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Resumen Objetivo La dificultad para el diagnostico y la variedad de manifestaciones clinicas que pueden determinar la eleccion del tratamiento del sindrome antifosfolipido (SAF) primario ha impulsado a la Sociedad Espanola de Reumatologia (SER) en la elaboracion de recomendaciones basadas en la mejor evidencia posible. Estas recomendaciones pueden servir de referencia para reumatologos y otros profesionales implicados en el manejo de pacientes con SAF. Metodos Se creo un panel formado por 4 reumatologos, una ginecologa y una hematologa, expertos en SAF, previamente seleccionados mediante una convocatoria abierta o por meritos profesionales. Las fases del trabajo fueron: identificacion de las areas claves para la elaboracion del documento, analisis y sintesis de la evidencia cientifica (utilizando los niveles de evidencia de SIGN, Scottish Intercollegiate Guidelines Network) y formulacion de recomendaciones a partir de esta evidencia y de tecnicas de «evaluacion formal» o «juicio razonado». Resultados Se han elaborado 46 recomendaciones que abordan 5 areas principales: diagnostico y evaluacion, medidas de tromboprofilaxis primaria, tratamiento del SAF o tromboprofilaxis secundaria, tratamiento del sindrome antifosfolipido obstetrico y situaciones especiales. Esta incluido tambien el papel de los nuevos anticoagulantes orales, el problema de las recurrencias o los principales factores de riesgo identificados en estos individuos. En este documento se reflejan las ultimas 25, referidas a las areas de: SAF obstetrico y situaciones especiales. El documento contiene una tabla de recomendaciones y algoritmos de tratamiento. Conclusiones Se presentan las recomendaciones de la SER sobre SAF. Este documento corresponde a la parte 2.a relacionada con el SAF obstetrico y las situaciones especiales. Estas recomendaciones se consideran herramientas en la toma de decisiones para los clinicos, teniendo en consideracion tanto la decision del medico experto en SAF como la opinion compartida con el paciente. Se ha elaborado tambien una parte I que aborda aspectos relacionados con el diagnostico, evaluacion y tratamiento.

Objective The difficulty in diagnosis and the spectrum of clinical manifestations that can determine the choice of treatment for primary antiphospholipid syndrome (APS) has fostered the development of recommendations by the Spanish Society of Rheumatology (SER), based on the best possible evidence. These recommendations can serve as a reference for rheumatologists and other specialists involved in the management of APS. Methods A panel of four rheumatologists, a gynaecologist and a haematologist with expertise in APS was created, previously selected by the SER through an open call or based on professional merits. The stages of the work were: identification of the key areas for drafting the document, analysis and synthesis of the scientific evidence (using the Scottish Intercollegiate Guidelines Network [SIGN] levels of evidence) and formulation of recommendations based on this evidence and formal assessment or reasoned judgement techniques (consensus techniques). Results 46 recommendations were drawn up, addressing five main areas: diagnosis and evaluation, measurement of primary thromboprophylaxis, treatment for APS or secondary thromboprophylaxis, treatment for obstetric APS and special situations. These recommendations also include the role of novel oral anticoagulants, the problem of recurrences or the key risk factors identified in these subjects. This document reflects the first 21, referring to the areas of: diagnosis, evaluation and treatment of primary APS. The document provides a table of recommendations and treatment algorithms. Conclusions An update of the SER recommendations on APS is presented. This document corresponds to part I, related to diagnosis, evaluation and treatment. These recommendations are considered tools for decision-making for clinicians, taking into consideration both the decision of the physician experienced in APS and the patient. A part II has also been prepared, which addresses aspects related to obstetric SAF and special situations.

Objectives Lipid profiles appear to be altered in SLE patients due to disease activity and inflammation. Cholesterol efflux capacity (CEC) is the ability of high-density lipoprotein cholesterol to accept cholesterol from macrophages. CEC has been linked to cardiovascular events in the general population and is impaired in SLE patients. The aim of this study was to establish whether CEC is related to subclinical carotid atherosclerosis in SLE patients. Methods The present report is of a cross-sectional study that encompassed 418 individuals: 195 SLE patients and 223 controls. CEC, using an in vitro assay, and lipoprotein serum concentrations were assessed in patients and controls. Carotid intima-media thickness and carotid plaques were evaluated in SLE patients. A multivariable analysis was performed to study the relationship of CEC to SLE-related data, lipid profile and subclinical carotid atherosclerosis. Results CEC was downregulated in SLE patients [8.1 (4.2) % vs 16.9 (10.4) %, P = 0.004). This occurred independently of traditional cardiovascular risk factors, statin use or other variations in the lipid profile related to the disease. Traditional cardiovascular risk factors, both in patients and controls, and SLE-related data such as activity, severity or damage were not associated with CEC. After multivariable regression analysis including lipid profile–related molecules, CEC was inversely and independently associated with the presence of carotid plaques in SLE patients [odds ratio 0.87 (95% CI: 0.78, 0.97), P = 0.014]. Conclusion CEC is impaired in SLE patients independently of other inflammation-related lipid profile modifications that occur during the disease. CEC is associated with carotid plaques in SLE patients.

Cholesterol efflux capacity (CEC) is the ability of high-density lipoprotein (HDL) cholesterol to accept cholesterol from macrophages. CEC is linked to cardiovascular events in the general population, and it has been shown to be disrupted in inflammatory states. The aim of this study was to establish whether CEC is impaired in PsA patients and if this could be explained by disease-related features like disease activity. Case-control study that encompassed 105 individuals: 52 PsA patients and 53 controls. CEC, using an in vitro assay, and lipoprotein serum concentrations were assessed in patients and controls. Disease activity in patients with PsA was measured using the Disease Activity Index for Psoriatic Arthritis (DAPSA). Multivariate analysis was performed to study the differences between CEC in patients and controls, and the relation of CEC with PsA activity-related data and lipid profile. Total cholesterol, apolipoprotein A1, and LDL cholesterol serum levels were downregulated in PsA patients. CEC did not differ between controls and patients (17 ± 10 vs. 18 ± 2%, p = 0.15) after adjusting for traditional cardiovascular risk factors or other variations in the lipid profile related to the disease. Traditional cardiovascular risk factors, both in patients and controls, were not related to CEC. After multivariate regression analysis, the DAPSA score was inversely and independently associated with CEC (beta coefficient − 0.75 [95%CI − 1.39–− 0.11] %, p = 0.023). CEC is inversely associated with disease activity in PSA patients, reinforcing the role of disease activity as a key factor in the development of accelerated atherosclerosis in these patients.

Amylin is a pancreatic hormone that participates in glucose homeostasis. We aimed to investigate how serum amylin levels are expressed in patients with systemic lupus erythematosus (SLE) compared to matched controls, and their possible relationship to disease-related characteristics, such as activity or damage.144 SLE patients and 96 non-diabetic sex- (female 96% vs. 91%, p=0.43) and age-matched controls (49±11 vs. 51±8 years, p=0.09) were included. Amylin, insulin and C-peptide serum levels, as well as insulin resistance indexes were assessed in both groups. Multivariable regression analysis was performed to compare amylin between groups and to explore its interrelations with SLE features. The analyses were adjusted for glucocorticoids intake and for insulin resistance classic risk factors.Patients with SLE exhibited significant higher serum levels of amylin when compared to controls after multivariable analysis (beta coef. 1.56 [95%CI 1.01-2.11], p=0.000). Moreover, SLE patients not on prednisone (beat coef. 1.54 [95%CI 0.98-2.10] ng/ml, p=0.000) and those on prednisone (beta coef. 1.51 [95%CI 0.96-2.07] ng/ml, p=0.000) disclosed higher amylin serum levels compared to controls in the fully multivariable analysis. Hyperamylinaemia in SLE patients remained significant even adjusting for differences in the insulin resistance and beta cell production rates between patients and controls. The damage produced by the disease and its severity were independently and positively associated with amylin serum levels.Amylin is upregulated in SLE patients compared to controls, regardless of the insulin resistance that SLE may present. The damage produced by the disease and its severity independently explains this upregulation.

Additional file 1: Supplementary Figure 1. Multivariable analysis of the differences between scleroderma patients and controls in main lipid profile-related molecules (total cholesterol, triglycerides, HDL-cholesterol, apolipoprotein B and lipoprotein -mg/dl-, and cholesterol efflux capacity -%-).

Additional file 2: Supplementary Table 1. Differences in cardiovascular risk factors, lipid profiles and disease-related data between SS types.

Objective: Cholesterol efflux capacity (CEC) is the ability of high-density lipoprotein (HDL) cholesterol to accept cholesterol from macrophages. Lipid profiles and CEC appear to be altered in patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) due to disease activity and inflammation. CEC has been linked to cardiovascular events in the general population and to subclinical atherosclerosis in SLE and RA patients. The aim of this study was to establish whether CEC varies between patients with SLE and those with RA. Methods: The study encompassed 460 individuals (195 SLE patients and 265 patients with RA). CEC (using an in vitro assay) and concentrations of lipoprotein serum were assessed in both populations. A multivariable regression analysis was performed to study whether CEC differs between SLE patients and RA patients. Results: Comparison of lipid patterns revealed that patients with RA have lower HDL cholesterol and higher apolipoprotein B serum levels than SLE patients. CEC was downregulated in SLE patients compared to patients with RA (β -12 [95% confidence interval -13, -10], P < 0.001). It occurred independently of traditional cardiovascular risk factors, statin use, disease-related data, and other variations in the lipid profile related to the diseases. Conclusion: Patients with RA have a more proatherogenic lipid pattern compared to those with SLE. However, CEC seems to be more damaged in SLE patients than in RA patients. Sin financiación 5.178 JCR (2021) Q2, 12/34 Rheumatology 1.566 SJR (2021) Q1, 7/61 Rheumatology No data IDR 2021 UEC

Objective It is well established that patients with systemic sclerosis (SSc) have a disrupted lipid profile and an increased cardiovascular risk. Cholesterol efflux capacity (CEC), the ability of high-density lipoprotein (HDL)-cholesterol to accept cholesterol from macrophages, has been linked to cardiovascular events. The aim of this study was to establish whether CEC and lipid profile were impaired in SSc patients with respect to controls and whether these changes were associated with disease-related data. Methods Cross-sectional study encompassed 188 individuals: 73 SSc patients and 115 controls. CEC, using an in vitro assay, and lipoprotein serum concentrations were assessed in patients and controls. A multivariable analysis was performed to study the differences in CEC between patients and controls, and if SSc-related data could explain such differences. Results The multivariable analysis adjusted for demographic characteristics, cardiovascular risk factors, and lipid-related molecules showed that total cholesterol (beta coefficient: − 22 [95%CI – 37 to – 7], p = 0.004), triglycerides (beta coefficient: 24 [95%CI 2–47], p = 0.033), lipoprotein A (beta coefficient: 22 [95%CI 2–43], p = 0.033), and CEC (beta coefficient: – 6 [95%CI − 10 to – 2]%,p = 0.002) were significantly different between patients and controls. Skin thickness, as assessed by modified Rodnan skin score, was independently associated with a lower CEC (beta coefficient: – 0.21 [95%CI – 0.37 to – 0.05]%, p = 0.011) after multivariable adjustment. Conclusion SSc patients show an abnormal lipid profile with respect to controls including CEC. Skin thickness is independent and inversely associated with CEC in SSc patients.

The purpose of this study was to compare physical activity (PA) in a group of patients with psoriatic arthritis (PsA) versus healthy controls and to determine whether the mobility of these patients is affected by disease activity.A group of 52 patients with PsA and 53 controls were included in this case-control study. PA was assessed by accelerometry in both groups and additionally with the International Physical Activity Questionnaire (IPAQ) in patients with PsA. Multiple regression analysis was used to compare PA between groups and to determine the relationship between PA and PsA features, including disease activity, as assessed by the 28-joint Disease Activity Score (DAS28) and the Disease Activity Index for Psoriatic Arthritis (DAPSA) score. In a group of 36 patients, a test-retest study was carried out after 6 months.The time engaged in moderate-to-vigorous physical activity (MVPA) per day, as evaluated by accelerometry, and adjusted by confounders, proved similar in patients with PsA and controls. In patients with PsA, disease activity was inversely related to PA as assessed either by IPAQ or accelerometry. When PA was compared in patients with PsA between the 2 visits, a significant difference in the amount of time doing MVPA was found (42 ± 33 versus 30 ± 22 minutes/day; P = 0.004). Interestingly, in the test-retest study, variations in disease activity over time based on DAPSA scores (r = -0.49, P = 0.002) and DAS28 using the C-reactive protein level (r = -0.4, P = 0.017) were inversely correlated with changes in PA, as determined by accelerometry.Patients with PsA show levels of PA like healthy controls. In patients with PsA, disease activity and PA are inversely correlated and the evaluation of PA by accelerometry is sensitive to changes in disease activity.

Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a serine protease that regulates cholesterol metabolism through low-density lipoprotein receptor degradation and that has been linked to cardiovascular (CV) disease. The purpose of the present study was to examine whether PCSK9 levels are disrupted compared with controls in patients with systemic lupus erythematosus (SLE). We additionally sought to establish whether PCSK9 is related to both the abnormalities in the lipid profile and to the disease activity or damage of patients with SLE. Methods: We performed a cross-sectional study that encompassed 366 individuals: 195 SLE patients and 171 age-, sex-, and statin intake-matched controls. PCSK9, lipoproteins serum concentrations, and lipid profiles were assessed in patients and controls. A multivariable analysis, adjusted for standard CV risk factors, was performed to evaluate the role of PCSK9 in SLE-related dyslipidemia. Results: Most lipid related-molecules were decreased in patients with SLE compared with controls. This downregulation included PCSK9, with PCSK9 levels being lower in patients than controls in the full multivariable analysis, including the modifications in lipid profiles that the disease itself produces {beta coefficient ?73 [95% confidence interval (CI) ?91 to ?54] ng/ml, p???0.001}. Both SLICC and SLEDAI scores were independently and positively related to PCSK9. Patients currently on hydroxychloroquine exhibited decreased levels of PCSK9 compared with those that were not taking hydroxychloroquine [beta coefficient ?30 (95% CI ?54 to ?6) ng/ml, p?=?0.015]. Conclusion: PCSK9 is downregulated in SLE compared with controls, but SLE patients with higher disease activity and damage exhibited higher PSCK9 serum levels. The authors disclosed receipt of the following financial support for the research, authorship, and/ or publication of this article: this work was supported by a grant to IF-A from the Spanish Ministry of Health, Subdirección General de Evaluación y Fomento de la Investigación, Plan Estatal de Investigación Científica y Técnica y de Innovación 2013–2016 and by Fondo Europeo de Desarrollo Regional - FEDER - (Fondo de Investigaciones Sanitarias, FIS PI14/00394, PI17/00083). The research of MAG-G is supported by the Instituto de Salud Carlos III (ISCIII) (Fondo de Investigación Sanitaria grants PI06/0024, PI09/00748, PI12/00060, PI15/00525, PI18/00043) and the ISCIII RETICS program (RD12/0009 and RD16/0012).

Cholesterol efflux capacity (CEC) is the ability of high-density lipoprotein (HDL) cholesterol to accept cholesterol from macrophages. CEC is linked to cardiovascular events in the general population, and it has been shown to be disrupted in inflammatory states. The aim of this study was to establish whether CEC is impaired in PsA patients and if this could be explained by disease-related features like disease activity.Case-control study that encompassed 105 individuals: 52 PsA patients and 53 controls. CEC, using an in vitro assay, and lipoprotein serum concentrations were assessed in patients and controls. Disease activity in patients with PsA was measured using the Disease Activity Index for Psoriatic Arthritis (DAPSA). Multivariate analysis was performed to study the differences between CEC in patients and controls, and the relation of CEC with PsA activity-related data and lipid profile.Total cholesterol, apolipoprotein A1, and LDL cholesterol serum levels were downregulated in PsA patients. CEC did not differ between controls and patients (17 ± 10 vs. 18 ± 2%, p = 0.15) after adjusting for traditional cardiovascular risk factors or other variations in the lipid profile related to the disease. Traditional cardiovascular risk factors, both in patients and controls, were not related to CEC. After multivariate regression analysis, the DAPSA score was inversely and independently associated with CEC (beta coefficient - 0.75 [95%CI - 1.39-- 0.11] %, p = 0.023).CEC is inversely associated with disease activity in PSA patients, reinforcing the role of disease activity as a key factor in the development of accelerated atherosclerosis in these patients.Key Points• Cholesterol efflux capacity is linked to cardiovascular events in the general population.• In patients with psoriatic arthritis, cholesterol efflux capacity is inversely associated with disease activity (beta coefficient - 0.75[95% CI - 1.39-- 0.11] %, p = 0.023).• This finding reinforces the role of disease activity as a key factor in increasing cardiovascular risk in psoriatic arthritis patients.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a serine protease that regulates cholesterol metabolism through low-density lipoprotein receptor degradation, and which has been linked to cardiovascular risk. The purpose of the present study was to examine whether PCSK9 serum levels are disrupted in patients with systemic sclerosis (SS) compared to controls, and if PCSK9 is related to disease-related data and the subclinical atherosclerosis that occurs in these patients.Cross-sectional study that encompassed 146 individuals; 73 patients with SS and 73 age- and sex-matched controls. PCSK9, lipoproteins serum concentrations, and standard lipid profiles were assessed in patients and controls. Carotid intima-media thickness (cIMT) and the presence of carotid plaques were evaluated in SS patients. A multivariable analysis, adjusted for traditional cardiovascular risk factors, was performed to evaluate the differences in PCSK9 between patients and controls, the association of SS-related manifestations with PCSK9 levels, and if PCSK9 was associated with subclinical carotid atherosclerosis in SS patients.After multivariable analysis, PCSK9 was downregulated in SS patients compared to controls (beta coefficient -78 (95%CI -106 - -50) ng/ml, p=0.000) and skin thickness was associated with higher serum levels of PCSK9 (beta coef. 22 (7-37) units, p=0.005). PCSK9 was significantly and positively associated with cIMT (beta coef. 0.65 (0.06-1.24) ng/ml, p=0.031) in SS patients after multivariable adjustment.PCSK9 serum concentration is downregulated in SS patients compared to controls and is directly associated with disease severity subrogated parameters. PCSK9 was independently related to cIMT in SS patients.

Patients with rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE) have an increased premature prevalence of atherosclerosis. We aimed to determine whether there are differences in the prevalence of classic cardiovascular risk factors between SLE and RA. We also analysed the effect of traditional cardiovascular risk factors on the development of subclinical atherosclerosis in both conditions and if some disease-characteristic features are associated with these traditional cardiovascular risk factors.This was a cross-sectional study encompassing 602 individuals, 276 SLE and 326 RA patients. Subclinical atherosclerosis (presence of carotid plaques and carotid intima-media thickness [cIMT]) was determined by carotid ultrasonography. A multivariable regression analysis was performed to evaluate whether classic cardiovascular-related risk factors differentially influence subclinical carotid atherosclerosis in SLE compared to RA patients.Age (interaction factor [if] p=0.000), hypertension (if p=0.034), and diabetes (if p=0.037) had a higher effect on cIMT in RA than in SLE subjects. However, these traditional cardiovascular factors did not yield different effects on the presence of carotid plaques in RA and SLE when the univariate interaction was analysed. In addition, no differences were found in the influence of hypertension, diabetes, dyslipidaemia or current smoking on cIMT or carotid plaque after adjusting for demographics, the presence of other traditional cardiovascular factors, and disease-related data. Moreover, the additive effect of several cardiovascular risk factors on the subclinical carotid atherosclerosis did not differ between the two diseases.The influence of traditional cardiovascular risk factors on cIMT and carotid plaque is similar in RA and SLE.

Background Both rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) patients are associated with an increased and premature prevalence of atherosclerosis. This has been characteristically attributed to the inflammation present in both diseases Objectives To analyze the differences in the role of traditional cardiovascular risk factors in the subclinical atherosclerosis between the two diseases. Methods Cross-sectional study encompassing 602 subjects, 276 SLE and 326 RA patients. Carotid plaques were assessed by ultrasonography. A multivariable regression analysis was performed to evaluate if classic cardiovascular-related risk factors influence differentially on subclinical carotid atherosclerosis in SLE compared to RA patients. Results Traditional cardiovascular risk factors were found to be prevalent in RA and SLE patients. Age (interaction factor p=0.000), hypertension (interaction factor p=0.034), and diabetes (interaction factor p=0.037) were found to have a higher effect on cIMT in RA patients compared to SLE subjects. No differences between RA and SLE were discovered in the effect of traditional cardiovascular factors over the presence of carotid plaque when univariate interaction was performed. After final adjustment for demographics, the presence of others traditional cardiovascular factors, and disease related data, no differences were found in the influence of hypertension, diabetes, dyslipidemia or current smoking over cIMT or the presence of carotid plaque. Moreover, the effect of the addition of various cardiovascular risk factors on the subclinical carotid atherosclerosis did not differ between both diseases. Conclusion The influence of traditional cardiovascular risk factors (hypertension, diabetes, dyslipemia and smoking) over cIMT and carotid plaque is equal in RA and SLE. No interaction was found between traditional cardiovascular risk factors and disease related data in the effect of the former on subclinical atherosclerosis. Disclosure of Interests Hiurma Sanchez-Perez: None declared, Juan Carlos Quevedo-Abeledo: None declared, Inigo Rua-Figueroa: None declared, Beatriz Tejera-Segura: None declared, Vanessa Hernandez-Hernandez: None declared, Antonia de Vera-Gonzalez: None declared, Alejandra Delgado-Gonzalez: None declared, Raquel Lopez-Mejias: None declared, Soledad Ojeda Grant/research support from: AMGEN, Speakers bureau: AMGEN, Miguel A Gonzalez-Gay Grant/research support from: Prof. MA Gonzalez-Gay received grants/research supports from Abbvie, MSD, Jansen and Roche., Speakers bureau: Consultation fees/participation in company sponsored speaker’s bureau from Pfizer, Lilly, Sobi, Celgene, Novartis, Roche and Sanofi., Ivan Ferraz-Amaro: None declared

Background:It is well established that patients with systemic sclerosis (SS) show a disrupted lipid profile and an increased cardiovascular risk. Cholesterol efflux capacity (CEC) is the ability of high-density lipoprotein (HDL)-cholesterol to accept cholesterol from macrophages. CEC has been linked to cardiovascular events in the general population and to subclinical atherosclerosis in patients with rheumatoid arthritis and systemic lupus erythematosus.Objectives:The main purpose of our study was to assess, for the first time, whether CEC is disrupted in patients with SS compared to controls. We also aimed to identify patients’ characteristics that could explain such potential CEC disturbance.Methods:Cross-sectional study that encompassed 188 individuals; 73 SS patients and 115 age- and sex-matched controls. CEC, using anin vitroassay, and lipoprotein serum concentrations were assessed in patients and controls. A multivariable analysis was performed to study the differences in CEC between patients and controls, and if SS-related data could explain CEC differences.Results:CEC was downregulated in SS patients as compared to controls (beta coefficient -6 [95%CI -10- -2] %, p=0.002). This occurred independently of traditional cardiovascular risk factors, statin use or other variations in the lipid profile produced by the disease. Demographics and lipid profile were, in general, not related with CEC in both patients and controls. In this sense, only abdominal circumference showed a positive association with CEC in patients (beta coefficient 0.09 [95%CI 0.03-0.14], p=0.002) but not in controls. Similarly, no traditional cardiovascular risk factors were related with CEC in both populations. Regarding lipid profile, no correlations were identified between the standard lipid profile molecules and CEC. Remarkably, the use of statins was not related to CEC in both patients and controls. Lastly, concerning SS related data, a negative association between mRSS and CEC was identified (beta coef. -1.08 [95%CI -2.03- -0.12] %, p=0.028).Skin thickness through modified Rodnan (mRSS) was positively related to age and the presence of hypertension, but negatively associated with apolipoprotein B, apo B:A1 ratio, and CEC when univariate correlations were assessed (Table 4). When the relation of mRSS to these lipid-related molecules was adjusted for traditional CV risk factors, the statistical significance of mRSS with those molecules was maintained. Moreover, when the relation between mRSS and CEC was additionally adjusted for other lipid-related molecules, its significance was conserved (beta coef. -1.35 [95%CI -2.62- -0.08]) %, p=0.038)Conclusion:CEC is downregulated in SS patients independently of other inflammation-related lipid profile modifications that occur in the disease. Skin thickness is independent and inversely associated with CEC in SS patients.Disclosure of Interests:Iván Ferraz-Amaro Grant/research support from: Pfizer, Abbvie, Speakers bureau: Pfizer, Abbvie, MSD., delgado frias esmeralda Speakers bureau: Pfizer, Abbvie, MSD, Vanessa Hernández-Hernández Speakers bureau: Pfizer, Abbvie, MSD, Hiurma Sánchez-Pérez: None declared, Laura de Armas-Rillo: None declared, Estefania Armas González: None declared, Jose David Machado: None declared, Federico Díaz-González Grant/research support from: Abbvie, Pfizer, MSD, Speakers bureau: Abbvie, Pfizer, MSD

The difficulty in diagnosis and the spectrum of clinical manifestations that can determine the choice of treatment for primary antiphospholipid syndrome (APS) has fostered the development of recommendations by the Spanish Society of Rheumatology (SER), based on the best possible evidence. These recommendations can serve as a reference for rheumatologists and other specialists involved in the management of APS.A panel of four rheumatologists, a gynaecologist and a haematologist with expertise in APS was created, previously selected by the SER through an open call or based on professional merits. The stages of the work were: identification of the key areas for drafting the document, analysis and synthesis of the scientific evidence (using the Scottish Intercollegiate Guidelines Network [SIGN] levels of evidence) and formulation of recommendations based on this evidence and formal assessment or reasoned judgement techniques (consensus techniques).46 recommendations were drawn up, addressing five main areas: diagnosis and evaluation, measurement of primary thromboprophylaxis, treatment for APS or secondary thromboprophylaxis, treatment for obstetric APS and special situations. These recommendations also include the role of novel oral anticoagulants, the problem of recurrences or the key risk factors identified in these subjects. This document reflects the first 21, referring to the areas of: diagnosis, evaluation and treatment of primary APS. The document provides a table of recommendations and treatment algorithms.An update of the SER recommendations on APS is presented. This document corresponds to partI, related to diagnosis, evaluation and treatment. These recommendations are considered tools for decision-making for clinicians, taking into consideration both the decision of the physician experienced in APS and the patient. A partII has also been prepared, which addresses aspects related to obstetric SAF and special situations.

Objective.Composite scores of cardiovascular (CV) risk factors underestimate the CV risk in patients with systemic lupus erythematosus (SLE). Carotid artery ultrasound (US) was found useful in identifying high CV–risk patients with inflammatory arthritis. We assessed the effect of carotid US assessments on the CV risk stratification of patients with SLE.Methods.This cross-sectional study included 276 patients with SLE. These indices were measured: lipid profile, Systematic COronary Risk Evaluation (SCORE) risk calculation, and disease activity (SLE Disease Activity Index), severity (Katz), and damage [Systemic Lupus International Collaborating Clinics (SLICC)/American College of Rheumatology Damage Index]. Carotid plaques were assessed by US. A multivariable regression analysis, adjusted for classic CV-related factors, was performed to evaluate how risk reclassification was influenced by disease characteristics in patients with SLE.Results.Thirty-six percent of patients had carotid plaques. However, only 6% of them fulfilled the definitions for high or very high risk according to the SCORE risk charts. Following carotid US assessment, 32% of the patients were reclassified as very high risk. Disease duration (OR 1.04, 95% CI 1.00–1.07, p = 0.025) and a SLICC > 0 (OR 2.48 95% CI 1.15–5.34, p = 0.020) were independently associated with a higher risk of reclassification. A predictive model for reclassification included age (cutoff 52 yrs, sensitivity 60%, specificity 86%), disease duration (cutoff 24 yrs, sensitivity 40%, specificity 82%), presence of hypertension, SLICC > 0, waist circumference (cutoff 102 cm, sensitivity 48%, specificity 84%), and C3 (cutoff 127 mg/dl, sensitivity 52%, specificity 92%) and triglyceride (cutoff 140 mg/dl, sensitivity 68%, specificity 79%) serum levels.Conclusion.Reclassification into a very high–risk category is frequent after carotid US assessments in patients with SLE. This is independently influenced by disease damage.

Background Systemic lupus erythematosus (SLE) is associated with a higher cardiovascular risk (CVR), at least doubled when compared with the general population, as well as an increased prevalence of atherosclerosis,which occurs prematurely and independently of traditional CVR factors. The presence of atheromatous plaques documented with carotid ultrasound (US) examination implies a change in the patient9s CVR category to “very high risk”,according to the “European Guidelines on cardiovascular disease prevention in clinical practice, 2016”. General guidelines do not take into account the specific increase in CVR risk that it9s present in patients with autoimmune diseases. Objectives To examine if the use of carotid US leads to a more accurate CVR classification in SLE patients, and in that way to a better CVR management. Methods Cross-sectional study that emcompassed 102 SLE patients currently being followed in our Rheumatology Department. Demographic variables, the presence of CVR factors and previous/current CV events, disease duration and drug use were analysed; lipid profile was assessed using blood tests, as well as carotid intima media thickness and the presence of carotid plaques using US scan. The current CVR status was calculated using the SCORE classification (low risk 10%). Results 95% of our patients were women,mean age was 51.6+/- years,median disease duration was 16 years (IQR 9–28). 35.29% of patients presented with at least one CVR factor before the SLE diagnosis,and 61.76% at the time of the research (19.60% current smokers, 39.21% high blood pressure (HBP),33.33% dyslipidemia, 7.84% type II diabetes. A CV event was diagnosed in 11.76% of our patients throughout their SLE disease. According to the SCORE classification,55 of them had a low CVR (53.92%),26 moderate CVR (25.49%),6 high CVR (5.88%) and 15 of them very highCVR (14.70%). Carotid plaques were found in 28 patients (27.45%): 23 of them had never had a CV event (22.54%),21.42% of them were current smokers,64.28% had HBP,53.57% dyslipidemia and 17.86% type II diabetes. After adjustment of the SCORE classification with the presence of carotid plaques,16.36% of patients from the “low CVR” category would be re-classified has having “very high CVR”, as well as 30.76% from the “moderate CVR” category and 50% from the “high CVR” category. Of note,8 patients within the “very high CVR” category also presented carotid plaques. Out of this patients with atheroma plaque,13 were not using statins,and in 2 of them it would have been mandatory in order to achieve the LDL Conclusions More than half of our SLE patients presented with at least 1 CVR factor. Around 15% of patients were categorised as “very high CVR” according to the SCORE classification.The presence of carotid plaque was found in 27.45% of our patients,and 82% of them hadn9t suffered any CV event. The use of carotid US examination allowed us to re-classify 20 patients (19.60%)in the “very high risk” category according to the SCORE classification. The need for a change in CVR management (ie., change in statin regime)was demonstrated in 4 of this 20 “re-classified” patients. Disclosure of Interest None declared

Background Insulin resistance (IR) may contribute to an increase in cardiovascular risk in general population as well as in Systemic Lupus Erythematosus (SLE) patients. Objectives The aim of this study was to examine the association between IR and disease activity, disease characteristics, drug exposure and subclinical atherosclerosis in patients with SLE. Methods Cross-sectional study that encompassed 87 SLE patients and 82 sex-matched controls. IR by homeostatic model assessment (HOMA2), insulin, C-peptide serum levels and lipid profile were assessed in both groups. Activity (SLEDAI), severity (Katz) and damage (SLICC) scores, carotid intima-media thickness (cIMT) and carotid plaques (ultrasound) were assessed in SLE patients. A multivariable regression analysis, adjusted for IR related factors, was performed to evaluate the differences between groups in IR indexes and, in SLE patients, the interrelation between IR and disease activity/characteristics as well as subclinical atherosclerosis. Results Median disease duration was 16 years (IQR 9–21). Body mass index, abdominal circumference, hypertension or dyslipidemia did not differ between groups. According to the SLEDAI score, 40% of patients were in no activity, while 32, 21, 18 and 1% were in mild, moderate, high and very high activity respectively. HOMA-IR-C-peptide (beta coefficiente 0.53, [95% CI 0.25–0.82], p=0.00) was increased in SLE patients when compared to controls, as well as HOMA %B C peptide levels (beta coef. 35, 95% CI 18–52, p=0.00). Similarly, insulin sensitivity estimated through HOMA-S% was inferior in SLE patients (-beta coef. -37, 95% CI -63–11, p=0.01).This diferences remained significant even after adjustment for IR related factors. SLICC damage index was clearly asociated with IR indexes; higher index values were related to higher HOMA-IR-C-peptide (beta coef. 37, [95% CI 16–57], p=0.00) and lower HOMA-S% levels (beta coef. 30%, [95% CI -47–14], p=0.00). Katz severity index showed correlation with HOMA-IR-C-peptide (beta coef.-5, [95% CI -11–0], p=0.04). These associations remained significant after adjustment for age, gender, smoking, hypertension and dyslipidemia, and, in relation with the SLICC index, also after adjustment for prednisone intake. SLEDAI activity index was not related to IR indexes. The use of prednisone was positively associated with HOMA-IR both when considered binary (beta coef 47, [95% CI 31–63], p=0.00) and continous (beta coef 2 [95% CI 0–5] per mg, p=0.03). Hydroxycloroquine (or other drugs) use was not associated with IR indexes, neither were disease duration, antiDNA titers and complement serum levels. Carotid plaques were found in 20% of the SLE patients. The presence of carotid plaques was correlated with a higher HOMA-IR-C-peptide (OR 3.15 [95% IC 1.17–8.51], p=0.02), and a higher cIMT value was associated with a lower HOMA-IR-S%>C-peptide (beta coef. 0.98 [95% CI 0.96–0.99], p=0.03). Nevertheless, after adjustment for cardiovascular risk factors this relation was lost. Conclusions Activity and damage indexes in SLE patients are independently related to the development of IR. IR is associated with subclinical carotid atherosclerosis in SLE patients on the univariate analysis. Disclosure of Interest None declared

Insulin resistance (IR) plays a role in the increased cardiovascular risk of systemic lupus erythematosus (SLE) patients. This study aimed to determine the potential association of IR with disease activity, drug exposure and subclinical atherosclerosis in patients with SLE.This cross-sectional study encompassed 87 non-diabetic SLE patients and 82 sex-matched controls. Insulin and C-peptide serum levels, IR indexes by homeostatic model assessment (HOMA2) (both insulin-based: HOMA2-IR, and with C-peptide: HOMA2-IR-C-peptide) and lipid profiles were assessed in patients and controls. Activity (SLEDAI), severity (Katz) and damage (SLICC) index scores, as well as carotid intima-media thickness (cIMT) and carotid plaques, were determined in SLE patients. A multivariable regression analysis, adjusted for classic IR related factors, was performed to evaluate the differences in IR indexes between patients and controls and how IR is associated with disease-related characteristics, including carotid ultrasound results, in SLE patients.SLE patients had higher C-peptide serum levels (2.61±1.51 vs. 1.34±0.62 ng/ml, p=0.00) and elevated HOMA2-IRC-peptide index (1.90±1.12 vs. 0.97±0.45, p=0.00) than controls. These differences remained statistically significant after adjusting for classic cardiovascular risk factors and prednisone intake. Traditional IR-related factors, such as body mass index, waist circumference or hypertension, and prednisone intake were significantly associated with HOMA2-IR and HOMA2-IRC-peptide in SLE patients. SLICC damage index was independently associated with HOMA2-IR-C-peptide. The presence of carotid plaques and cIMT values were associated with IR indexes in SLE patients only in the univariate analysis.C-peptide serum levels are independently up-regulated in SLE patients. Although classic IR factors and prednisone are associated with IR, SLE damage over time also contributes to IR in an independent way.