Objectives To evaluate the annual direct medical cost of managing adult systemic lupus erythematosus (SLE) patients with active autoantibody positive disease in Europe. Methods A 2-year, retrospective, multicentre, observational study was conducted in five countries (France, Germany, Italy, Spain and the UK). Data included patients' characteristics, disease activity and severity, flare assessments and health resource use (eg, laboratory tests, medications, specialist visits and hospitalisations). Costs were assessed from the public payers' perspective. Cost predictors were estimated by multivariate regression models. Results Thirty-one centres enrolled 427 consecutive eligible patients stratified equally by disease severity. At baseline, mean (SD) age was 44.5 (13.8) years, 90.5% were women and mean (SD) SLE duration was 10.7 (8.0) years. The SELENA-SLEDAI (11.2 vs 5.3) and SLICC/ACR index (1.0 vs 0.7) scores were higher in severe patients. Over the study period, patients experienced on average 1.02 (0.71) flares/year. The mean annual direct medical cost was higher in severe compared to non-severe patients (€4748 vs €2650, p<0.001). Medication costs were €2518 in severe versus €1251 in non-severe patients ( p<0.001). Medications represented 53% and 47% of the total cost for severe and non-severe patients, respectively, primarily due to immunosuppressants and biologics. Flares, especially severe flares, were identified as the major cost predictor, with each flare increasing the annual total cost by about €1002 ( p<0.001). Conclusions The annual direct medical cost of SLE patients in Europe is related to disease severity and flares. Medical treatments were the main cost drivers. Severe flares and major organ involvement were identified as important cost predictors.

Triple therapy is independently associated with a higher survival rate among patients with CAPS.

Background and Purpose The aims of this prospective and multicenter study were to determine the frequency of anticardiolipin and antinuclear antibodies in an unselected ischemic and hemorrhagic stroke population and to evaluate the clinical significance of these autoantibodies.Methods Over a 1-year period, we collected plasma from 481 consecutive patients with ischemic or hemorrhagic stroke attending four different hospitals. Blood (10 mL) was drawn from each subject into a citrated glass tube. Plasma was obtained immediately by centrifugation and was stored at -70°C until use. Concentrations of IgM and IgG anticardiolipin antibodies were measured at room temperature in normal (not heat-treated) plasma by standardized enzyme-linked immunosorbent assay. All sera were treated by indirect immunofluorescence on mouse liver and kidney sections for antinuclear antibodies.

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Background Statins may have beneficial vascular effects in systemic lupus erythematosus (SLE) beyond their cholesterol-lowering action, although involved mechanisms remain incompletely understood Objectives To investigate the potential mechanisms participating in the efficacy of fluvastatin in preventing atherothrombosis in SLE Methods Eighty five SLE patients and 62 healthy donors were included in the study. Selected SLE patients (n=27) received 20 mg/day fluvastatin for one month. Blood samples were obtained before the starting and at the end of treatment. Parallel in vitro studies were conducted to evaluate the underlying mechanisms involved in the response to the fluvastatin treatment Results Increased prothrombotic and inflammatory parameters were found in SLE patients. Gene expression analysis showed that monocytes from SLE patients were major players in the altered proinflammatory parameters. Moreover, SLE monocytes displayed altered mitochondrial membrane potential and increased oxidative stress. Correlation and association analyses demonstrated a complex interplay among autoimmunity, oxidative stress, inflammation, and increased risk of atherothrombosis in SLE. Treatment of normal monocytes with SLE serum or exogenous IFNα altered inflammatory and oxidative stress markers as well as mitochondrial membrane potential and biogenesis. Effects were stronger in SLE serum treated monocytes, particularly on thrombotic and inflammatory parameters. One-month fluvastatin treatment of SLE patients reduced SLEDAI and lipid levels, oxidative status, and vascular inflammation. Array studies on monocytes demonstrated differential expression in 799 genes after fluvastatin treatment. Novel target genes and pathways modulated by fluvastatin were uncovered, including gene networks involved in cholesterol and lipid metabolism, inflammation, oxidative stress and mitochondrial activity. Electron microscopy analyses showed increased density volume of mitochondria in monocytes from fluvastatin-treated SLE patients, which also displayed higher expression of genes involved in mitochondrial biogenesis. The in vitro treatment of monocytes purified from SLE patients with fluvastatin showed similar results to in vivo studies, including reduced inflammatory and oxidative stress parameters and induced gene changes similar to those observed in the microarray analysis. Furthermore, mitochondrial biogenesis was also increased, as indicated by EM analysis and the increased expression of specific genes Conclusions Our overall data suggest that fluvastatin improves the impairment of a redox-sensitive pathway participating in processes that collectively orchestrate the pathophysiology of atherothrombosis in SLE Acknowledgements Supported by: P08-CVI-04234, CTS-7940, PI12/01511 and the Spanish Rheumatology Society Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.4340