BackgroundThis 4 phase project1 jointly supported by EULAR and ACR has led to draft criteria.2 ObjectivesTo simplify and validate the new criteria in a large international cohort.Methods23 expert centres each contributed up to 100 patients with SLE and with non-SLE diagnoses. Diagnoses were verified by 3 independent reviewers for 1,193 SLE and 1059 non-SLE patients. 500 randomly selected SLE and non-SLE patients formed the derivation cohort and the remainder the validation cohort.ResultsThe criteria were fine-tuned and simplified, using ANA of ≥1:80 as entry criterion and a classification threshold of 10.RenalClass III/IV nephritis10Class II/V nephritis8Proteinuria≥0.5 g/day4 Specific antibodiesAnti-Sm orAnti-dsDNA6Muco-cutaneousACLE6SCLE orDLE4Alopecia or oral ulcers2SerosaAcute pericarditis6Effusion5Musculo-skeletalArthritis6CNSSeizures5Psychosis3Delirium2BloodAutoimmune hemolysis or thrombocytopenia4Leukopenia3ComplementLow C3 and C44Low C3 or C43Anti-phospholipidAnti-Cardiolipin or anti-β2-GPI or lupus anticoagulant2ConstitutionalFever2Sensitivity was close to the SLICC 2012 criteria, specificity maintained at the level of the ACR 1997 criteria. This performance was independently confirmed in the validation cohort.ACR 1997 criteriaSLICC criteriaNew criteria DerivationSensitivity84.6396.8198.00Specificity95.2090.0096.40ValidationSensitivity82.7696.7096.12Specificity93.3883.6293.38ConclusionsThe new criteria developed with EULAR/ACR support achieved sensitivity close to the SLICC criteria, while maintaining the specificity of the ACR criteria.References[1] Aringer, et al. Ann Rheum Dis2017;76(S2):4.[2] Tedeschi, et al. Ann Rheum Dis2017;76(S2):50.Disclosure of InterestNone declared

flare cluster included Delaware, Delaware Bay area, and Chesapeake Bay area between 2003 and 2014. Maps were generated highlighting the study area, flares, and identified clusters from all analyses. The space-time effects of environmental and demographic variables on the identified clusters will be considered in subsequent analysis. Conclusions We describe the first space-time clusters of lupus organ-specific disease activity strongly supporting the role of environmental factors as drivers of lupus activity.

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BackgroundSLE is a known disease for the study of ethnic and gender minorities. In Spain, from 1998 to 2011, occurred a significant immigration from Latin American people. The English speakers consider “Hispanics” as the same ethnic group. But there are differences between the Hispanics from Spain (with ethnicity European Caucasian) and the Hispanics from Latin America (with ethnicity Mestizo Latin American).ObjectivesTo know the demographic, clinical, severity, activity, damage, mortality and comorbidity of SLE in Hispanics with ethnicity European Caucasian (EC) and in Hispanic Mestizos from Latin American (MLA) residents in Spain. To identify differences between the groups.MethodsDesign: observational, multicentric, crossover study. Patients with SLE (ACR 1987) and <16 years old were included in 45 rheumatology Units in Spain. The RELESER methodology has been informed. Statistical analysis: we grouped the patients from the registry in two groups: EC and MLA and descriptive, univariate and multivariate statistics were done.Results3,490 patients with SLE were included, 90% females; 3,305 (92%) Hispanics EC y 185 (5%) Hispanics MLA. The Table shows the main variables. Patients MLA had higher levels of activity (SLEDAI), severity (KATZ INDEX) and number of admissions to the hospital for SLE activity. The damage index (SLICC), mortality, and comorbidity Index showed no differences. In the multivariate analysis several models were constructed with adjusted for age, sex and disease duration. The patients MLA had a higher risk for Severity (Katz Index >3) OR 1,45 (1,038 – 2, 026, p=0,02. This differences were not found for activity: OR 0,98 (0.30 - 1.66), may be for collinearity.Table 1VariableEuropean CaucasianMestizos Latin Americanpn, %n, %Total3.305, 92185, 5Women2.891, 90176, 950.02Myositis113, 315, 80.001Hemolytic anemia271, 824. 140.01Lupus nephritis952, 2979, 44<0.0001Serositis49, 19, 5<0.001Admissions related to LES activity1.741, 54120, 670.0001Median (IQR)Median (IQR)Age at SLE diagnosis (years)35.5 (24.3–44.5)30.5 (22.6–36.9)0.001Age at the study inclusion32.8 (22–42)28.6 (21–36)<0.001SLA disease duration (years) 1st symptom to diagnosis12.5 (5.7–17.5)7.9 (2.5–10.7)<0.0001Activity (SLEDAI)2.5 (0–4)3.8 (0–4)0.01Severity (KATZ)2.6 (1–3)2.9 (2–4)0.01Damage (SLICC)1.1 (0–2)0.9 (0–1)0.6Comorbidity (Charlson)2.3 (1–3)1.7 (1–2)0.2ConclusionsThe SLE of Hispanics MLA patients had clinical differences when it was compared with Hispanics EC patients, mainly higher severity and activity. This shows that all the Hispanics are not equal.Disclosure of InterestNone declared

Background:The mortality in Systemic Lupus Erythematosus (SLE) varies largely across different countries most probably due to social, healthcare and ethnic differences.Objectives:To analyze the causes and identify predictive factors of mortality of SLE in Spain in the present century.Methods:We performed a cross-sectional and retrospective study analyzing data from the RELESSER cohort (Spanish Registry of Systemic Lupus Erythematosus of the Spanish Society of Rheumatology). We included all patients diagnosed with SLE since the year 2000 and recorded sociodemographic, clinical and serological variables, comorbidities and treatments, as well as indicators of disease activity, damage and severity. The characteristics of the deceased patients were compared with those of the survivors, and variables with clinical significance or statistical significance were grouped into multivariate models to determine which ones were independently associated with the outcome of the disease.Results:A total of 2004 patients were included, 88.6% female, the mean age at diagnosis was 38.3 (± 15.3) years, with a mean delay in diagnosis of 28.9 (± 52.6) months. Up to 2.84% of the individuals had died. The leading cause of death was SLE activity (n=16), followed by infections (n=14), vascular events (n=7) and cancer (n=6). The mean age of death was 54.68 (± 20.13) years, and neither age, sex nor delay in diagnosis was independently associated with mortality. The presence of nephritis, depression, severe infections, organ damage (SLICC/ACR DI) or disease activity (SLEDAI), as well as the use of cyclophosphamide, rituximab or high doses of corticosteroids, were predictors of mortality in our cohort. Antimalarial treatment and skin manifestations were linked to improved survival.Conclusion:In the RELESSER cohort, clinical factors, co-morbidities, as well as therapeutic attitudes were associated with a significant increase in mortality in SLE. Interestingly, depression was independently associated to mortality. The activity of the disease and infections continue to be the main causes of death at the beginning of the 21st century amongst our patients.Disclosure of Interests:Clara Moriano: None declared, Jaime Calvo Grant/research support from: Lilly, UCB, Consultant of: Abbvie, Jansen, Celgene, Iñigo Rua-Figueroa: None declared, Elvira Diez Alvarez: None declared, Cristina Bermúdez: None declared, Francisco J López-Longo Grant/research support from: AbbVie and GSK, Speakers bureau: AbbVie, Actelion, Bristol Myers Squibb, GSK, MSD, Pfizer, Roche, and UCB Pharma, María Galindo-Izquierdo: None declared, Alejandro Olive: None declared, Eva Tomero Muriel: None declared, Antonio Fernandez-Nebro: None declared, Mercedes Freire González: None declared, Olaia Fernández- Berrizbeitia: None declared, Ana Pérez Gómez: None declared, Esther Uriarte Isacelaya: None declared, Carlos Marras Fernandez Cid: None declared, Carlos A. Montilla-Morales: None declared, Gregorio Santos Soler: None declared, Ricardo Blanco Grant/research support from: AbbVie, MSD, and Roche, Speakers bureau: AbbVie, Pfizer, Roche, Bristol-Myers, Janssen, and MSD, M. Rodíguez-Gómez: None declared, Paloma Vela-Casasempere: None declared, Alina Boteanu: None declared, J. Narváez: None declared, Victor Martinez Taboada: None declared, Blanca Hernández-Cruz Speakers bureau: Abbvie, Lilly, Sanofi, BMS, STADA, José Luis Andreu: None declared, José A Hernandez Beriain: None declared, Lorena Expósito: None declared, Raúl Menor-Almagro: None declared, Mónica Ibañez Barceló: None declared, Ivan Castellví Consultant of: Boehringer Ingelheim, Actelion, Kern Pharma, Speakers bureau: Boehringer Ingelheim, Actelion, Bristol-Myers Squibb, Roche, Carles Galisteo: None declared, Enrique Raya: None declared, Víctor Quevedo Vila: None declared, Tomas Vazquez Rodriguez: None declared, Jesus Ibañez: None declared, Jose M Pego-Reigosa: None declared