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Hidradenitis suppurativa (HS) is a chronic inflammatory disease associated with an increased prevalence of subclinical atherosclerosis and cardiovascular risk. Angiopoietin-2 (Ang-2), asymmetric dimethylarginine (ADMA), and osteoprotegerin (OPG) are molecules related to endothelial dysfunction (ED) and atherosclerosis, but also to disease severity in patients with chronic inflammatory disorders. In this case-control study, we aimed to investigate serum Ang-2, ADMA, and OPG levels in patients with HS, and to assess the potential relationship between these levels and disease severity. Seventy-five patients with HS and 60 controls were assessed. Serum Ang-2, ADMA, and OPG concentrations were determined in all participants. HS patients had significantly higher Ang-2 and ADMA levels than controls after adjusting for confounders. Besides, Ang-2 concentrations positively correlated with disease severity in the adjusted multivariable analysis. Nevertheless, serum OPG levels did not significantly differ between HS patients and controls. Our results indicate that serum Ang-2 and ADMA levels are significantly increased in patients with HS. Furthermore, Ang-2 might be a suitable marker of HS severity.

Introduction: Recent studies suggest a role of adipokines in the pathogenesis of hidradenitis suppurativa (HS). Omentin-1 and apelin are two recently identified adipokines that have been involved in the regulation of metabolic and inflammatory responses. Aim: To investigate serum omentin-1 and apelin levels in patients with HS and to assess their associations with metabolic parameters, disease severity and HS risk. Material and methods: This case-control study included 139 non-diabetic individuals (78 HS patients and 61 ageand sex-matched controls). Serum concentrations of omentin-1 and apelin and the homeostasis model assessment of insulin resistance (HOMA-IR) were measured in all participants. Results: Serum omentin-1 concentrations were significantly higher in HS patients compared to controls, whereas apelin serum levels did not significantly differ between both groups. These differences in omentin-1 concentrations remained significant even after adjusting for age, sex, and body mass index (BMI). The results of logistic regression analysis showed that increased omentin-1 plasma levels were an independent risk factor for HS. However, we found no association between serum levels of both omentin-1 and apelin with HS severity. Conclusions: Our results show that patients with HS have raised omentin-1 serum levels, which are associated with HS risk.

Objective To investigate if the Systematic Coronary Risk Evaluation (SCORE) and the QRISK3 algorithms as well as the carotid ultrasound are useful predictors of cardiovascular (CV) events and death in a prospectively defined population-based rheumatoid arthritis (RA) inception cohort. Methods A set of 327 consecutive RA patients without history of diabetes, chronic kidney disease or CV events were studied by carotid ultrasound between 2012 and 2013. At that time, CV risk was calculated according to the modified EULAR systematic coronary risk evaluation (mSCORE) for RA. A five-year prospective follow-up study was conducted by survival analysis models. The EULAR mSCORE based on the 2015/2016 updated EULAR recommendations and the QRISK3 algorithms were retrospectively tested using baseline data. Results After 1,984.25 patient-years of follow-up, 23 had died and 27 had experienced CV events. Linearized mortality rate was 1.16/100 patient-years (95% confidence interval [CI]: 0.74--1.73). Adjusting for age, gender and disease duration, a model with carotid plaques (Hazard ratio [HR]: 6.10 [95% CI:0.74--50.0]; p = 0.09) and another model with carotid plaques and QRISK3 (HR for carotid plaques: 6.12 [95% CI: 0.74--50.5]; p = 0.09 and HR for each 1% in QRISK3: 1.03 [95% CI: 0.99--1.07], p = 0.11, respectively were the best predictors of death whereas a model with carotid plaques (HR: 5.25 [95% CI:1.41--19.50]; p = 0.01) and another model with carotid plaques and QRISK3 (HR for carotid plaques: 5.13 [95% CI: 1.36--19.3]; p = 0.02 and HR for each 1% in QRISK3: 1.03 [95% CI: 0.99--1.07], p = 0.12, respectively, were the best predictors of CV events. In contrast, the mSCORE was a weaker predictor of the risk of death or CV events. Conclusions The presence of carotid plaques predicts the development of CV events and death in patients with RA. The predictable capacity of carotid plaques and QRISK3 is higher than that of mSCORE in RA patients.

Objective Because carotid plaques predict the development of cardiovascular events in RA, we aimed to assess if the combined use of the systematic coronary risk evaluation (SCORE) and the QRISK3 algorithms allows for the identification of RA patients with carotid plaques in a defined population-based RA inception cohort. Methods A set of consecutive RA patients without a history of diabetes, chronic kidney disease or cardiovascular events were studied by carotid US between 2012 and 2019. Modified SCORE (mSCORE) for RA based on the 2015/2016 updated EULAR recommendations and QRISK3 algorithms were retrospectively tested using baseline data obtained at the time of the carotid US assessment. Results A total of 466 (54%) of 865 patients had carotid plaques. Using dichotomized QRISK3 and EULAR mSCORE, 73.2% (95% CI: 68.4.8, 77.6) of patients with QRISK ≥ 10% and EULAR mSCORE Conclusions . The combined use of QRISK3 and EULAR mSCORE allows for the identification of most RA patients at high risk of carotid plaques.

Objectives: To identify disease-related factors associated with subclinical atherosclerosis and cardiovascular (CV) events in a large series of patients with axial spondyloarthritis (axSpA) and to identify possible differences in the effect of the potential pro-atherogenic factors between ankylosing spondylitis (AS) non-radiographic axSpA (nr-axSpA). Methods: This is a cross-sectional observational study of the AtheSpAin cohort, a Spanish multicenter cohort to study atherosclerosis in axSpA. Subclinical atherosclerosis determined by carotid ultrasound included assessment of carotid intima-media thickness (cIMT) and plaque detection. Results: 639 AS and 167 nr-axSpA patients were recruited. CV risk factors (CRF) and several disease-related factors showed a statistically significant association with subclinical atherosclerosis in the crude analysis. After adjustment for age, sex, and smoking (model 1), associations remained statistically significant for spinal mobility, inflammatory bowel disease, use of prednisone, and Disease-modifying antirheumatic drugs (DMARD) when assessing carotid plaques and for acute phase reactants (APR) at diagnosis, use of prednisone, DMARD, and TNF-inhibitors when measuring cIMT. In model 2, which also included classic CRF as confounding factors to identify axSpA features with a potential independent pro-atherogenic effect, the functional status was the only variable significantly associated with plaques and the use of prednisone and APR at diagnosis with cIMT. No association differences were found between both subtypes of patients. Besides, APR at diagnosis were also associated with subsequent development of CV events that had occurred in 33 patients. Conclusion: Apart from CRF, atherosclerotic disease in AxSpA is associated with disease-related factors such as inflammatory response and disease severity, with no differences between AS and nr-axSpA.

To determine the potential impact of extra-articular manifestations (EAMs) on disease characteristics and cardiovascular (CV) risk in patients with axial spondylarthritis (axSpA).This is a cross-sectional study from the AtheSpAin cohort, a Spanish multicenter cohort to study atherosclerosis in axSpA. Data on the history of CV events, subclinical carotid atherosclerosis, and disease-related features, including EAMs, were collected.888 axSpA patients were recruited. Concomitant acute anterior uveitis (AAU), psoriasis (PSO), and inflammatory bowel disease (IBD) were present in 177 (19.9%), 96 (10.8%), and 57 (6.4%) patients, respectively. When compared with axSpA patients without EAMs, a significant increase in past CV events was observed in patients with PSO (9% versus 4%, p = 0.048) and in those with at least one EAM (7% versus 4%, p = 0.032) or with more than one EAM (11% versus 4%, p = 0.022). The frequency of carotid plaques and the values of cIMT were higher in patients with EAMs than in those without EAMs, although only the univariable analysis for carotid plaques in patients with PSO (39% versus 30%, p = 0.038) and for cIMT in patients with AAU (665 ± 156 µm versus 637 ± 139 µm, p = 0.042) and those with at least one EAM (661 ± 155 µm versus 637 ± 139 µm, p = 0.024) showed significant results. In addition, patients with PSO or IBD were found to have specific disease-related features, such as higher ESR at diagnosis, and more frequent use of glucocorticoids and TNF inhibitors than those without EAMs. Also, PSO patients had more commonly peripheral involvement and those with AAU more severe radiographic damage than those without EAMs. The frequency of HLA B27 was higher in patients with AAU and lower in those with PSO or IBD compared to those without EAMs.Patients with axSpA and EAMs, in addition to displaying their own disease-related features, are likely to have an increased CV risk that appears proportional to the number of EAMs and could be related to proatherogenic factors other than traditional CV risk factors, such as the inflammatory load and the use of glucocorticoids.

Background: Interstitial lung diseases (ILD) lead to an increase in the patient’s morbidity and mortality. According to the etiology, ILD can be divided in disorders with either an unknown or known possible cause such as an underlying connective tissue disease (CTD) [1]. A specific T cell subset termed angiogenic T cells (TAng), that promote endothelial repair and revascularization, has been involved in the pathogenesis of CTD [2]. Nevertheless, little is known about their role in ILD. Objective: To assess the potential role of TAng in ILD. Methods: Peripheral venous blood was collected from 61 patients with ILD (composed of 21 with idiopathic pulmonary fibrosis (IPF) and 40 with CTD-ILD+), 44 CTD-ILD- patients and 20 healthy controls (HC). Quantification of TAng was performed by flow cytometry. TAng were considered as triple-positive for CD3, CD31 and CXCR4. Results: Patients with ILD exhibited a significantly lower TAng frequency than CTD-ILD- patients and HC (mean ± standard deviation: 11.98 ± 4.75 versus 16.24 ± 5.03 and 11.98 ± 4.75 versus 16.50 ± 4.83, respectively, p Conclusion: Our results disclose a decrease of TAng frequency related to the presence of ILD. References: [1] J Clin Med 2020;9(6):1606; [2] Ann Rheum Dis 2015 74(5):921-7. Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: INNVAL20/06 (IDIVAL); RP-F: START PROJECT (FOREUM); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).

Hidradenitis suppurativa (HS) is a chronic inflammatory disease associated with insulin resistance (IR), metabolic syndrome and increased cardiovascular risk. Adipokines are biologically active, pleotropic molecules which have been involved in the development of IR and in the pathogenesis of several chronic inflammatory conditions. The aim of the present study was to analyze serum concentrations of adiponectin, leptin, resistin and visfatin in patients with HS, and investigate their possible associations with IR, HS risk and disease severity. This case-control study enrolled 137 non-diabetic individuals (76 HS-patients and 61 age and sex-matched controls). Serum concentrations of adiponectin, leptin, resistin and visfatin, and the homeostasis model assessment of IR (HOMA-IR) were measured in all the participants. Serum adiponectin concentrations were found to be significantly lower, and leptin, resistin and visfatin levels were significantly higher in HS-patients than in controls. These differences remained significant even after adjusting for age, sex and body mass index, except for leptin. In a multivariate regression analysis, HOMA-IR was inversely correlated with adiponectin and positively associated with resistin levels. Furthermore, serum levels of resistin and visfatin were independently associated with HS risk. However, we found no association between serum levels of adipokines and HS severity. Our results suggest that reduced adiponectin and increased resistin serum levels may be surrogate biomarkers for IR in patients with HS. Moreover, resistin and visfatin might be independent risk factors for the development of HS.

Background: Previous studies have shown that risk chart algorithms, such as the Systematic Coronary Risk Assessment (SCORE), often underestimate the actual cardiovascular (CV) risk of patients with rheumatoid arthritis (RA). In contrast, carotid ultrasound was found to be useful to identify RA patients at high CV. In the present study, we aimed to determine if specific disease features influence the CV risk reclassification of RA patients assessed by SCORE risk charts and carotid ultrasound. Methods: 1279 RA patients without previous CV events, diabetes, or chronic kidney disease were studied. Disease characteristics including disease activity scores, CV comorbidity, SCORE calculation, and the presence of carotid plaque by carotid ultrasound were assessed. A multivariable regression analysis was performed to evaluate if the reclassification into very high CV risk category was independently associated with specific features of the disease including disease activity. Additionally, a prediction model for reclassification was constructed in RA patients. Results: After carotid ultrasound assessments, 54% of the patients had carotid plaque and consequently fulfilled definition for very high CV risk. Disease activity was statistically significantly associated with reclassification after fully multivariable analysis. A predictive model containing the presence of dyslipidemia and hypertension, an age exceeding 54 years, and a DAS28-ESR score equal or higher than 2.6 yielded the highest discrimination for reclassification. Conclusion: Reclassification into very high CV risk after carotid ultrasound assessment occurs in more than the half of patients with RA. This reclassification can be independently explained by the activity of the disease. Funding: This work was supported by a grant to I.F-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). Prof. González-Gay’s research 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 programs (RD12/0009 and RD16/0012).

Background: Axial spondyloarthritis (axSpA) patients are known to have a higher prevalence of several comorbidities, including, among others, an increased risk of atherosclerosis, hypertension, dyslipidemia, and diabetes. The purpose of the present study was to determine whether the sum of traditional cardiovascular (CV) risk factors is related to disease characteristics, such as disease activity, in patients with axSpA. Methods: A cross-sectional study that encompassed 804 patients with axSpA was conducted. Patients were assessed for the presence of five traditional CV risk factors (diabetes mellitus, dyslipidemia, hypertension, obesity, and smoking status), and disease activity measurements. A multivariable regression analysis was performed to evaluate whether the number of classic CV risk factors was independently associated with specific features of the disease, to include disease activity. Results: A multivariable analysis showed that Ankylosing Spondylitis Disease Activity Score-C reactive protein (ASDAS-CRP) activity score was significantly higher in patients with 1 [beta coefficient 0.3 (95% confidence interval (CI) 0.1-0.5), p = 0.001] and ?2 [beta coefficient 0.5 (95% CI 0.3-0.7), p = 0.000] CV risk factors compared with those without CV risk factors. Similarly, patients with 1 [OR 2.00 (95%CI 0.99-4.02), p = 0.053] and ?2 [OR 3.39 (95%CI 1.82-6.31), p = 0.000] CV risk factors had a higher odds ratio for the presence of high disease activity compared with the zero CV category. The Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) activity score was significantly associated with the number of CV risk factors, being higher in patients with more CV risk factors. These relationships showed a CV risk factor-dependent effect being beta coefficients and ORs higher for the effect of ?2 over 1 CV risk factor. Conclusion: Among patients with axSpA, as the number of traditional CV risk factors increased, disease activity similarly increases in an independent manner. Funding: The authors disclosed receipt of the following financial support for the research, authorship, and/ or publication of this article: This research was funded by a grant to MAG-G from 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 programs (RD12/0009 and RD16/0012).

Endothelial progenitor cells (EPC), which are key effectors in the physiologic vascular network, have been described as relevant players in autoimmune diseases. We previously showed that EPC frequency may help to identify the presence of interstitial lung disease (ILD) in rheumatoid arthritis patients. Given that ILD constitutes the main cause of mortality in systemic sclerosis (SSc) patients, we aimed to determine the EPC contribution to the pathogenic processes of vasculopathy and lung fibrosis in SSc-ILD+. EPC quantification was performed by flow cytometry on blood from 83 individuals: 21 SSc-ILD+ patients and subjects from comparative groups (20 SSc-ILD− and 21 idiopathic pulmonary fibrosis (IPF) patients and 21 healthy controls (HC)). EPC were considered as CD34+, CD45low, CD309+, and CD133+. A significant increase in EPC frequency was found in SSc-ILD+ patients when compared to HC (p &lt, 0.001). SSc-ILD+ patients exhibited a higher EPC frequency than SSc-ILD− patients (p = 0.012), whereas it was markedly reduced compared to IPF patients (p &lt, 0.001). EPC frequency was higher in males (p = 0.04) and negatively correlated to SSc duration (p = 0.04) in SSc-ILD+ patients. Our results indicate a role of EPC in the processes of vasculopathy and lung fibrosis in SSc-ILD+. EPC frequency may be considered as a biomarker of ILD in SSc patients.

Hidradenitis suppurativa (HS) is a chronic inflammatory disease associated with insulin resistance (IR). Retinol binding protein 4 (RBP4) and ghrelin are two bioactive proteins that have been involved in glucose metabolism and IR, but also in the regulation of immune and inflammatory processes. The aim of this study was to determine the serum levels of RBP4 and ghrelin in patients with HS, and to assess the possible relationship between these levels and IR, disease severity and HS risk. A total of 137 subjects (77 HS patients and 60 controls) without diabetes mellitus were enrolled in this cross-sectional study. Patients with HS had significantly higher RBP4 but lower ghrelin plasma levels than controls, independently of body mass index (BMI). Serum RBP4 levels were positively correlated to disease severity and IR in HS patients. However, we found no association between ghrelin levels and any clinical or laboratory parameters. Moreover, high serum RBP4 and low ghrelin levels were associated with an increased risk for HS. Our results suggest that high RBP4 levels may be a surrogate biomarker for IR in patients with HS. Moreover, increased RBP4 and decreased ghrelin levels could also be independent risk factors for the development of HS.

Cardiovascular (CV) disease is the main cause of mortality in axial spondyloarthritis (axSpA). CV risk is enhanced by dysregulation of adipokines. Low omentin levels were associated with metabolic dysfunction and CV disease in conditions different from axSpA. Accordingly, we evaluated the genetic and functional implication of omentin in CV risk and subclinical atherosclerosis in a cohort of 385 axSpA patients. Subclinical atherosclerosis was evaluated by carotid ultrasound. Omentin rs12409609, in linkage disequilibrium with a polymorphism associated with CV risk, was genotyped in 385 patients and 84 controls. Serum omentin levels were also determined. omentin mRNA expression was assessed in a subgroup of individuals. Serum and mRNA omentin levels were lower in axSpA compared to controls. Low serum omentin levels were related to male sex, obesity, inflammatory bowel disease (IBD) and high atherogenic index. rs12409609 minor allele was associated with low omentin mRNA expression in axSpA. No association was observed with subclinical atherosclerosis at the genetic or functional level. In conclusion, in our study low omentin serum levels were associated with CV risk factors in axSpA. Furthermore, rs12409609 minor allele may be downregulating the expression of omentin. These data support a role of omentin as a CV risk biomarker in axSpA. We wish to thank all the patients and controls that participated in this study. This work was supported by funds of a NEXT-VAL grant (NVAL17/10) (Instituto de Investigación Sanitaria IDIVAL) awarded to FG. SR-M is supported by funds of the RETICS Program (RD16/0012/0009) from the ‘Instituto de Salud Carlos III´ (ISCIII), co-funded by the European Regional Development Fund (ERDF). VP-C is supported by a pre-doctoral grant from IDIVAL (PREVAL 18/01). VM is supported by funds of a Miguel Servet type I programme (grant CP16/00033) (ISCIII, co-funded by the European Social Fund (ESF)). LL-G is supported by funds of PI18/00042 (ISCIII, co-funded by ERDF). RL-M is a recipient of a Miguel Servet type I programme fellowship from the ISCIII, co-funded by the ESF (grant CP16/00033).

Calprotectin (CPT) is released during inflammation, also in the context of atherosclerosis. The link between CPT and the atherosclerotic process was evaluated in several diseases. However, studies in axial spondyloarthritis (axSpA), associated with a high incidence of subclinical atherosclerosis, are scarce. Therefore, we assessed the association of CPT with subclinical atherosclerosis and metabolic risk factors in axSpA. CPT serum levels were measured by enzyme-linked immunosorbent assay in 163 axSpA patients and 63 controls. Subclinical atherosclerosis was determined in patients by carotid ultrasonography (assessing the presence/absence of carotid plaques and carotid intima-media thickness [cIMT]). Data on inflammation, disease activity, lipid profile and treatment were collected to evaluate its relationship with CPT. axSpA patients evidenced lower CPT levels than controls. CPT showed no association with plaques or cIMT in axSpA. CPT and HDL-cholesterol negatively correlated, while a positive association of CPT with the atherogenic index was disclosed. Additionally, axSpA patients with C-reactive protein values at diagnosis higher than 3?mg/L displayed higher CPT levels. Our study shows no relationship between CPT and markers of subclinical atherosclerosis in axSpA. Nevertheless, it demonstrates an association of CPT with adverse lipid profiles and inflammatory biomarkers, which could further influence on the development of atherosclerosis. We wish to thank all the patients and controls that participated in this study and Begoña Ubilla for technical assistance. FG is a recipient of a Sara Borrell post-doctoral fellowship from the Instituto de Salud Carlos III (ISCIII) (Spain), co-funded by the European Social Fund (ESF, “Investing in your future”) (grant CD15/00095). SR-M is supported by funds of the RETICS Program (RIER) RD16/0012/0009 (ISCIII, co-funded by the European Regional Development Fund, ERDF). VM is supported by funds of a Miguel Servet type I programme (grant CP16/00033) (ISCIII, co-funded by ERDF). RL-M is a recipient of a Miguel Servet type I programme fellowship from the ISCIII, co-funded by the ESF (grant CP16/00033). This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Background:The prevalence of inflammatory bowel disease (IBD) in ankylosing spondylitis (AS) has been reported to range between 6%-15%. As occurs with axial spondyloarthrtitis (axSpA), patients with IBD have an increased risk of cardiovascular (CV) events because of a process of accelerated atherosclerosis1. However, it is unknown whether the presence of IBD confers an increased cardiovascular CV risk in patients with axSpA.Objectives:To compare the atherosclerotic burden, CV events, CV risk factors and disease related factors including structural damage in axSpA patients with and without IBD.Methods:Cross-sectional analysis of the AtheSpAin cohort, a Spanish multicenter cohort designed for the study of atherosclerosis in axSpA, comparing axSpA patients with and without concomitant IBD. Background information on CV and disease-related factors was reviewed. Data on CV risk and disease status at the time of the study were also obtained, including the structural damage assessed by the presence of syndesmophytes, the severity of the sacroiliitis (defined as grade 3 or 4 according to New York criteria), and the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS). Carotid ultrasound (US) was performed in all patients at the time of the study, including measurement of carotid intima-media wall thickness (cIMT) and plaque detection according to the Mannhein consensus criteria.Results:A set of 886 axSpA patients were included. 829 (93.6%) of them had no concomitant IBD, which was present in 57 (6.4%) patients. Age, sex and AS/nr-axSpA ratio were comparable in both groups (Table 1. next page). Patients with IBD were characterised by a lower prevalence of HLA B27 (46% vs 72%, p=0.01) and a higher presence of concomitant psoriasis (21% vs 10%, p=0.01)Regarding peripheral disease (history of synovitis, enthesitis, dactylitis) and hip involvement, no differences were found between both groups. There were either no differences in the structural damage found in patients with and without IBD (Table 1. next page).With respect to the management of the disease, prednisone (21% vs 13%, p = 0.03), DMARDs (54% vs 35%, p = 0.01) and anti-TNFα therapy (54% vs 31%, p = 0.00) were more commonly used in the group with IBD, while treatment with NSAIDs was more frequent in patients without IBD (81% vs 70%, p = 0.04).Regarding CV risk features, smoking was more frequent in patients without IBD (34% vs 21%, p = 0.045) (Table 1. next page). No differences were observed neither in the lipid profile or blood pressure at the time of the study, nor in the prevalence of CV events (5% vs 4%, p=0.99) (Table 1) and the subclinical atherogenic burden assessed both by the presence of carotid plaques (31% vs 37%, p=0.45) and the cIMT (645 ± 147 mm vs 636 ± 112 mm, p = 0.64) (Table 1. next page).Conclusion:The presence of IBD does not confer additional CV risk to axSpA. In our series, patients with axSpA and IBD showed a lower frequency of HLA B27 and a higher prevalence of psoriasis.Table 1.axSpA without IBD (n=829)axSpA with IBD (n=57)pMen/Women, n272/55715/420.33Mean age (years) ±SD at the time of study49 ± 1349 ± 100.99AS/nr-AxSpa656/17345/120.97History of CV risk factors Current smoker285 (34)12 (21)0.045 Obesitty Dyslipemia280 (34)16 (28)0.42 Hypertension223 (27)16 (28)0.79 Diabetes Mellitus60 (7)4 (7)0.99 Chronic Kidney Disease20 (2)2 (4)0.65History of cardiovascular events, n (%)40 (5)2 (4)0.99Structural damage at the time of studyPresence of syndesmophytes, n (%)307 (37%)23 (49%)0.66mSASSS5 (1-15)6 (3-23)0.64Severe sacroiliitis (grade 3,4), n (%)436 (53)34 (60)0.42CV data at the time of studyCarotid plaques261 (31)21 (37)0.45IMT (mm)645 ± 147636 ± 1120.64IMT >= 0.9 mm46 (6)0 (0)0.066Abbreviations: AS = ankylosing spondylitis. AxSpA= axial spondylitis. CV = cardiovascular. IBD = Inflammatory bowel disease. IMT = intima-media wall thickness. Nr-axSpA = no-radiographic axial spondylitis.Disclosure of Interests:None declared

Psoriasis patients have high risk of atherosclerosis, characterized by endothelial dysfunction. We aimed to study the association of the endothelial activation biomarkers monocyte chemoattractant protein 1 (MCP-1), soluble (s) E-selectin and P-selectin with disease activity and severity in psoriasis patients treated with anti-TNF-α therapy. Also, to evaluate the relationship of metabolic syndrome features with these biomarkers and the effect of anti-TNF-α therapy on these molecules.Twenty-nine consecutive non-diabetic patients with moderate-to-severe psoriasis who underwent 6 months of anti-TNF-α-adalimumab therapy were studied. Metabolic and clinical evaluation was performed prior to anti-TNF-α treatment (time 0) and 6 months later. MCP-1, sE-selectin and sP-selectin serum levels were determined by ELISA.Dyslipidemic and obese patients showed higher MCP-1 levels at month 6 from the onset of anti-TNF-α therapy (p = .05 and .01, respectively). sE-selectin positively correlated with pro-inflammatory molecules such as asymmetric dimethylarginine, sP-selectin and resistin at baseline and month 6 (p .05). sE-selectin levels significantly reduced after 6 months of therapy (p = .0006).Metabolic syndrome features are associated with endothelial activation in patients with moderate-to-severe psoriasis. Adalimumab therapy led to a reduction in sE-selectin levels, supporting the beneficial effect of anti-TNF-α therapy on mechanisms associated with the development of atherosclerosis in psoriasis.

Background:Rheumatoid arthritis is an autoimmune disorder in which patients have an increased risk of developement of serious infections. This risk may be augmented due to RA itself and to immunosuppressive drugs, specially biologic therapy. Vaccination programs may change this condition.Objectives:Our aim in this study was to evaluate the incidence of serious infections in a vaccinate RA patients cohort.Methods:Prospective study of 401 patients diagnosed with RA who were invited to participate in the vaccination program of the Preventive Medicine department of our hospital from October 2011 to October 2016. The follow up was made until June 2017 with a minimun follow-up period of 8 months and maximun of 5.5 years. Serious infections were defined as those that required hospitalization or at least one dose of intravenous antibiotic treatement at emergency room. Information was retrieved from dthe hospital records.Only 7 patients refused vaccination (2%). Information was not obtained in 4 of the remaining 394 patients. Therefore, these 4 patients were not incuded in the assessment.Survival análisis was assessed by Kaplan-Meier method.Results:We finally studied 390 patients (307♀/83♂) mean age±SD 61,28 ± 12,9 years that participate in the vaccination program and followed-up. The main features at the time of vaccination were: median disease duration (4years), positive rheumatoid factor (56,7%), subcutaneous nodules (4.9%), erosive arthritis (36.9%), pulmonary fibrosis (3.8%), secondary Sjögren syndrome (5.1%), other extraartocular manifestations (14.6%) and rheumatoid vasculitis (5.6%) Most patients had received imunosuppressive drugs before the vaccination program. The most frequently used were systemic corticosteroids (n=228), methotrexate (n=362) and biologic agents (40.3%).During the follow-up, 42 patients (10.7%) had required hospital admissions due to infections, 17 of them were severe respiratory infections (4.35%). The remaining 25 admissions were in the setting of urinary tract infections (n=12), intraabdominal infections (7), skin and soft tissues (12) and articular (1). Also 12 of these patients had a zoster herpes.Afeter a median follow-up of 1061,89 ± 417 days, the incidence of serious infection, with a CI (95%), was 4.00 (2.95-5.41) for 100 patients yearly. Concerning to admissions due to serious respiratory infections, with a CI (95%), was 1.55 (0.9-2.47) for 100 patients yearly.Images 1 and 2.Image 1.Survival analysis on serious infectionsImage 1.Survival analysis on serious respiratory infectionsConclusion:In this stydy we can concluded that our RA vaccinated patients present a dicrease of the incidence of serious infeccions, similar to other published cohorts. The incidence of serious respiratory infections shows a dicrease even lower to other published cohorts. The vaccination program seems to be effective to prevent hospital admissions due to infections.Disclosure of Interests:Lucia Domínguez: None declared, Paz Rodriguez Cundin: None declared, Vanesa Calvo-Río Grant/research support from: MSD and Roche, Speakers bureau: AbbVie, Lilly, Celgene, Grünenthal, UCB Pharma, Nuria Vegas-Revenga Grant/research support from: AbbVie, Roche, Pfizer, Lilly, Gebro Pharma, MSD, Novartis, Bristol-Myers, Janssen, and Celgene, Virginia Portilla: None declared, Francisco Manuel Antolin-Juarez: None declared, Maria Henar Rebollo Rodriguez: None declared, Alfonso Corrales Speakers bureau: Abbvie, Natalia Palmou-Fontana: None declared, D. Prieto-Peña: None declared, Monica Calderón-Goercke: 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

Objective. Because the addition of carotid ultrasound (US) into composite cardiovascular (CV) risk scores has been found effective for identifying patients with inflammatory arthritis and high CV risk, we aimed to determine whether its use would facilitate the reclassification of patients with psoriatic arthritis (PsA) into the very high Systematic Coronary Risk Evaluation (SCORE) risk category and whether this might be related to disease features. Methods. This was a cross-sectional study involving 206 patients who fulfilled ClASsification for Psoriatic ARthritis criteria for PsA, and 179 controls. We assessed lipid profile, SCORE, disease activity measurements, and the presence of carotid plaques and carotid intima-media thickness by ultrasonography. A multivariable regression analysis, adjusted for classic CV risk factors, was performed to evaluate whether the risk of reclassification could be explained by disease-related features and to assess the most parsimonious combination of risk reclassification predictors. Results. Forty-seven percent of patients were reclassified into a very high SCORE risk category after carotid US compared to 26% of controls (p < 0.001). Patients included in the low SCORE risk category were those who were more commonly reclassified (30% vs 14%, p = 0.002). The Disease Activity Index for PsA (DAPSA) score was associated with reclassification (? 1.10, 95% CI 1.02?1.19; p = 0.019) after adjusting for age and traditional CV risk factors. A model containing SCORE plus age, statin use, and DAPSA score yielded the highest discriminatory accuracy compared to the SCORE-alone model (area under the receiver-operating characteristic curve 0.863, 95% CI 0.789?0.936 vs 0.716, 95% CI 0.668?0.764; p < 0.001). Conclusion. Patients with PsA are more frequently reclassified into the very high SCORE risk category following carotid US assessment than controls. This was independently explained by the disease activity. Funding: This work was supported by a grant to I.F-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) Professor González-Gay research was supported by European Union FEDER funds and by the “Fondo de Investigación Sanitaria” (grants PI06/0024, PS09/00748, PI12/00060, PI15/00525 and PI18/00043) of the ‘Instituto de Salud Carlos III’ (ISCIII, Health Ministry, Spain). It was also partially supported by RETICS Programs RD12/0009 (RIER), RD12/0009/0013 and RD16/0012 from the ‘Instituto de Salud Carlos III’ (ISCIII, Health Ministry, Spain).

Background Immunosuppressed patients such as Rheumatoid Arthritis (RA) patients have a greater risk (1.5-2 times) of presenting herpes zoster (HZ). Both, the disease itself and the use of immunosuppressive drugs, are involve in this increased risk. Furthermore, in these patients is more frequent a disseminated presentation of zoster involving several dermatomes. Objectives In a series of RA patients our aim was analyzed HZ infections and to assess a) HZ prevalence and b) HZ general features Methods Prospective Single center study of 390 RA patients included in the vaccination program of the Preventive and Rheumatology department of our hospital between october 2011 and october 2016. The follow-up was made until December 2017. HZ vaccination is not included in our program. RA was diagnosed according to the ACR/EULAR 2010 proposed criteria (Arthritis Rheum 2010; 62: 2569–2581) The diagnose of HZ was made according to the clinical manifestations and was confirmed by a dermatologist. These manifestations were characteristic skin rash and blisters, paresthesia and local pain, in one (localized) or more dermatomes (generalized) Results We studied 390 patients (307♀/83♂), average age 61.28±12.9 years that were included in the vaccination program and followed-up. HZ infection was observed in 12 of 390 (3.07%) in the follow-up (TABLE). The 12 RA patients (11 women/1 man) with a mean±SD age of 67.5±11.67. More than half of patients, 7 (58.33%) were taking corticosteroids. 8 patients (66.66%) were receiving conventional disease modifying drugs (DMARDs) methotrexate (33.33%), leflunomide (16.66%) and hydroxychloroquine (16.66%). Besides corticosteroids and conventional DMARDs, 7 patients (58.33%) were in treatment with biologic drugs, tocilizumab (n=2), etanercept (n=2), adalimumab (n=2), and rituximab (n=1). Conclusion Herpes zoster is a relative frequent viral infection in RA patients non-vaccine for HZ. The female sex, older age, more aggressive RA and treatment with corticosteroids were more frequent. Probably in this group of patients HZ vaccination may be useful. Abbreviatures: MTX: methotrexate, LFN: leflunomide, HCQ: hydroxicloroquine, TCZ: tocilizumbas, ADA: adalimumab, ETN: etanercept Disclosure of Interests: Lucia Dominguez: None declared, Vanesa Calvo-Rio: None declared, Paz Rodriguez-Cundin: None declared, Virginia Portilla: None declared, Nuria Vegas-Revenga: None declared, Francisco Manuel Antolin-Juarez: None declared, Maria Henar Rebollo Rodriguez: None declared, Alfonso Corrales: None declared, D. Prieto-Pena: None declared, Monica Calderon-Goercke: None declared, 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., Ricardo Blanco Grant/research support from: Abbvie, MSD, and Roche, Consultant for: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen, Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen

Background RA is associated with the development of cardiovascular (CV) disease and subclinical atherosclerosis1. The presence of carotid plaques assessed by ultrasonography studies is a surrogate marker for subclinical atherosclerosis2. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is involved in homeostasis of cholesterol, a traditional CV risk factor related to RA and atherosclerosis1,3. PCSK9 polymorphisms can both increase and decrease the risk of CV disease in patients with atherosclerosis3. Moreover, PCSK9 levels have been also related with CV risk4. However, there is little information on PCSK9 in RA. Objectives To assess the role of several PCSK9 polymorphisms in RA and subclinical atherosclerosis in RA as well as to determine if these ones may influence on PCSK9 mRNA and protein levels. Methods PCSK9 rs2479409, rs11583680, rs2483205, rs2495477 and rs562556 polymorphisms were genotyped in 1,169 Spanish RA patients, who met the 1987 ACR and the 2010 ACR/EULAR criteria for RA5-6, and 528 healthy controls. Associations were estimated using odds ratios (OR) and 95% confidence intervals (CI). The potential association between PCSK9 polymorphisms in both RA and controls and the presence/absence of carotid plaques in RA was evaluated by logistic regression. PCSK9 mRNA expression and PCSK9 serum levels were determined by qPCR and ELISA, respectively. All results were adjusted by sex, age and traditional CV risk factors. Results Significant differences in the allele frequencies of PCSK9 rs2495477 between RA patients and controls were found (minor allele: OR=0.55, 95% CI=0.34-0.89, p=0.01). A significant association between minor allele of rs2495477 and carotid plaques was also disclosed in RA patients (OR=0.72, 95% CI=0.56-0.92, p=0.01). PCSK9 levels were significantly decreased in RA patients carrying rs2495477 minor allele compared to controls (97.8 ± 104.9 vs 235.8 ± 93.5 ng/mL, p=0.001). None of the five PCSK9 polymorphisms influenced on its expression. Conclusion Our study showed for the first time that PCSK9 rs2495477 confers protection against RA susceptibility and the development of subclinical atherosclerosis in RA patients. Furthermore, rs2495477 decreased PCSK9 serum levels in RA that may be crucial to control the disease. References [1] Autoimmun Rev. 2016; 15: 1013–30. [2] Ann Rheum Dis. 2014; 73: 722–7. [3] J Am Coll Cardiol. 2005; 45: 1611–9. [4] Atherosclerosis. 2016; 252: 50–60. [5] Arthritis Rheum. 1988; 31: 315–24. [6] Arthritis Rheum. 2010; 62: 2569–81. Acknowledgement Study supported by ERDF and PI15/00525 (ISCIII).Personal funds, SR-M: RD16/0012/0009 (ISCIII-ERDF); FG: Sara Borrell fellowship CD15/00095 (ISCIII-ESF); VP-C: PREVAL18/01 (IDIVAL); VM and RL-M: Miguel Servet type I CP16/00033 (ISCIII-ERDF,ISCIII-ESF). Disclosure of Interests Sara Remuzgo-Martinez: None declared, Fernanda Genre: None declared, Veronica Pulito-Cueto: None declared, Alfonso Corrales: None declared, Javier Llorca: None declared, Veronica Mijares: None declared, Leticia Lera-Gomez: None declared, Virginia Portilla: None declared, Ivan Ferraz-Amaro: None declared, Santos Castaneda Consultant for: Amgen, BMS, Pfizer, Lilly, MSD, Roche, Sanofi, UCB, Oreste Gualillo: None declared, Javier Martin Ibanez: None declared, Ricardo Blanco: None declared, Raquel Lopez-Mejias: None declared, 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.

Background Cardiovascular (CV) disease is one of the main causes of mortality in axial spondyloarthritis (axSpA). The higher incidence of CV risk factors and systemic chronic inflammation increase CV risk in axSpA.1 This is enhanced by a dysregulation of adipokines. Low levels of omentin, an anti-inflammatory adipokine, have been associated with metabolic dysfunction and CV disease in general population and conditions different from axSpA.2,3 Objectives To evaluate the implication of omentin in CV risk and subclinical atherosclerosis in axSpA at the genetic and functional (mRNA and protein) level. Methods 382 patients fulfilling the ASAS classification criteria for axSpA4 and 84 controls were included. Carotid ultrasound was performed to evaluate the presence of subclinical atherosclerosis. Serum omentin levels were assessed by ELISA. mRNA expression of ITLN1, coding omentin, was evaluated by RT-qPCR. ITLN1 rs12409609 (C/T), in complete linkage disequilibrium with a polymorphism previously associated with coronary artery disease,5 was genotyped by TaqMan probes. Results were adjusted by potential confounding factors (STATA® v.11.1). Results Serum and mRNA levels of omentin were lower in axSpA compared to controls (p Conclusion style=”font-family: ‘Times New Roman’,’serif’; font-size: 10.0pt; margin: 0cm; margin-bottom: 8.0pt; line-height: 106%; margin-left: 0cm; margin-right: 0cm; margin-top: 0cm; mso-style-name: Normal_0; text-align: justify;” fontsize=”11.0” data-pos-index=”15” class-name=”Deleted”>Omentin is linked to obesity and adverse lipid profiles in axSpA. Additionally, low serum levels of omentin are associated with the presence of IBD in axSpA. These data support a role of omentin as a CV risk biomarker in axSpA. References [1] Joint Bone Spine.2014;81:57-63. [2] Cardiovasc Hematol Disord Drug Targets.2013;13:59-72. [3] Curr Issues Pharm Med Sci.2015;28:176-80. [4] Ann Rheum Dis.2009;68:777-83. [5] Asian Cardiovasc Thorac Ann.2017;25:199-203. Acknowledgement Study supported by NVAL17/10 (IDIVAL). Personal funds: FG: Sara Borrell fellowship CD15/00095 (ISCIII-ESF); SR-M: RD16/0012/0009 (ISCIII-ERDF); VP-C: PREVAL18/01 (IDIVAL); VM and RL-M: Miguel Servet type I CP16/00033 (ISCIII-ERDF, ISCIII-ESF). Disclosure of Interests Fernanda Genre: None declared, Javier Rueda-Gotor: None declared, Sara Remuzgo-Martinez: None declared, Veronica Pulito-Cueto: None declared, Alfonso Corrales: None declared, Veronica Mijares: None declared, Leticia Lera-Gomez: None declared, Virginia Portilla: None declared, Rosa Exposito: None declared, Cristina Mata: None declared, Ivan Ferraz-Amaro: None declared, Vanessa Hernandez-Hernandez: None declared, Santos Castaneda Consultant for: Amgen, BMS, Pfizer, Lilly, MSD, Roche, Sanofi, UCB, Esther Vicente: None declared, Cristina Fernandez-Carballido: None declared, Maria Paz Martinez-Vidal: None declared, David Castro-Corredor: None declared, Joaquin Anino-Fernandez: None declared, Juan Carlos Quevedo-Abeledo: None declared, Carlos Rodriguez-Lozano: None declared, Ricardo Blanco Grant/research support from: Abbvie, MSD and Roche, Consultant for: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Oreste Gualillo: None declared, Javier Martin Ibanez: None declared, Javier Llorca: None declared, Raquel Lopez-Mejias: None declared, 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.

Background:Endothelial progenitor cells (EPC), involved in vasculogenesis and endothelial tissue repair, have been described as relevant players in vascular and connective tissue diseases [1-2]. In this regard, a previous study of our group disclosed that the degree of EPC frequency may help to identify the presence of interstitial lung disease (ILD) in rheumatoid arthritis patients [3]. Given that ILD is the main cause of mortality in patients with systemic sclerosis (SSc) [1, 4-6], the understanding of the role of EPC in the mechanism of SSc-ILD+ vasculopathy is crucial.Objectives:To assess the potential role of EPC on vascular dysfunction associated with the presence of ILD in patients with SSc.Methods:Peripheral venous blood was collected from a total of 39 patients with SSc, 20 with ILD (SSc-ILD+) and 19 without ILD (SSc-ILD-). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of EPC was analyzed by flow cytometry. EPC were considered as CD34+, CD45Low, CD309+ and CD133+.Results:Statistically significant differences in EPC frequency between patients with SSc-ILD+ and patients with SSc-ILD- were disclosed. Specifically, an increase of EPC frequency was observed in SSc-ILD+ patients when compared to patients with SSc-ILD- (mean ± standard deviation: 0.033 ± 0.012 versus 0.021 ± 0.017, respectively, p=0.012).Conclusion:Our results suggest a potential role of EPC on vascular damage associated with the manifestation of ILD in patients with SSc.References:[1]Eur J Rheumatol 2020;7(Suppl 3):S139-S146.[2]Arthritis Rheum 2009;60(11):3168-79.[3]J Clin Med 2020;9(12):4098.[4]Ann Rheum Dis 2007;66(7):940-4.[5]Rheumatology (Oxford) 2010;49(12):2375-80.[6]Eur Respir Rev 2015;24(135):102-14.Acknowledgements:Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: INNVAL20/06 (IDIVAL); RP-F: START PROJECT (FOREUM); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).Disclosure of Interests:Verónica Pulito-Cueto: None declared, Sara Remuzgo Martinez: None declared, Fernanda Genre: None declared, Belén Atienza-Mateo: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe-Fernández: None declared, Leticia Lera-Gómez: None declared, Raquel Pérez-Fernández: None declared, Diana Prieto-Peña: None declared, Virginia Portilla: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Alfonso Corrales: None declared, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD

Background:Anterior uveitis (AU) is one of the most frequent extra articular manifestations of axial spondyloarthritis (axSpA), present in around 25% of patients. As with axSpA, AU has also been associated with the development of accelerated atherosclerosis1. If the presence of AU confers an increased cardiovascular (CV) risk or specific disease-related features to patients with axSpA remains unclear.Objectives:To compare the atherosclerotic burden, CV events, CV risk factors and disease related factors including structural damage in axSpA patients with and without AU.Methods:Cross-sectional analysis of the AtheSpAin cohort, a Spanish multicenter cohort designed for the study of atherosclerosis in axSpA, comparing axSpA patients with and without concomitant uveitis. Background information on CV and disease-related factors was reviewed. Data on CV risk and disease status at the time of the study were also obtained, including the structural damage assessed by the presence of syndesmophytes, the severity of the sacroiliitis (defined as grade 3 or 4 according to New York criteria), and the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS). Carotid ultrasound (US) was performed in all patients at the time of the study, including measurement of carotid intima-media wall thickness (cIMT) and plaque detection according to the Mannhein consensus criteria.Results:A set of 886 axSpA patients were included. 709 (80.0%) of them had no history of concomitant AU, which was present in the remaining 177 (20.0%). The group with AU was older (50 ± 11 vs 48 ± 13 years, p=0.05), had a higher proportion of patients with AS (90.1% vs 76.3%, p=0.00) (Table 1) and a longer disease duration 13(7-23) vs 7(2-16) years, p=0.00]. The prevalence of HLA-B27 was higher in AU patients (82% vs 67%).Remarkably, structural damage showed interesting differences between both groups (Table 1). AU patients had a higher prevalence of severe sacroiliits (69% vs 49%, p=0.00), which remained significant after adjustment for age, disease duration and AS/nr-axSpA ratio. Furthermore, a non-significant trend towards a higher prevalence of syndesmophytes (44% vs 36%, p=0.06) and hip involvement (20% vs 15%, p=0.09) was observed in the group of AU.Regarding CV risk features, no differences were observed in the prevalence of CV risk factors and events (Table 1). Patients with AU showed a higher cIMT in the crude analysis (665 ± 156 mm vs 640 ± 142 mm, p = 0.047), but no significant differences were observed after adjustment by age and sex (p=0.6). Prevalence of carotid plaques was comparable in both groups (32% Vs 32%, p=0.84).Table 1.axSpA without uveitis (n=709)axSpA with uveitis (n=177)pP (adjusted model)Men/Women, n477/232122/550.68Mean age (years) ±SD at the time of study48 ± 1350 ± 110.049AS/nr-AxSpa541/168160/170.000History of CV risk factors, n (%) Current smoker247 (35)50 (28)0.096 Obesitty Dyslipemia233 (33)63 (36)0.48 Hypertension188 (27)50 (28)0.63 Diabetes Mellitus50 (7)14 (8)0.69 Chronic Kidney Disease18 (3)4 (2)0.99History of cardiovascular events, n (%)29 (4)12 (7)0.13Structural damage at the time of studyPresence of syndesmophytes, n (%)253 (36)77 (44)0.063mSASSS5 (1-15)6 (0-16)0.31Severe sacroiliitis (grade 3,4), n (%)348 (49)122 (69)0.0000.000*Carotid US data at the time of studyCarotid plaques, n (%)225 (32)57 (32)0.84IMT (mm)640 ± 142665 ± 1560.0470.6**IMT >= 0.900 mm36 (5)10 (6)0.72*: adjusted by age, disease duration and AS/nr-axSpA ratio**: adjusted by age and sexAbbreviations: AS = ankylosing spondylitis. AxSpA= axial spondylitis. CV = cardiovascular. IMT = intima-media wall thickness. Nr-axSpA = no-radiographic axial spondylitis.Conclusion:The presence of AU does not confer additional CV risk to axSpA patients, although it is associated with a more severe structural damage in our series.References:[1]Conkar S, Güven Yilmaz S, Koska İÖ, Berdeli A, Mir S. Evaluation of development of subclinical atherosclerosis in children with uveitis. Clin Rheumatol. 2018 May;37(5):1305-1308.Disclosure of Interests:None declared

Background:Vaspin is a novel anti-inflammatory adipokine associated with cardiovascular (CV) disease and inflammation in chronic inflammatory conditions different from axial spondyloarthritis (axSpA).1 Given the high incidence of CV disease (mainly due to accelerated atherosclerosis) exhibited by axSpA patients,2 we wondered if vaspin could also be a key molecule in this process. However, data on the role of vaspin regarding atherosclerotic disease in the context of axSpA is scarce.3Objectives:To evaluate the implication of vaspin, at the genetic and serological level, in subclinical atherosclerosis and CV risk in axSpA.Methods:510 patients who fulfilled the ASAS criteria for axSpA4 were included in this study. Carotid ultrasound (US) was performed to evaluate the presence of subclinical atherosclerosis. Three vaspin gene variants (rs2236242 T/A, rs7159023 G/A and rs35262691 T/C) were genotyped by TaqMan probes. Serum vaspin levels were assessed by Enzyme-Linked ImmunoSorbent Assay. Analysis was performed using a statistical software.Results:Serum vaspin levels were significantly higher in female patients than in males and also in obese patients when compared to those with normal weight (pConclusion:Our results revealed that vaspin is linked to CV risk factors that may influence on the atherosclerotic process in axSpA. Additionally, we disclosed that serum vaspin concentration is genetically modulated in a large cohort of patients with axSpA.References:[1]Adv Exp Med Biol. 2019;1111:159-88.[2]Front Med (Lausanne). 2018;5:62.[3]Braz J Med Biol Res. 2016;49(7):e5231.[4]Ann Rheum Dis. 2009;68(2):ii1-44.Acknowledgements:Personal funds: RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF); SR-M: RD16/0012/0009 (ISCIII-ERDF); VP-C: PREVAL18/01 (IDIVAL); LL-G: INNVAL20/06 (IDIVAL).Disclosure of Interests:Javier Rueda-Gotor: None declared, Raquel López-Mejías: None declared, Sara Remuzgo-Martínez: None declared, Verónica Pulito Cueto: None declared, Alfonso Corrales: None declared, Leticia Lera-Gómez: None declared, Virginia Portilla: None declared, Iñigo González-Mazón: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Rosa Expósito: None declared, Cristina Mata: None declared, Javier Llorca: None declared, Vanessa Hernández-Hernández: None declared, Carlos Rodríguez-Lozano: None declared, Nuria Barbarroja Puerto: None declared, Rafaela Ortega Castro: None declared, Noelia García Castañeda: None declared, Cristina Fernández-Carballido: None declared, Maria Paz Martínez-Vidal: None declared, David Castro-Corredor: None declared, Joaquín Anino-Fernández: None declared, Diana Peiteado: None declared, Chamaida Plasencia: None declared, E Galindez: None declared, María L. García Vivar: None declared, Oreste Gualillo: None declared, Juan Carlos Quevedo-Abeledo: None declared, Santos Castañeda: None declared, Iván Ferraz-Amaro: None declared, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD, Fernanda Genre: None declared

Background:Interstitial lung disease (ILD) is one of the most significant complications of connective tissue diseases (CTD), leading to an increase of the morbidity and mortality in patients with CTD [1]. A specific T cell subset termed angiogenic T cells (TAng), that promote endothelial repair and revascularization, have been involved in the pathogenesis of CTD [2-4]. However, to the best of our knowledge, no information regarding the role of TAng in CTD-ILD+ is available.Objectives:To study, for the first time, the potential role of TAng related to vascular damage in CTD-ILD+.Methods:Peripheral venous blood was collected from 40 patients with CTD-ILD+ and three comparative groups: 44 CTD-ILD- patients, 21 idiopathic pulmonary fibrosis (IPF) patients and 20 healthy controls (HC). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of TAng was performed by flow cytometry. TAng were considered as triple-positive for CD3, CD31 and CXCR4.Results:Patients with CTD-ILD+ exhibited a significantly lower TAng frequency than CTD-ILD- patients (p+ were compared with HC (p=0.004) although no difference was observed between CTD-ILD+ and IPF. In addition, a significant increase of TAng frequency was shown in patients with CTD-ILD- in relation to IPF patients (p- and HC.Conclusion:Our results reveal a decrease of TAng frequency related to vascular damage in CTD-ILD+. Furthermore, we disclose that the presence of ILD is associated with lower TAng frequency.References:[1]Expert Rev Clin Immunol 2018;14(1):69-82.[2]Circulation 2007;116(15):1671-82.[3]Ann Rheum Dis 2015 74(5):921-7.[4]PLoS One 2017;12(8):e0183102.Acknowledgements:Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: INNVAL20/06 (IDIVAL); RP-F: START PROJECT (FOREUM); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).Disclosure of Interests:Verónica Pulito-Cueto: None declared, Sara Remuzgo Martinez: None declared, Fernanda Genre: None declared, Belén Atienza-Mateo: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe-Fernández: None declared, Leticia Lera-Gómez: None declared, Raquel Pérez-Fernández: None declared, Pilar Alonso Lecue: None declared, Javier Rodriguez Carrio: None declared, Diana Prieto-Peña: None declared, Virginia Portilla: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Alfonso Corrales: None declared, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD

Background:Patients with rheumatologic immune-mediated diseases (R-IMID) with Latent tuberculosis infection (LTBI) requiring biologic therapy (BT) are at an increased risk of active tuberculosis (TB). Screening of LTBI with tuberculin skin test (TST) and/or Interferon (IFN)-γ release assays (IGRA) is recommended before starting of BT.Objectives:In patients with R-IMID previously to BT our aim was to assess a) prevalence of LTBI, b) importance of using a booster test in negative TST and c) to compare TST with the IGRA test.Methods:Cross-sectional single University Hospital study including all patients diagnosed with R-IMID who underwent a TST and/or IGRA in the last five years (2016-2020).TST was performed by a subcutaneous injection of 0.1 ml of purified protein derivative (PPD) with a reading after 72 hours. TST was considered positive with an induration of more than 5 mm of diameter. If the first TST was negative, a new TST (Booster) was performed between 1 and 2 weeks after the first TST.LTBI was diagnosed by a positive IGRA and/or TST and absence of active TB (Chest radiograph). Diagnosis with IGRA vs TST was compared (Cohen’s kappa coefficient).Results:We included 1117 patients (741 women/376 men), mean age 53±15 years with LTBI. Chest radiograph was normal in most of the patients, only 39 patients (3.5%) presented signs of previous TB infection, mostly granuloma. Total LTBI prevalence was 31.7% (354/1117). LTBI prevalence in different underlying R-IMID ranges from 35% in vasculitis up to 26.5% in conectivopathies (Figure 1).Booster was positive in 66 patients (7.7%) out of 859 patients with a negative simple TST. Results of TST (+booster) and IGRA tests are shown in Table 1. TST (+booster) was positive in 187 patients (22.9%) out of 817 with a negative or indeterminate IGRA test. IGRA test was positive in 30 (3.8%) out of 793 patients with a negative TST (+booster). Cohen’s Kappa coefficient between TST (+booster) and IGRA (QFT-plus), was 0.381.Conclusion:LTBI is frequent between patients with R-IMID. Booster after negative simple TST may be useful, since it can detect false negatives for LTBI. IGRA and TST(+booster) show a low grade of agreement. Therefore, performing both tests before BT may be recommendable.Table 1.Results of TST (+booster) and IGRA testIGRA (QFT-Plus)PositiveNegativeIndeterminateUnavailableTotalTST(+Booster)Positive891424548324Negative30500130133793Total1196421751811117* Cohen’s kappa coefficient: 0.381Figure 1.Prevalence of LTBI in different underlying R-IMIDLTBI: Latent tuberculosis infection, PsA: Psoriatic arthritis, RA: Rheumatoid arthritis, SpA: Axial spondyloarthritis.Diagnosis of LTBI: Positive TST(+booster) and/or IGRA test.Disclosure of Interests:David Martínez-López: None declared, Joy Osorio-Chavez: None declared, Carmen Álvarez-Reguera: None declared, Virginia Portilla: None declared, Miguel A González-Gay Speakers bureau: Abbvie, Pfizer, Roche, Sanofi and MSD, Consultant of: Abbvie, Pfizer, Roche, Sanofi and MSD, Grant/research support from: Abbvie, MSD, Jansen and Roche, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen, Lilly and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen, Lilly and MSD, Grant/research support from: Abbvie, MSD, and Roche

Background:Tuberculosis (TB) may be increased with biologic therapy (BT). Diagnosis and treatment of latent TB infection (LTBI) is the best strategy to prevent TB. In Rheumatic Immune-Mediated Diseases (R-IMID) and LTBI, chemoprophylaxis must be used before BT. The drugs more frequently used are Isoniazid (INH), Rifampicin (RIF) and Fluoroquinolones (FQ). These drugs may be associated with side-effects, especially hepatotoxicity.Objectives:To assess, in a single University Hospital, a) used chemoprophylactic drugs and, b) adverse events with these drugs.Methods:We included all consecutive patients in the last five years (2016-2020) with a diagnosis of R-IMID and a positive LTBI test (positive tuberculin skin test and/or interferon-γ–release assay), who received chemoprophylaxis prior to BT.Dose of chemoprophylactic drugs were a) INH (5 mg/kg/d, maximum, 300 mg; for 9 months with vitamin B6), b) RIF (10 mg/kg/d, maximum, 600 mg for 4 months) and c) FQ levofloxacin (500 mg/day for 9 months).In all patients analytic controls that included liver enzymes were performed at the 1st and 3rd month and then at a variable time.Results:240 patients were analyzed (165 women/ 75 men), mean age of 56±11 years. The underlying R-IMID of patients receiving chemoprophylaxis were rheumatoid arthritis (n=74, 30.8%), axial spondyloarthritis (n=59, 24.6%), psoriatic arthritis (n=62, 25.8%), conectivopathies (n=17, 7.1%), vasculitis (n=12, 5%), sarcoidosis (n=2, 0.8%), Behçet’s disease (n=1, 0.4%), inflammatory myopathies (n=1, 0.4%) and other (n=12, 5%).At the onset of chemoprophylaxis they were taking: Prednisone in 61 patients (24 of them above 10 mg/day) and the following conventional DMARD, methotrexate (n=109, 45.4%), hydroxychloroquine (n=20, 8.3%), sulfasalazine (n=11, 4.6%), leflunomide (n=4, 1.7%) and azathioprine (n=2, 0.8%).The first-line chemoprophylactic drug was INH in 232 (96.7%) patients and RIF in the remaining 8 (3.3%). Due to adverse events, second-line therapy was used in 18 (RIF, n=17 and Levofloxacin, n=1) patients previously treated with INH.Adverse events were more frequent with INH, being observed in 55 patients (23.7%) out of 232. (Table 1 next page, Figure 1 below). By contrast, only 1 out of 25 (4%) receiving RIF presented an adverse event, which was hepatotoxicity, requiring suspension of RIF. No adverse events were described in the only patient receiving levofloxacin.Figure 1.Liver enzyme elevation over baseline in patients in treatment with isoniazid. * Patients with higher liver enzyme elevation are included in the previous groups.Conclusion:INH is the most used first-line treatment for LTBI. RIF was mainly used as second-line therapy if an adverse event with INH was observed. Treatment was generally well tolerated and most adverse events did not require the withdrawal of the treatment. Hepatotoxicity was the most frequent adverse event with INH and the most frequent cause of treatment withdrawal.Table 1.Adverse events with isoniazid at months 1 and 3 and after month 3Month 1(n=232)Month 3(n=222)After month 3(n=214)Adverse events, n (%)TotalRequiring switchingRequiring suspensionTotalRequiring switchingRequiring suspensionTotalRequiring switchingRequiring suspensionHepatotoxicity38 (16.4)6 (2.6)033 (14.9)5(2.3)2 (0.9)16 (7.5)2 (0.9)0Gastrointestinal side effects4 (1.3)3 (1.3)1 (0.4)3 (1.5)03 (1.5)2 (0.9)01 (0.5)Cutaneous toxicity2 (0.9)1 (0.4)0000000Dizziness1 (0.4)1 (0.4)0000000Total44 (19)11 (4.7)1 (0.4)36 (16.2)5 (2.3)5(2.2)18 (8.4)2 (0.9)1 (0.5)Disclosure of Interests:David Martínez-López: None declared, Javier Rueda-Gotor: None declared, Joy Osorio-Chavez: None declared, Carmen Álvarez-Reguera: None declared, Virginia Portilla: None declared, Miguel A González-Gay Speakers bureau: Abbvie, Pfizer, Roche, Sanofi and MSD, Consultant of: Abbvie, Pfizer, Roche, Sanofi and MSD, Grant/research support from: Abbvie, MSD, Jansen and Roche, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen, Lilly and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen, Lilly and MSD, Grant/research support from: Abbvie, MSD, Roche

Background:Cardiovascular disease (CVD) risk in patients with rheumatoid arthritis (RA) is substantially elevated compared to the general population. In RA, as in the general population, CVD control includes the detection and treatment of CV risk factors based, among others, on blood pressure, smoking, diabetes, and lipid profiles. Little is known about the real impact of the use of carotid ultrasound in the prevention of CVD in patients with RA.Objectives:To determine whether the use of carotid ultrasound in the routine clinical care of patients with RA can improve the achievement of LDL-cholesterol targets over time.Methods:We conducted a retrospective, real-world study of 327 RA patients in which a carotid ultrasound was performed as part of routine clinical care. Participants were followed from 2012 to 2018. LDL-c levels were measured before and after the carotid ultrasound intervention. The achievement of the LDL-c goals recommended by the international guidelines was compared before and after the carotid ultrasound. Predictive factors of achievement of LDL-cholesterol targets were studied.Results:When considering the 2010 EULAR RA SCORE risk categories, serum LDL-c levels in the moderate CV risk category was significantly lower when follow-up finished (126 ± 33 to 109 ± 29 mg/dl, p=0.000) (Table 1). This was not the case for other CV risk categories. Similarly, LDL-c goal attainment in the moderate CV risk category was significant higher at the end of the study compared to baseline. Based on the 2016 European Society of Cardiology LDL-c targets, the achievement of a LDL-cholesterol inferior to 115 mg/dl for the moderate CV risk category significantly increased from 35 to 64% (p=0.000) after follow-up. However, significant changes were not observed in this regard for the low, high, and very-high CV risk categories.Table 1.LDL cholesterol serum levels and LDL goals differences between baseline and final follow-upLDL, mg/dlLDL (mg/dl) ESC 2016 goalsn%BaselineFinal follow-upGoalBaselineFinal follow-upp2010 EULAR RA SCORELow12037116 ± 37119 ± 320.081< 13068%66%0.99Moderate19560126 ± 33109 ± 290.000< 11535%64%0.000High72121 ± 26104 ± 220.14< 10014%33%0.99Very High50131 ± 41115 ± 460.080< 700%20%0.99ESC: European Society of Cardiology; EULAR: European League Against Rheumatism. SCORE: Systematic COronary Risk Evaluation; RA: Rheumatoid Arthritis; LDL: low-density lipoprotein. Significant ‘p’ value are depicted in bold.When patients with RA, regardless the SCORE risk they had, were divided between those that attained LDL-cholesterol target or not, those that achieved their LDL goal, were more frequently female and had less diabetes mellitus. Moreover, the probability of achieving LDL-cholesterol goal was higher in those with an inferior total cholesterol, LDL-c and atherogenic index at baseline. Interestingly, no differences were observed in both populations regarding the baseline use of statins, aspirin or hypertension treatment at baseline. Concerning disease related data when study started, no differences about disease duration and activity or treatments were observed between dose that reached LDL-cholesterol goal and those that did not.Those that achieved LDL-c objectives had a higher decrease in smoking quit and a superior control of hypertension. Besides, in those that attained objectives a superior increase in statins prescription was observed (36% vs. 13%, p=0.000), as well in hypertension and aspirin treatment. However, no differences were noticed in the changes in disease-related data that occur during the time the study was carried out.Conclusion:This real-world study demonstrates that incorporating carotid ultrasound into routine clinical practice in RA patients is effective in achieving LDL-cholesterol targets for the prevention of cardiovascular disease. This effect is not only mediated by the increase in the prescription of statins, but also by the better control of other cardiovascular risk factors that occurred after carotid ultrasound evaluation.Disclosure of Interests:None declared

Background:Patients with axial spondyloarthritis (axSpA) may present with concomitant psoriasis (Ps) in approximately 10% of cases. As with axSpA, Ps is also associated with an accelerated atherosclerosis process1. However, it is unknown whether the presence of Ps confers an increased cardiovascular (CV) risk in patients with axSpA.Objectives:To compare factors related to the disease, CV risk factors, atherosclerotic burden, and CV events in patients with axSpA with and without Ps.Methods:Cross-sectional analysis of the AtheSpAin cohort, a Spanish multicenter cohort designed for the study of atherosclerosis in axSpA. We compared axSpA patients with and without concomitant psoriasis, focusing mainly on CV risk characteristics. Background information on CV risk factors, CV events, and disease-related factors was reviewed, and data on maximum body index, blood pressure, lipid profile, and disease status at the time of the study were also obtained. Carotid ultrasound (US) was performed in all patients at the time of the study, including measurement of carotid intima-media wall thickness (cIMT) and plaque detection according to the Mannhein consensus criteria.Results:A set of 882 axSpA patients were included. 786 (89.1%) of them had no concomitant Ps, which was present in 96 (10.9%) patients. Although the mean age was similar, male sex was more prevalent in axSpA patients with Ps (79.1% Vs 66.5%, p=0.01) (Table 1).Furthermore, it was found that axSpA with Ps had a more frequent history of synovitis (50% vs 33%, p = 0.001), dactylitis (13% vs 6%, p = 0.011) and concomitant inflammatory bowel disease (13% vs 6%, p = 0.01). AxSpA patients with Ps had a non-significant trend towards a higher prevalence of asymmetric sacroiliitis (23 vs 16%, p = 0.064) and had a lower frequency of positive HLA-B27 status (56% vs 72%, p = 0.003). Regarding the management of the disease, prednisone (23% vs 12%, p = 0.02), methotrexate (30% vs 15%, p = 0.000) and anti-TNFα therapy (50% vs 34%, p = 0.002) were more commonly used in the group with Ps.Regarding CV risk characteristics, no differences were observed either in the prevalence of traditional CV risk factors (Table 1), nor in the total serum level, HDL and LDL, blood pressure and body mass index at that time of the study. However, axSpA patients with Ps showed a higher prevalence of CV events (9% vs 4%, p = 0.05), including ischemic heart disease (6% vs 3%, p = 0.042) and ischemic stroke (4% vs 1%, p = 0.016) (Table 1). The subclinical atherogenic burden was also more severe in the group with Ps, with a higher prevalence of carotid plaques (39% vs 31%, p = 0.098), and higher values of cIMT (0.664 ± 0.170 mm vs 0.642 ± 0.142 mm, p = 0.16), although the differences did not reach statistical significance.Table 1.Main sociodemographic and cardiovascular differences among axSpA patients with and without psoriasis.axSpA without psoriasis (n=786)axSpA with psoriasis (n=96)pMen/Women, n523/26876/200.010Mean age (years) ±SD at the time of study49 ± 1349 ± 130.81AS/nr-AxSpa625/16677/190.79History of CV risk factors Current smokers267 (34)30 (31)0.60 Obesitty174 (22)26 (27)0.29 Dyslipidemia262 (33)35 (36)0.48 Hypertension211 (27)28 (29)0.57 Diabetes Mellitus56 (7)8 (8)0.65 Chronic Kidney Disease19 (2)3 (3)0.72History of cardiovascular events, n (%)33 (4)9 (9)0.023 Ischemic heart disease20 (3)6 (6)0.042 Congestive heart failure2 (0)1 (1)0.29 Ischemic stroke6 (1)4 (4)0.016 Peripheral artery disease6 (1)0 (0)0.99CV data at the time of studyCarotid plaques244 (31)38 (39)0.098IMT mm0.642 ± 0.1420.664 ± 0.1700.16IMT >= 900 mm40 (5)6 (6)0.66Abbreviations: AS = ankylosing spondylitis. AxSpA= axial spondylitis. CV = cardiovascular. IMT = intima-media wall thickness. Nr-axSpA = no-radiographic axial spondylitis.Conclusion:The presence of Ps may confer additional CV risk to axSpA patients and is associated with particular disease related factors.References:[1]Fang N, Jiang M, Fan Y. Association Between Psoriasis and Subclinical Atherosclerosis: A Meta-Analysis. Medicine (Baltimore). 2016;95(20):e3576.Disclosure of Interests:None declared.

Background:Interstitial lung disease (ILD) is one of the most significant comorbidities of rheumatoid arthritis (RA), increasing the mortality in these patients [1,2]. Although the pathogenesis of ILD associated to RA (RA-ILD+) remains poorly defined [1], it is known that vascular tissue plays a crucial role in lung physiology [3]. In this context, a population of cells termed endothelial progenitor cells (EPC) are involved in vasculogenesis and endothelial tissue repair [4]. Previous reports suggest the implication of EPC in different conditions such as RA and idiopathic pulmonary fibrosis (IPF), the most common and destructive ILD [5,6]. Nevertheless, little is known about their specific role in RA-ILD+.Objectives:The purpose of this study was to shed light on the potential role of EPC in endothelial damage in RA-ILD+.Methods:Peripheral venous blood was collected from a total of 68 individuals (18 with RA-ILD+, 17 with RA-ILD-, 19 with IPF and 14 healthy controls). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of EPC was analyzed by the expression of surface antigens by flow cytometry. The combination of antibodies against the stem cell marker CD34, the immature progenitor marker CD133, the endothelial marker VEGF receptor 2 (CD309) and the common leukocyte antigen CD45 was used. EPC were considered as CD34+, CD45Low, CD309+and CD133+. All statistical analyses were performed using Prism software 5 (GraphPad).Results:EPC frequency was significantly increased in patients with RA-ILD+, RA-ILD-and IPF compared to controls (p=0.001, p=0.002, p< 0.0001, respectively). Nevertheless, patients with RA, both RA-ILD+and RA-ILD-, showed a lower frequency of EPC than those with IPF (p= 0.048, p= 0.006, respectively).Conclusion:Our results provide evidence for a potential role of EPC as a reparative compensatory mechanism related to endothelial damage in RA-ILD+, RA-ILD-and IPF patients. Interestingly, EPC frequency may help to establish a differential diagnostic between patients with IPF and those who have an underlying autoimmune disease (RA-ILD+).References:[1] J Clin Med 2019; 8: 2038;[2] Arthritis Rheumatol 2015; 67: 28-38;[3] Nat Protoc 2015; 10: 1697-1708;[4] Science 1997; 275: 964-966;[5] Rheumatology (Oxford) 2012; 51: 1775-1784;[6] Angiogenesis 2013; 16: 147-157.Acknowledgments:Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: PI18/00042 (ISCIII-ERDF); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).Disclosure of Interests:Verónica Pulito-Cueto: None declared, Sara Remuzgo-Martínez: None declared, Fernanda Genre: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe Fernández: None declared, Sonia Fernández-Rozas: None declared, Leticia Lera-Gómez: None declared, Pilar Alonso Lecue: None declared, Javier Rodriguez Carrio: None declared, Belén Atienza-Mateo: None declared, Virginia Portilla: None declared, David Merino: None declared, Ricardo Blanco Grant/research support from: AbbVie, MSD, Roche, Consultant of: Abbvie, Eli Lilly, Pfizer, Roche, Bristol-Myers, Janssen, UCB Pharma and MSD, Speakers bureau: Abbvie, Eli Lilly, Pfizer, Roche, Bristol-Myers, Janssen, UCB Pharma. MSD, Alfonso Corrales Speakers bureau: Abbvie, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Grant/research support from: Pfizer, Abbvie, MSD, Speakers bureau: Pfizer, Abbvie, MSD

Background Cardiovascular (CV) disease and atherosclerosis are common causes of morbidity in axial spondyloarthritis (axSpA),1 a disease characterised by changes in the osteoproliferative process. A dysregulation in the molecules involved in bone remodelling could also affect the atherosclerotic process, since both processes are linked.2 3 Osteonectin (ON), a key molecule in bone homeostasis,4 was associated to obesity, insulin resistance and diabetes.5 Objectives Since the exact role of ON on CV risk in axSpA has not been elucidated yet, we evaluated its role in the development of subclinical atherosclerosis and its association with CV risk factors in axSpA patients at the serological and genetic level. Methods 171 axSpA patients fulfilling the classification criteria for axSpA6,7 and 84 controls were included in this study. Serum ON levels were measured by multiplex assays. Carotid ultrasound was performed to evaluate the presence of markers of subclinical atherosclerosis. Five ON polymorphisms (rs1054204 [G/C], rs11950384 [G/A], rs13182103 [A/G], rs11745387 [G/A] and rs4958487 [A/G]) were selected by tagging and genotyped using TaqMan assays. Results No difference was observed in ON levels between axSpA and controls. Serum ON and CRP levels at study positively correlated in axSpA (p=0.008). Higher ON levels were observed in men, smokers and patients with an atherogenic index indicative of dyslipidemia (p=0.008, 0.01 and 0.001, respectively). No association was found between ON and subclinical atherosclerosis in axSpA. Interestingly, we disclosed that the presence of the A allele of rs13182103 and rs11950384 ON polymorphisms led to lower ON serum levels in axSpA (p Conclusions Our results show that ON is linked to inflammation and CV risk factors in axSpA and suggest that the A allele of rs13182103 and rs11950384 ON polymorphisms may have a protective effect in axSpA, leading to reduced ON serum levels and later diagnosis of the disease. These data support an implication of ON in the development and progression of atherosclerotic disease in axSpA. References [1] Joint Bone Spine2014;81(1):57–63. [2] Clin Chim Acta2015;438:401–14. [3] Arterioscler Thromb Vasc Biol2001;21(12):1998–2003. [4] J Bone Miner Res2015;30(4):723–32. [5] Int J Clin Exp Med2015;8(10):19290–6. [6] Ann Rheum Dis2009;68:777–83. [7] Arthritis Rheum1984;27:361–8. Acknowledgements FG is a recipient of a Sara Borrell post-doctoral fellowship from Instituto de Salud Carlos III (ISCIII, Spain), co-funded by European Social Fund (ESF,CD15/00095). SR-M is supported by funds of RETICS Program (RD16/0012/0009,ISCIII,co-funded by European Regional Development Fund,ERDF). RL-M is a recipient of a Miguel Servet type I fellowship from ISCIII, co-funded by ESF(CP16/00033). VM is supported by funds of a Miguel Servet type I (CP16/00033)(ISCIII, co-funded by ERDF). Disclosure of Interest None declared

Background Ankylosing spondylitis (AS) is associated with increased rates of cardiovascular (CV) mortality. CV events can be prevented by identifying patients with high CV risk who can beneficiate from strict primary prevention measures. The systematic coronary risk evaluation (SCORE) is the predictive model recommended in Europe, but it underestimates the CV risk in individuals under 50 years old. Objectives To determine if the use of the relative risk (RR) chart score (figure 1) may help to identify young AS patients at high risk of CV disease. Methods A set of 73 AS patients younger than 50 years old without history of CV events, diabetes mellitus or chronic kidney disease was assessed. CV risk was calculated according to the total cholesterol systematic coronary risk evaluation (TC-SCORE) and the RR chart score. A value of C-reactive protein (CRP) >3 mg/L at diagnosis, cut-off point associated with an increased risk of CV events, and carotid ultrasound data performed at the time of the assessment were also analysed. Results Twenty (27.4%) of 73 patients exhibited carotid plaques and, consequently, they were classified into the category of very high CV risk. CRP>3 mg/L at disease diagnosis was associated with the presence of carotid plaques after adjustment for confounding factors (odds ratio 5.66, 95% confidence interval 1.11–28.77; p=0.03). None of these young patients were included in the category of high/very high CV according to the TC-SCORE. Whereas only 5 (14.2%) of the 35 patients with RR=1 had carotid plaques, 15 (39.5%) of 38 with RR >1 showed plaques. A model that included the performance of carotid US in patients with RR >1 who had CRP>3 mg/L at disease diagnosis allowed us to identify 60% of young AS with very high CV risk, with a specificity of 77.4% (area under the curve [AUC]: 0.69). The performance of carotid US in young AS patients with RR >1 regardless of CRP data at diagnosis increased the sensitivity up to 75% at the expense of a significant decline in the specificity to 56.6% (AUC: 0.66) (table 1). The gold standard used to define high/very high cardiovascular risk was the presence of TC-SCORE ≥5% or carotid plaques. Conclusions RR chart score assessment may help to identify young AS at high risk who are underdiagnosed as having very high CV risk by the SCORE. Disclosure of Interest None declared

Background Rheumatoid arthritis (RA) is associated with accelerated atherosclerosis, which results in high cardiovascular morbidity and mortality. The European Atherosclerosis Society recommends a strict control of cardiovascular (CV) risk factors, focusing in a healthy lifestyle, for the prevention of future CV events. Objectives Our aim was to assess the characteristics of healthy lifestyle in patients with RA and very high risk of CV events. Methods Prospective study that included a group of 113 patients, of whom 65 presented carotid plaques on carotid ultrasound study and, due to this, were categorised as having very CV high risk at the baseline visit. At this time, patients were informed about the risks associated to their disease and the high risk of having CV events. They were even warned of the need of healthy lifestyle habits. Data on lifestyle, smoking, obesity and diabetes mellitus were collected at baseline and last visit (with an interval of more than 5 years) Results The results of the 65 patients at the last visit are shown in table 1. The average age was of 67 years, with a disease duration of 17 years and high prevalence of dyslipidemia (72%), HTA (62%) and obesity (40%). Data obtained at the basal and last visit (with an average difference of 5.5 years) were compared in table 2. At last follow-up none of the smokers at baseline had discontinued smoking. There were no significant differences in the body mass index (BMI) average. Nevertheless, there was increase in the number of patients with a BMI 3 times/week) and did not have a sedentary lifestyle (50%), despite having a mean age of 67 years and long disease duration at baseline. Poor control of diabetes mellitus (DM), was found in more than half of the patients. Conclusions Despite having been informed on the high risk of CV events, patients with RA included in the category of very high CV risk performed poor long-term control of factors that include a healthy lifestyle. Disclosure of Interest None declared

Background Ankylosing spondylitis (AS) is associated with increased rates of cardiovascular (CV) disease. CV events in these patients can be prevented by identifying patients at high risk who can benefit from appropriate primary prevention measures. The systematic coronary risk evaluation (SCORE) is the predictive model recommended in Europe, but it underestimates the CV risk in AS. Objectives To determine if a lateral lumbar radiography, which is available in most of AS patients, may help to identify AS patients at high risk of CV disease. Methods 125 AS patients older than 35 years old without history of CV events, diabetes mellitus or chronic kidney disease were recruited. All patients underwent a carotid ultrasound (US) and lateral lumbar spine radiography and a multi-detector coronary tomography (MDCT) was also performed in a subgroup of 43 AS patients. Carotid plaques were defined according to the Mannheim consensus and the presence of AAC as calcific densities visible in an area parallel to the lumbar spine and anterior to the lower part of the spine. A Coronary Artery Calcification Score (CACS) superior to 100 were considered as a surrogate marker of coronary atherosclerosis. CV risk was calculated according to the total cholesterol systematic coronary risk evaluation (TC-SCORE). Results CV risk was categorised according to the TC-SCORE as low ( Conclusions Several AS patients at high CV risk who are underdiagnosed as having very high CV risk by the SCORE can be detected by a lateral lumbar radiography. Disclosure of Interest None declared

Background Rheumatoid arthritis (RA) patients are at increased risk of severe infections. Besides the disease itself, the immunosuppressive treatment appears to play an important role in the risk of infections. Vaccination programs are designed to decrease the risk of infections in these patients. Objectives Our aim was to assess the incidence of severe respiratory infections in patients with RA and to determine the underlying risk factors for the development of these complications. Methods Retrospective study of 401 patients diagnosed with RA who were invited to participate in a vaccination program from October 2011 to October 2016. The follow-up was made until June 2017 with a minimum follow-up period of 8 months and maximum of 5.5 years. Information on severe respiratory infection episodes was retrieved from the hospital medical records. Serious infections were defined as those that required hospitalisation or at least one dose of intravenous antibiotic treatment at the emergency room. Only 7 patients refused vaccination (2%). Information was not obtained in 4 of the remaining 394 patients. Therefore, these 4 patients were not included in the assessment. Results 390 patients (307♀/83 ♂) average age 61.28±12.9 years were vaccinated a followed-up. The main features at the time of vaccination were: median disease duration (4 years), positive rheumatoid factor (56.7%), subcutaneous nodules (4.9%), erosive arthritis (36.9%), pulmonary fibrosis (3.8%), Sjogren syndrome (5.1%) other extraarticular manifestations (14.6%) and rheumatoid vasculitis (5.6%). Most patients had received immunosuppressive drugs before the vaccination program. The most frequently used were systemic corticosteroids (n=228), methotrexate (n=362) and biologic agents (40.3%). During the follow-up, 42 patients (10.7%) had required hospital admissions due to infections, 17 of them were severe respiratory infections (4.35%) The remaining 25 admissions were in the setting of urinary tract infections (n=12), intraabdominal infections (n=7), skin and soft tissues (n=12) and articular (n=1). Also 12 of these patients had a zoster herpes. The presence of anti-citrullinated protein antibodies (ACPA) was associated with an increased frequency of admissions due to these infections. It was also the case for the presence of a history of biologic therapy prior to vaccination. No association of severe respiratory infection with rheumatoid factor, erosions or pulmonary fibrosis was found. (table 1). Conclusions Vaccinated patients with RA present a low incidence of severe respiratory infections. Positivity for ACPA and the use of biologics prior to vaccination are associated with increased risk of severe respiratory infections in these patients. Therefore, vaccination should be performed prior to the onset of biologic treatment. Disclosure of Interest None declared