from: Actelion, Roche, MSD, Consultant of: GlaxoSmithKline, VivaCell Biotechnology, Emerald Health Pharmaceuticals, Boehringer Ingelheim, Roche, Speakers bureau: Actelion, GlaxoSmithKline, Roche, Natalia Mena-Vázquez: None declared, C. Peralta-Ginés: None declared, ANA URRUTICOECHEA-ARANA: None declared, Luis Marcelino Arboleya Rodríguez: None declared, J. Narváez: None declared, DESEADA PALMA SANCHEZ: None declared, Olga Maiz-Alonso: None declared, J. Fernández-Leroy: None declared, I. Cabezas-Rodriguez: None declared, Ivan Castellví Consultant of: Boehringer Ingelheim, Actelion, Kern Pharma, Speakers bureau: Boehringer Ingelheim, Actelion, Bristol-Myers Squibb, Roche, A. Ruibal-Escribano: None declared, JR De Dios-Jiménez Aberásturi: None declared, Paloma Vela-Casasempere: None declared, C. González-Montagut Gómez: None declared, J M Blanco: None declared, Noelia Alvarez-Rivas: None declared, N. Del-Val: None declared, M. Rodíguez-Gómez: None declared, Eva Salgado-Pérez: None declared, Carlos Fernández-López: None declared, E.C. Cervantes Pérez: None declared, A. Devicente-DelMas: None declared, Blanca Garcia-Magallon Consultant of: MSD, Speakers bureau: Pfizer, Amgen, Celgene, MSD, Cristina Hidalgo: None declared, Sabela Fernández: None declared, Edilia García-Fernández: None declared, R. López-Sánchez: None declared, S. Castro: None declared, P. Morales-Garrido: None declared, Andrea García-Valle: None declared, Rosa Expósito: None declared, L. Exposito-Perez: None declared, Lorena Pérez Albaladejo: None declared, Ángel García-Aparicio: None declared, Miguel A González-Gay Grant/research support from: Pfizer, Abbvie, MSD, Speakers bureau: Pfizer, Abbvie, MSD, Ricardo Blanco Grant/research support from: AbbVie, MSD, and Roche, Speakers bureau: AbbVie, Pfizer, Roche, Bristol-Myers, Janssen, and MSD

Background:The prevalence of joint hypermobility (JH) and Joint Hypermobility Syndrome (JHS) in patients with fibromyalgia (FM) is considerable and is much more than can be explained at random(1). Some authors propose that FM and JHS share a common pathophysiological mechanism is some patients. Currently it is accepted that Ehlers-Danlos Syndrome Hypermobility subtype (EDSh) and JHS are the same entity. We regard the subgroup of FM patients with JHS a different subtype of FM, even phenotypically similar to EDSh.Objectives:Determine the possible differences between both groups according to their body composition, bone metabolism and clinical findings.Methods:Our study is observational, descriptive, transverse cohort study in which we included 86 women with fibromyalgia recruited at the Fibromyalgia and Chronic Fatigue Unit at Parc Salut-Mar in Barcelona, Spain. The patients were grouped according to the presence or absence of JHS, following the Brighton Criteria. Diverse clinical data was collected: Pain Visual Analogue Scale (PVAS), time from pain onset, time from diagnosis, somatic symptoms, state of mind, presence of a FM trigger, concurrent medication, anxiety, quality of life, disease impact, anthropometric data, Bioelectrical Impedance Analysis (BIA), bone density test (BMD) and bone metabolism data in blood samples.Results:51 patients were included in the FM group and 35 patients in the FM-JHS group. We did not find differences between groups PVAS; time from pain onset; somatic symptoms using the Psychiatric Disorder and Somatic Pathology Scale (TOPYPS); nor Fibromyalgia Impact Questionnaire (FIQ). Both groups scored similarly on SF-36 Health Questionnaire. The use of opioids was more common in the FM group (p0,05)Conclusion:Our work revealed that FM patients with JHS are different from FM without JHS, by manifesting differences in certain clinical, anthropometric, and bone metabolism features.References:[1]Lai S, Goldman JA, Child AH, Engel A, Lamm SH. Fibromyalgia, hypermobility, and breast implants. J Rheumatol. 2000;27(9):2237-41.[2]Malfait, F., Francomano, C., Byers, P., Belmont, J., Berglund, B., Black, J., ... & Castori, M. (2017, March). The 2017 international classification of the Ehlers–Danlos syndromes. InAmerican Journal of Medical Genetics Part C: Seminars in Medical Genetics(Vol. 175, No. 1, pp. 8-26).Disclosure of Interests: :None declared

Background:Interstitial Lung Disease (ILD) is a severe extraarticular manifestation of rheumatoid arthritis (RA). In this line, several radiological patterns of RA-ILD have been described: i) usual interstitial pneumonia (UIP), ii) nonspecific interstitial pneumonia (NSIP), iii) obliterating bronchiolitis, iv) organized pneumonia and mixed patterns. Abatacept (ABA) could be an effective and safe option for patients with RA-ILD, although the response in the different radiological patterns is not well defined.Objectives:Our aim was to assess the response to ABA in different radiological patterns of ILD.Methods:Observational retrospective multicenter study of RA-ILD treated with ABA. ILD was diagnosed by HRCT and classified by radiological patterns in 3 different subgroups of RA-ILD: a) UIP, b) NSIP and c) “other”. ABA was used sc. or iv. at standard dose. We assessed: a) Dyspnoea (MMRC scale; significant variation ≥1); b) Respiratory function tests (significant changes ≥10% in FVC and DLCO); c) HRCT imaging; d) DAS28 e)prednisone dose.Variables were collected at months 0, 3, 6, 12 months and subsequently every 12 months until a maximum of 60 months.Results:We included 263 patients: 106 UIP, 84 NSIP and 73 others (150 women / 113 men), mean age 64.64±10 years. Total patients positive for RF or CCPA were 235 (89.4%) and 233 (88.6%), respectively. In 26 out of 263 patients, the development of ILD was closely related to the administration of sDMARDs (MTX n = 11 and LFN n = 1) or bDMARDs (ETN n = 5, ADA n = 4, CZP n = 2 and IFX n = 3). Patient characteristics are shown in table 1. Figure 1 shows the evolution of the cases with available data after a mean follow-up of 22.7±19.7 months. Mean DLCO and FVC remained stable in the 3 groups without statistically significant changes, and all the groups showed a statistically significant reduction in DAS28 and prednisone dose.Conclusion:ABA could be a good choice of treatment in patients with RA-ILD independently of the radiological pattern of ILD.Disclosure of Interests:Carlos Fernández-Díaz Speakers bureau: Brystol Meyers Squibb, Santos Castañeda: None declared, Rafael Melero: None declared, J. Loricera: None declared, Francisco Ortiz-Sanjuán: None declared, A. Juan-Mas: None declared, Carmen Carrasco-Cubero Speakers bureau: Janssen, MSD, AbbVie, Novartis, Bristol Myers Squibb, and Celgene, S, Rodriguéz-Muguruza: None declared, S. Rodrigez -Garcia: None declared, R. Castellanos-Moreira: None declared, RAQUEL ALMODOVAR Speakers bureau: Abbvie, Celgene, Janssen, Lilly, Novartis, Pfizer., CLARA AGUILERA CROS: None declared, Ignacio Villa-Blanco Consultant of: UCB, Speakers bureau: Novartis, MSD, Lilly, Sergi Ordoñez: None declared, Susana Romero-Yuste: None declared, C. Ojeda-Garcia: None declared, Manuel Moreno: None declared, Gemma Bonilla: None declared, I. Hernández-Rodriguez: None declared, Mireia Lopez Corbeto: None declared, José Luis Andréu Sánchez: None declared, Trinidad Pérez Sandoval: None declared, Alejandra López Robles: None declared, Patricia Carreira Grant/research support from: Actelion, Roche, MSD, Consultant of: GlaxoSmithKline, VivaCell Biotechnology, Emerald Health Pharmaceuticals, Boehringer Ingelheim, Roche, Speakers bureau: Actelion, GlaxoSmithKline, Roche, Natalia Mena-Vázquez: None declared, C. Peralta-Ginés: None declared, ANA URRUTICOECHEA-ARANA: None declared, Luis Marcelino Arboleya Rodríguez: None declared, J. Narváez: None declared, DESEADA PALMA SANCHEZ: None declared, Olga Maiz-Alonso: None declared, J. Fernández-Leroy: None declared, I. Cabezas-Rodriguez: None declared, Ivan Castellví Consultant of: Boehringer Ingelheim, Actelion, Kern Pharma, Speakers bureau: Boehringer Ingelheim, Actelion, Bristol-Myers Squibb, Roche, A. Ruibal-Escribano: None declared, JR De Dios-Jiménez Aberásturi: None declared, Paloma Vela-Casasempere: None declared, C. González-Montagut Gómez: None declared, J M Blanco: None declared, Noelia Alvarez-Rivas: None declared, N. Del-Val: None declared, M. Rodíguez-Gómez: None declared, Eva Salgado-Pérez: None declared, Carlos Fernández-López: None declared, E.C. Cervantes Pérez: None declared, A. Devicente-DelMas: None declared, Blanca Garcia-Magallon Consultant of: MSD, Speakers bureau: Pfizer, Amgen, Celgene, MSD, Cristina Hidalgo: None declared, Sabela Fernández: None declared, R. López-Sánchez: None declared, Edilia García-Fernández: None declared, S. Castro: None declared, P. Morales-Garrido: None declared, Andrea García-Valle: None declared, Rosa Expósito: None declared, L. Exposito-Perez: None declared, Lorena Pérez Albaladejo: None declared, Ángel García-Aparicio: None declared, Miguel A González-Gay Grant/research support from: Pfizer, Abbvie, MSD, Speakers bureau: Pfizer, Abbvie, MSD, Ricardo Blanco Grant/research support from: AbbVie, MSD, and Roche, Speakers bureau: AbbVie, Pfizer, Roche, Bristol-Myers, Janssen, and MSD

Background:Blocking of the Tumor Necrosis Factor (TNF) activity is a successful therapeutic approach for 2 out of 3 Rheumatoid Arthritis patients. Identifying the patients that will not respond to this therapeutic approach is a major translational goal in RA. Association of seropositivity to rheumatoid factor (RF) or anti-cyclic-citrullinated antibodies (anti-CCP) with anti-TNF response has proven inconclusive, suggesting that other yet unexplored biomarkers could be more informative for this goal.Objectives:We tested the association of two recently introduced biomarkers in RA: anti-carbamylated protein antibodies (anti-CarP) and anti-peptidylarginine deiminase type 4 (anti-PAD4).Methods:A prospective cohort of n=80 RA patients starting anti-TNF therapy was recruited and levels for all four autoantibodies -RF, anti-CCP, anti-CarP and anti-PAD4- were measured at baseline. The change in DAS28 score between baseline and week 12 of therapy was used as the clinical endpoint.Results:Single marker-analysis showed no significant association with drug response. However, when testing for interactions between autoantibodies, we found highly significant associations with drug response. Anti-CCP and RF showed a positive interaction with the response to anti-TNF therapy (P=0.00068), and anti-PAD4 and antiCarP titers showed a negative interaction with the clinical response at week 12 (P=0.0062). Using an independent retrospective sample (n=199 patients), we validated the interaction between anti-CCP and RF with the clinical response to anti-TNF agents. (P=0.044).Conclusion:The results of this study show that interactions between antibodies are important in the response to anti-TNF therapy and suggest potential pathogenic relationships.Acknowledgments :We would like to thank the clinical researchers and patients participating in the IMID Consortium for their collaborationDisclosure of Interests:Antonio Julià: None declared, Maria Lopez Lasanta: None declared, Francisco Blanco: None declared, Antonio Gómez: None declared, Isabel Haro: None declared, Antonio Juan Mas: None declared, Alba Erra: None declared, Mª Luz García Vivar: None declared, Jordi Monfort: None declared, Simon Sánchez Fernandez: None declared, Isidoro González-Álvaro Grant/research support from: Roche Laboratories, Consultant of: Lilly, Sanofi, Paid instructor for: Lilly, Speakers bureau: Abbvie, MSD, Roche, Lilly, Mercedes Alperi-López: None declared, Raúl Castellanos: None declared, Antonio Fernandez-Nebro: None declared, Cesar Diaz Torne: None declared, Núria Palau: None declared, Raquel M Lastra: None declared, Jordi Lladós: None declared, Raimon Sanmarti: None declared, Sara Marsal: None declared

Background Adult-onset Still’s disease (AOSD) is often refractory to standard immunosuppressive therapy. Tocilizumab (TCZ) has shown efficacy in isolated cases or in small series. Objectives We assess the efficacy of TCZ in AOSD. Methods Multicenter study of 27 patients with AOSD of 18 hospitals diagnosed according to Yamagouchi’s criteria (J Rheumatol 1992;19:424). TCZ was used due to lack of good response to standard therapy or to other biologic agents. Results The 27 patients (20 women/ 7 men), had a mean age of 37.2±15.9 (range 16-71) and an average duration of AOSD of 5.9±4.6 years (range 0.1-17) to onset of TCZ. Prior to the onset of TCZ and besides corticosteroids, patients had recived the following drugs: Metotrexate (26 patients), Anakinra (12), Etanercept (6), Adalimumab (5) and Infliximab (3). TCZ standard dose was 8 mg/k/iv/4 weeks. At TCZ onset, the most frequent clinical manifestations were joint (27 cases), cutaneous (14) and fever (18), along with analytical abnomalities, increase of ESR or CRP (20 cases), anemia (11) or leukocytosis (15). Clinical and analytical improvement was observed soon, 1 st month after the onset of TCZ therapy (TABLE). After a mean follow-up of 20.8±12 months, cutaneous manifestations disappeared in 13 of 14 patients (92,9%), fever in 17 of 18 (94.4%) and joint manifestation in 22 of 27 (81,5%). Improvement of analytical abnormalities was observed in most cases with normalization of the blood cell count in 9 of 15 (60%) patients, anemia in 11 of 11 (100%), ESR in 15 of 19 (78.9 % ), CRP in 17 of 20 (85%), hepatic enzymes (AST/ALT) in 3 of 4 (50 %) and ferritin seric levels in 11 of 13 (84,6%). The median [IQR] dose of steroids was reduced from 15 [8.8-25] to 5 [1.3-7.5]. Conclusions In refractory AOSD, TCZ yields early and maintained clinical-analytical response, even in refractory cases to other biological agents. Although TCZ showed global efficacy, joint are more refractory than other systemic manifestations. Disclosure of Interest None Declared