Explore the vast range of titles available.

Lecturer play an important role in the process of planning the learning activities, one of them is in the selection of learning model. This research aims to improve the student activities and learning outcomes in the course of chemistry food materials using problem solving learning models integrated with video media. This research was a classroom action research, which consists of 3 cycles. The participants were students of the chemistry education study program who enrol chemistry food materials courses in the odd semester of academic year 2017/2018, totally 35 people. The data analysis technique is by calculating the average value and classical learning completeness. The data were gathered from test in the end of every cycle. It was found that the student's ability in learning process improved after the implementation of Problem Solving model. It could be seen in the improvement of average score for each test, from 78,81 in cycle I, 80,18 in cycle II to 85,69 in cycle III. In addition, classically learning completeness of students also improved, from 82,86 % in cycle I, 88,57 in cycle II to 100 % in cycle III.

Anti-Tumor Necrosis Factor (anti-TNF) drugs are biologic agents commonly used to treat rheumatoid arthritis (RA). However, anti-TNFs are not effective in approximately one out of four treated patients. We conducted a Genome-Wide Association Study (GWAS) to identify the genetic variation associated with the response to anti-TNF therapy in RA. In the discovery stage, 372 RA patients treated with an anti-TNF agent (infliximab, adalimumab or etanercept) were analyzed and treatment response was defined at 12 weeks of therapy. We found a genome-wide significant association in the MED15 gene with the response to etanercept ( P <1.5e-8). Using an independent cohort of 245 RA patients, we performed a replication study of the most significant GWAS associations. We replicated the association at the MED15 locus and found suggestive evidence of association in the previously associated MAFB locus. The results of this study suggest novel mechanisms associated with the response to anti-TNF therapies.

BackgroundObesity (BMI ≥30 kg/m2) is a common cardiovascular risk factor in psoriatic disease1. Although the prevalence of obesity is high, the factors associated with it in psoriatic arthritis (PsA) are poorly understood.ObjectivesWe aimed to evaluate the prevalence and obesity-associated factors in patients with PsA.MethodsRetrospective cross-sectional study that included 205 consecutive patients with PsA according to CASPAR criteria. The prevalence of obesity was compared with that of 310 patients with skin psoriasis of similar age (±3 years). The factors associated with obesity were first analysed by a conditional logistic regression. The significant factors in this first model were then introduced in a multivariate model using a backward step approach (p-values<0.05 were considered significant).ResultsOne-hundred twelve men and 94 women were included, with a mean age of 53±13 years. Obesity was more prevalent among psoriatics (36.5%) compared to PsA patients (24%), OR 1.6 (1.1–2.3), p<0.05. The factors associated with obesity in the univariate analysis (p<0.05) were: onset of psoriasis >40 years (OR 2.4), onset of arthritis >40 years (OR 2.1), PsA family history (OR 3.1), polyarticular presentation (OR 1.9), axial presentation (OR 2.5), polyarticular evolution (OR 2.4), axial evolution (OR 4.2), diabetes (OR 3.6), HBP (OR 3.9), and dyslipidemia (OR 3.5). After correcting for age, sex, disease duration and other confounders, independent associations with obesity found in the multivariate model (p<0.05) were: PsA family history (OR 3.6, IC95%: 1.1–14.4), axial evolution (OR 4.4, IC95%: 1.0–22.4) and dyslipidemia (OR 3.5, IC95%: 1.5–8.6).ConclusionsObesity was more common among our patients with cutaneous psoriasis than in those with arthritis. The model that best explains obesity in this PsA series combines genetic factors (PsA family history), together with factors specific to the metabolic syndrome (dyslipidemia), with others owned to arthritis (axial evolution).Reference[1] Husni ME. Comorbidities in psoriatic arthritis. Rheum Dis Clin North Am2015;41:677–98.Disclosure of InterestNone declared

Background:Autoimmunity and immune dysregulation may account for the cardiovascular risk excess in rheumatoid arthritis (RA), although exact mechanisms are incompletely understood. Angiogenic T-cells (Tang) may counteract endothelial damage, by collaborating with endothelial progenitor cells (EPC) in vascular repair. Tang depletion was linked to overt cardiovascular disease in established RA. Whether Tang are disturbed in the early stages of the disease is unknown.Objectives:To evaluate circulating Tang levels in the earliest stages of arthritis, including clinically suspect arthralgia (CSA), and their associations with subclinical CV endpoints (subclinical atherosclerosis and vascular stiffness).Methods:84 untreated RA patients (2010 EULAR/ACR classification criteria; 68% RF, 65% ACPA; mean DAS28: 5.16±1.44), 14 CSA individuals (EULAR definition; 57% RF, 50% ACPA) and 28 matched healthy controls (HC) were recruited. Tang (CD3+CD31+CXCR4+) and EPC (CD34+VEGFR2+CD133+) subsets were assessed by flow cytometry in peripheral blood samples. Plaque occurrence, cIMT and stiffness parameters were analyzed by Doppler ultrasound. Lipoprotein analyses were performed by NMR. Cardiometabolic-related proteins were assessed in serum using high-throughput targeted proteomics.Results:Tang frequency was decreased in arthralgia and RA patients compared to HC (p<0.050 and p<0.001, respectively). Although both CD4+ and CD8+Tang subsets were reduced in RA (p<0.001) compared to HC, only the CD4+Tang subset was diminished in arthralgia (p<0.050). Tang counts paralleled those EPC in HC (r=0.671, p<0.001), but this association was absent in arthralgia (r=0.423, p=0.131) and RA (r=-0.157, p=0.168). Similarly, Tang were negatively correlated with very low density lipoproteins features (cholesterol and triglyceride content, size distribution and particle number) and positively with HDL (cholesterol content and particle number) in HC (all p<0.010), whereas no associations were retrieved in RA and CSA groups. Proteomic analyses revealed that Tang frequency was associated with protein signatures related to blood pressure and vascular tone regulation in HC, whereas associations in RA and CSA were limited and related to inflammatory circuits (Figure 1).Figure 1.In RA patients, Tang levels were unrelated to traditional risk factors, body mass index or waist circumference (all p>0.050). However, disease activity accounted for Tang depletion both in univariate and multivariate analyses (B [95%CI]; DAS28: -0.121 [-0.193, -0.049], p<0.001; SDAI: -0.013 [-0.022, -0.003], p=0.008; CDAI: -0.014 [-0.024, -0.004], p=0.008). Tang frequency paralleled stiffness parameters: vascular strain (VS: r=0.373, p=0.013), distensibility (VD: r=0.479, p=0.004), stiffness (VSf: r=-0.400, p=0.007) and pressure-strain elastic modulus (PSEM: r=-0.373, p=0.013) in RA. Tang frequency remained as an independent predictor of stiffness parameters after adjusting for confounders (all p<0.050).Conclusion:Circulating Tang showed (vasculo)-protective associations in healthy controls, which are absent in arthritis. Tang depletion occurs early along RA development, linked to inflammation and disease activity. Circulating Tang may be a biomarker of premature vascular stiffness during the first stages of the disease.REFERENCES:NIL.Acknowledgements:ISCIII (PI21/00054, and FI22/00148).Disclosure of Interests:None declared.

Background:immune responses underlie vascular insult in rheumatoid arthritis (RA), hence accounting for cardiovascular risk excess. However, candidate mechanisms are yet to be identified. GPR55 is a cannabinoid receptor expressed in a variety of haematopoietic and stromal tissues. GPR55 signalling has been reported to modulate atherosclerosis progression and vascular remodelling, especially in knock-out animal models. No evidence in human patients is available.Objectives:to evaluate the GPR55 expression in leukocyte populations in RA patients and their potential role as biomarker in atherosclerosis.Methods:GPR55 expression on monocytes (CD14+ and CD14low subsets) and B-cells (CD19+) was quantified by flow cytometry in Peripheral Blood Mononuclear Cells (PBMCs) samples from 63 RA patients (2010 EULAR/ACR classification criteria; 69% RF, 67% ACPA; mean DAS28: 5.32±1.14), 11 individuals with clinically-suspect arthralgia (EULAR definition; 57% RF, 50% ACPA) and 36 matched healthy controls (HC). All patients were recruited at onset (untreated). Lipoprotein profiles were evaluated by conventional and NMR-based approaches. Atherosclerosis occurrence was measured by Doppler-ultrasound. Serum levels of proinflammatory cytokines were evaluated by immunoassays. Serum proteins were evaluated through a pre-defined panel by using high-throughput targeted proteomics.Results:GPR55 was detected on human monocytes and B-cells by flow cytometry. RA patients exhibited lower GPR55 expression (measured as mean fluorescence intensity) in monocyte subsets (CD14+: p=0.002, and CD14low: p<0.001) and B-cells (p=0.002) compared to HC. Equivalent results were obtained when the number of GPR55+ cells was computed for each subset (p=0.052, p=0.010 and p=0.010, respectively). No differences were observed between CSA individuals and HC (all p>0.050).GPR55 expression was unrelated to disease activity, joint counts, symptom duration or traditional cardiovascular risk factors in RA patients (all p>0.050). No associations were retrieved for the lipoprotein profile (all p>0.050). However, smoking was associated to lower expression on B-cells (p=0.047). This effect was dose-dependent (cigarettes/day: r=-0.249, p=0.039) and restricted to patients carrying the Shared Epitope (p=0.050, and r=-0.375, p=0.027; respectively). Atherosclerosis occurrence or cIMT were not associated with GPR55 expression on B-cells (p=0.174, and r=0.027, p=0.841, respectively), neither on monocyte subsets (all p>0.050).GPR55 expression on B-cells was correlated with serum levels of proinflammatory cytokines (IL6: r=0.236, p=0.062; IL-18: r=0.410, p<0.001, and IL-8: r=0.317, p=0.011) in RA patients. Furthermore, GPR55 expression on B-cells was associated with several proteins related to vascular remodelling (PGF, CXCL1, IL-18, SERPINA12, MMP7, THBS2 and MMP12) and B-cell activation/differentiation (SLAMF7, IL-6, TNFRSF13B or VSIG2). These proteins informed signatures (protein-protein interaction: p=5.99·10-11) related to humoral adaptive responses, cytokine production and regulation of defence response. However, these associations were atherosclerosis-dependent, and were only restricted to patients with atherosclerosis, where specific proteomic pathways involved in the positive regulation of cytokine production and cellular response to lipopolysaccharide predominated. Equivalent findings were found for the associations with proinflammatory cytokines.Conclusion:this is the first study assessing GPR55 expression in patients with rheumatic and musculoskeletal conditions. Reduced GPR55 expression hallmarked monocyte and B-cell subsets in RA patients at onset, whereas no differences were found in earliest stages. GPR55 expression was linked to B-cell activation-related pathways, especially in patients with atherosclerosis. GPR55 may be a novel hub to understand the links between immune (humoral) responses and atherosclerosis.REFERENCES:NIL.Acknowledgements:ISCIII (PI21/00054 and FI22/00148).Disclosure of Interests:None declared.

Background:informing residual risk to improve cardiovascular risk stratification is a major unmet need in rheumatoid arthritis (RA). Autoimmune phenomena and immune dysregulation, including humoral responses, are thought to play a role in risk excess. However, exact mediators are unknown. Age-associated B cells (ABCs) have emerged as multi-faceted pro-inflammatory mediators, also in the atherosclerosis microenvironment. Despite being expanded in autoimmunity, their role is ill-defined.Objectives:to evaluate ABCs levels in the earliest stages of inflammatory arthritis and their potential role as biomarkers of atherosclerosis.Methods:ABCs (CD19+CD21-CD11c+) were quantified by flow cytometry in Peripheral Blood Mononuclear Cells (PBMCs) samples from 58 early RA patients (2010 EULAR/ACR classification criteria; 69% RF, 66% ACPA; DAS28 5.28±1.13), 11 individuals with clinical-suspect arthralgia (CSA) (EULAR definition; 54% RF, 45% ACPA) and 33 healthy controls (HC). All patients were untreated at recruitment. Atherosclerosis occurrence was measured by Doppler-ultrasound. Cardiometabolic-related proteins were evaluated using high-throughput targeted proteomics.Results:ABCs frequency within the CD19+ compartment was increased in RA patients compared with HC (2.96±2.47 vs 1.56±1.36 %, p=0.013). Equivalent results were observed within the total PBMC pool (p<0.001). CSA individuals showed similar ABCs levels than RA (p=0.495). No associations with disease activity, symptom duration or RF/ACPA positivity were retrieved (all p>0.050). Higher ABCs counts at onset were linked to poor/moderate response to DMARDs (EULAR criteria) at 6 months compared to patients presenting a good response (p=0.022). ABCs frequency was positively correlated with serum levels of proinflammatory cytokines (IL6, IFNg and TNF, all p<0.050) in RA. Proteomic analyses revealed that ABCs were associated with 11 proteins (protein-protein interaction: p=3.3·10-10) (Figure 1A) related to B-cell activation, T-cell-dependent B-cell activation and macrophages/foam cell activation (Figure 1B). ABCs numbers were associated with atherosclerosis occurrence (p=0.006) and correlated with the number of atheroma plaques (r=0.346, p=0.010) in RA patients, whereas no correlation between cIMT and ABCs was found (p=0.322). ABCs counts were associated with atherosclerosis occurrence in univariate models (OR [95% CI], p: 1.260 [1.051-1.510], p=0.012), and remained as independent predictors of atherosclerosis after adjusting for traditional risk factors (OR [95% CI], p: 1.284 [1.037-1.589], p=0.022). Moreover, adding ABCs levels to the mSCORE improved risk stratification over the mSCORE alone based on diagnostic/classification statistics and net reclassification improvement (Figure 1C).Figure 1.Conclusion:ABCs expansion may be an early biomarker of atherosclerosis in arthritis, with incremental value in improving risk stratification over existing algorithms. ABCs may be a missing link between humoral responses and atherosclerosis in autoimmunity.REFERENCES:NIL.Acknowledgements:ISCIII (PI21/00054 and FI22/00148 grants).Disclosure of Interests:None declared.

Background:The HLA-Cw6 allele has been shown to be the main driver of the genetic burden of psoriatic disease and has also been associated with marked phenotypic traits. Recently, associations have been found between this biomarker and some cardiometabolic factors such as hypertension and visceral adiposity1-3.Objectives:We aimed to analyze the associations between some psoriasis-related genetic biomarkers and the presence of cardiometabolic risk factors.Methods:Cross-sectional observational study of 572 patients with psoriatic disease (30% PsA). The following genetic biomarkers were determined: HLA-Cw6*0602 allele (SNP rs1050414 C/G) and the IFIH1/MDA5 gene variants: rs35337543, intron8 + 1G>C; rs35744605, Glu627Stop; and rs1990760, Ala946Thr. The potential associations between these markers and cardiometabolic risk factors were investigated both by crude and adjusted regression models (software R 4.3.1 “Beagle Scouts”).Results:We included 309 (54%) men and 263 women (46%). Table 1 summarizes the main characteristics of the study population. Regarding PsA, associations with psoriasis severity (OR: 2.14), female sex (OR: 1.63), and the rs1990760 TT genotype (OR: 1.62) were found, while HLA-Cw6 positivity resulted protective (OR: 0.65). Cw6+ patients had a lower waist perimeter with an average of 2.37 cm less, however this difference was explained by age, female sex and arthritis. These subjects had on average 0.81 units less in BMI, but again this difference was explained by age, female sex, and arthritis. The Cw6+ patients weighed on average 2.3 kg less than the Cw6 negative patients, but this difference was explained by female sex and arthritis. The presence of this marker was associated with a reduction in the risk of hypertension (OR: 0.52, 95% CI: 20-66), however this difference lost significance after adjustment for age and arthritis. Cw6 positive subjects had a lower risk of diabetes (OR: 0.36, 95%CI: 0.19-0.63), however this association was lost after adjusting for age. We found no association between cardiometabolic comorbidity and IFIH1/MDA5 gene variants.Conclusion:The apparent protection conferred by HLA-Cw6 against the development of hypertension, diabetes or a greater visceral adiposity was explained by other variables such as age, sex or arthritis. Since the worldwide distribution of HLA-Cw6 is not uniform, these findings need further confirmation.REFERENCES:[1] Biomed Res Int 2022; 2022: 1451193.[2] J Invest Dermatol 2022; 142(6): 1617-1628.[3] Acta Derm Venereol 2023; 103: adv5209.Table 1.Distribution of study variables stratified by sexVariablesMen, n: 309Women, n: 263Total, n: 572Age (yrs), mean (SD)47.5 (14.6)45.7 (14.3)46.7 (14.5)Age at disease onset (yrs), median (min, max)24.5 [1.00, 74.0]20.0 [1.00, 78.0]23.0 [1.00, 78.0]Disease duration (yrs), mean (SD)18.7 (14.3)20.3 (15.4)19.4 (14.8)PsA, n (%)81 (26.2)90 (34.2)171 (30)Weight, mean (SD)85.4 (14.6)69.3 (13.9)77.9 (16.4)BMI, mean (SD)28.5 (4.43)26.7 (5.48)27.6 (5.02)Waist perimeter (cm), mean (SD)101 (11.6)91.4 (14.7)96.7 (14.1)PASI, mean (SD)16.0 (11.9)14.0 (12.0)15.1 (12.0)PASI ≥ 10, n (%)174 (56.3)120 (45.6%)294 (51.4%)Nail disease, n (%)192 (62.1)136 (51.7%)328 (57.3%)Plaque psoriasis, n (%)281 (90.9)216 (82.1)497 (86.9)Smoking, n (%)99 (32.0)97 (36.9)196 (34.3)alcohol consumption (SDU), median (min, max)0 [0, 2.00]0 [0, 30.0]0 [0, 30.0]T1D, n (%)11 (3.6)11 (4.2)22 (3.8)T2D, n (%)29 (9.4)16 (6.1)45 (7.9)Hypertension, n (%)68 (22.0)46 (17.5)114 (20.0)Dyslipidemia, n (%)68 (22.0)45 (17.1)113 (19.8)NAFLD, n (%)99 (32.0)30 (11.4)129 (22.6)Patients with adverse coronary events, n (%)20 (6.5)13 (4.9)33 (5.8)Patients on systemic therapy, n (%)203 (65.7)167 (63.5)370 (64.7)yrs: years; PsA: psoriatic arthritis; BMI: body mass index; PASI: psoriasis area and severity index; SDU: standard drink unit; T1D: type 1 diabetes; T2D: type 2 diabetes; NAFLD: non-alcoholic fatty liver disease.Acknowledgements:NIL.Disclosure of Interests:None declared.

Background:Persistence and safety data for tofacinitib (TOF) in psoriatic arthritis (PsA) are scarce and little known in real clinical practice[1]. This information is crucial to know the true value of this treatment in clinical practice, thus allowing better decisions to be made in the management of these patients.Objectives:We aimed to analyze the persistence and safety of TOF in patients with PsA under real-life conditions.Methods:The entire population with PsA exposed to at least one dose of TOF from a university hospital in northern Spain was included. The Kaplan-Meier survival curves of the drug were analyzed in the total population, by sex, according to the smoking status, and depending on the line of treatment (1st/2nd vs. 3rd or more). To analyze the explanatory factors of persistence, a multivariate Cox regression model was carried out. Adverse events were also recorded. The Hazard Ratio (HR) was used as measure of association.Results:Seventy-two patients were included, 54 women and 18 men. The majority were previously exposed to biologic therapies and targeted oral molecules (refractory PsA). Table 1 summarizes the main characteristics of the study population. The median survival of TOF was 13 months (IQR: 5.3-29). Persistence rate at first year was 52.7% (95%CI: 42.4-65.6). Figure 1 shows Kaplan-Meier curve of all-cause TOF discontinuation. Neither sex nor cardiometabolic factors (including obesity) nor the line of treatment influenced TOF survival. Younger patients [HR 0.96 (95%CI: 0.92-0.99), p=0.011] and those with enthesitis [HR 0.37 (95%CI: 0.15-0.92), p= 0.033] showed lower odds of TOF discontinuation. On the other hand, former smokers had a significantly higher risk of discontinuing TOF [HR 2.58 (95%CI: 1.05-6.39), p=0.04]. Patients with a history of exposure to methotrexate showed a trend towards a higher risk of discontinuation, although this did not reach statistical significance [HR 2.16 (95%CI: 0.96-4.86), p=0.063]. Of the 45 patients who discontinued the drug, 24 (53.3%) did so due to loss or lack of effectiveness, 10 (22.2%) due to intolerance, and the rest (11, 24.4%) due to adverse events during exposure.Conclusion:Tofacinitib showed good persistence in a PsA population mostly refractory to biologics and small oral molecules. Patients with enthesitis could be a group that responds especially well to the drug. Regarding safety, we did not detect new alarm signals.REFERENCES:[1] J Rheumatol 2021 Oct;48(10):1552-1558.Table 1.Study population characteristicsVariableWomen, n: 54Men, n: 18Total, n:72Age (yr), mean (SD)51.8 (10.5)52.1 (13.0)51.9 (11.1)Pso duration (yr), mean (SD)16.4 (11.9)15.2 (7.79)16.1 (11.0)PsA duration (yr), mean (SD)10.3 (7.51)10.8 (5.36)10.4 (6.99)Weight (Kg), mean (SD)75.3 (18.1)83.1 (14.0)77.7 (17.3)High blood pressure, n (%)17 (31.5)5 (27.8)22 (30.6)Dyslipidemia n (%)16 (29.6)3 (16.7)19 (26.4)Diabetes, n (%)5 (9.3)2 (11.1)7 (9.7)Current smokers, n (%)16 (29.6)3 (16.7)19 (26.4)Former smokers, n (%)16 (29.6)3 (16.7)19 (26.4)Joint pattern, n (%) Peripheral Axial Mixed38 (70.4)3 (5.6)13 (24.1)10 (55.6)0 (0)8 (44.4)48 (66.7)3 (4.2)21 (29.2) Plaque psoriasis, n (%)32 (59.3)16 (88.9)48 (66.7) Nail disease18 (33.3)10 (55.6)28 (38.9) Dactylitis, n (%)13 (24.1)7 (38.9)20 (27.8) Enthesitis, n (%)11 (20.4)4 (22.2)15 (20.8) Depression, n (%)36 (66.7)4 (22.2)40 (55.6)Tofacinitib line, n (%) 1 2 3 4 ≥ 51 (1.9)17 (31.5)11 (20.4)13 (24.1)12 (22.2)0 (0)1 (5.6)8 (44.4)5 (27.8)4 (22.2)1 (1.4)18 (25.0)19 (26.4)18 (25.0)16 (22.2)Tofacinitib current intake, n (%) yes no19 (35.2)35 (64.8)8 (44.4)10 (55.6)27 (37.5)45 (62.5)Treatment duration (mo), median [min, max]7.44 [0.23, 42.8]14.7 [0, 40.0]10.0 [0, 42.8]DAPSA, mean (SD)14.2 (7.9)9.2 (6.1)12.4 (6.5)PsAID, mean (SD)4.1 (2.2)3.6 (3.2)3.7 (3.3)Figure 1.Kaplan-Meier curve of all-cause treatment discontinuationAcknowledgements:NIL.Disclosure of Interests:None declared.

BackgroundCardiovascular (CV) comorbidity is frequent in psoriatic arthritis (PsA). This population shows a higher frequency of traditional CV risk factors (CVRF) when compared to normal population. However, additional traits related to the inflammatory nature of the disease may also suppose an additional risk beyond that attributable to classic CVRF.ObjectivesTo analyze the prevalence and predictors of CV events in a wide cohort of PsA patients recruited at two rheumatology departments from Spain.MethodsWe included (cross-sectional) 340 PsA patients (CASPAR criteria) from two different rheumatology departments in Spain. There were 190 males and 150 females (mean age: 55 ± 13 yrs). Both subpopulations were similar in terms of age, sex distribution and disease duration. Prevalence and predictors of CV events (coronary heart disease, ictus and/or ischemic peripheral vascular disease) were analyzed. Initially, a univariate analysis was performed to examine unadjusted associations of potential risk factors. Significant variables in the univariate analysis were then introduced in a multivariate analysis with a backward stepwise approach. The statistical analysis software package used was SPSS v.19.0. Patients gave their informed consent and an institutional ethics committee approved the final version of the study.ResultsDistribution of classic CVRF was as follow: Diabetes 14%, hypertension 36%, dyslipidemia 31%, tobacco 27%, obesity 35% and 24% had overweight. Thirty two out of 340 subjects (9.4%) developed 41 CV events: 15 coronary events, 15 ictus and 11 events of ischemic peripheral vascular disease. Compared to men, women had more diabetes (29.5% vs. 18%, p=0.049) and obesity (44% vs. 29%, p=0–010), even though the frequency of CV events did not differ between sexes. In multivariate analysis, an age of psoriasis onset ≥40 yr (OR 4.1, 95%CI: 1.04–16.2, p<0.001) and dyslipidemia (OR 5.8, 95%CI: 1.5–22.8, p<0.001) were found independently related to the risk of coronary events. Hypertension was an independent predictor of ictus (OR 8.0, 95%CI: 1.7–38.1, p<0.001). When analyzing CV events as a whole, an age of psoriasis onset ≥40 yr (OR 3.4, p=0.03), a polyarticular pattern during evolution (OR 2.9, p=0.04), hypertension (OR 5.3, p=0.007) and dyslipidemia (OR 2.6, p=0.07), were found independently associated to the risk of CV events in multivariate analysis.ConclusionsIn our context, CV comorbidity of PsA may be explained by a conjunction of classic CVRF, late onset of psoriasis, and the inflammatory burden of joint disease. A better management of these factors should be the basis for improvement of CV health of these patientsReferencesOgdie A, Yu Y, Haynes K, Love TJ, Maliha S, Jiang Y, et al. Risk of major cardiovascular events in patients with psoriatic arthritis, psoriasis and rheumatoid arthritis: a population-based cohort study. Ann Rheum Dis 2015; 74:326–32.Horreau C, Pouplard C, Brenaut E, Barnetche T, Misery L, Cribier B, et al. Cardiovascular morbidity and mortality in psoriasis and psoriatic arthritis: a systematic literature review. JEADV 2013; 27 (Suppl. 3):12–29.Disclosure of InterestNone declared

BackgroundThe age of onset of psoriasis has been used for decades as an appropriate descriptor to define two subpopulations of psoriatic patients (types I and II). Clinical features of both types of psoriasis have been clearly delineated. However, the importance of this distinction in patients with psoriatic arthritis (PsA) has not been studied in depth.ObjectivesTo evaluate the importance of age of onset of both psoriasis and arthritis in dissecting the clinical features of PsA.MethodsThis cross-sectional study included 205 patients with PsA (CASPAR criteria) seen at a single university institution. Socio-demographic, clinical, radiographic, and laboratory variables were included and population was then stratified according to age at onset of psoriasis, as well as joint manifestations, in two groups: early-onset and late -onset, according to a cut off value of 40 years old. Uni and multivariate analysis were performed.All patients gave informed consent. This study was approved by an institutional ethics committee.ResultsEarly-onset psoriasis (EOP) showed extensive skin involvement (OR 2.3, p=0.011), higher prevalence of axial pattern as disease onset (OR 4.6, p=0.009) and mixed pattern during evolution (OR 2.4, p=0.019), increased frequencies of family history of both psoriasis (OR 3.1, p=0.003) and PsA (OR 4.0, p=0.021), higher prevalence of HLA-C*06 (OR 2.03, p=0.03) and HLA-B*27 (OR 2.7, p=0.02). Early onset arthritis (EOA) patients presented more family history of PsA (OR 2.9, p=0.007), as well as HLA-B*27 positivity (OR 5.9, p<0.0001). Patients with late-onset arthritis (LOA) had more DM (OR 4.0, p=0.009), hypertension (OR 2.5, p=0.004), dyslipidemia (OR 2.3, p=0.011), and obesity (OR 1.7, p=0.012). Late-onset psoriasis (LOP) showed more obesity (OR 1.9, p=0.035), DM (OR 9.4, p<0.0001), hypertension (OR 4.1, p<0.0001), and ischemic heart disease during follow-up (OR 5.9, p=0.021). In multivariate analysis, LOP predicted DM development (OR 12.1; CI: 2-73.1, p=0.006). Likewise, LOA was shown to be an independent risk factor for hypertension (OR 5.2; CI: 1.09-25.02, p=0.039).ConclusionsAge at disease onset is a key stratification factor to better characterize the clinical and cardiovascular risk profile of psoriatic disease. In psoriatic disease, diabetes risk seems to be related to age at skin disease onset whereas hypertension development appears linked to age at joint disease onset. Both conditions are more prevalent in late disease.ReferencesQueiro R, Tejόn P, Alonso S, Coto P. Age at disease onset: a key factor for understanding psoriatic disease. Rheumatology (Oxford) 2014; 53:1178-85.Disclosure of InterestNone declared