PsA is characterized by a high prevalence of cardiovascular (CV) comorbidities. Recognizing these comorbidities is critical due to their influence on the quality of life and the choice of therapy. Imaging techniques also play an important role in the evaluation of the CV risk in psoriatic disease, improving the prediction of CV events when combined with clinical scores as a predictive tool. Meta-analyses point to a significant reduction in the incidence of CV events associated with the suppression of inflammatory activity when using systemic therapies. Consequently, the mortality rate in PsA patients has fallen in the last 40 years and is now similar to that of the general population, including cardiovascular causes. Obesity is an especially relevant CV comorbidity in patients with psoriatic disease, most of whom are overweight/obese. Body mass index (BMI) is a risk factor for PsA and a causal relationship with psoriasis has been demonstrated by Mendelian randomized studies. The study of fat distribution shows that patients with psoriasis are characterized by visceral fat accumulation, which correlates with CV risk measurements. These findings suggest that approaches to the prevention and treatment of psoriatic disease might come from targeting adiposity levels, in addition to the immune pathways. Weight loss treatment with low energy diets in patients with PsA has been associated with significant improvements in disease activity. Novel strategies using a multimorbidity approach, focused more on patients outcomes, are necessary to better address comorbidities, improve clinical outcomes and the quality of life of patients with psoriatic disease.

BackgroundThe Charlson comorbidity index (CCI) is a prognostic scale, which gives a numerical value that indicates the burden of comorbidities in a patient. This index is obtained from the sum of 19 medical conditions that have been related to mortality and has been validated in several studies. Patients with rheumatoid arthritis (RA) are more at risk than the general population of developing comorbidities. However, these often go unnoticed despite the impact on the disease activity and to treatment response, as shown by different studies such as COMORA.ObjectivesTo determine the prevalence of comorbidities in a cohort of patients with RA and estimate CCI.MethodsCross-sectional descriptive study, patients diagnosed with RA according to the EULAR/ACR 2010 classification criteria were included. All patients were followed up in a rheumatology service in a tertiary hospital. Comorbidities were obtained from the medical records. To measure comorbidities, CCI was calculated, the diagnosis of RA was not included in the index. We defined three categories of comorbidity according to CCI: 0 (no comorbidity, applied to patients with no previous record of conditions included in the CCI), 1 to 2 (moderate) and 3 or more (severe). Others comorbidities not included in CCI, such as hypertension (HTN), dyslipidemias (DLP), thyroid disease (TD), osteoporosis (OP) were collected.Results130 patients (103 women) were analysed; mean age was 58.6±12.9 years and disease duration of 6.0±4.4 years. 82.8% were seropositive for rheumatoid factor (n: 83) and/or anti-CCP (n: 97). 44.6% had previous smoking history, 22 were current smokers. The most observed comorbidities in our cohort were: overweight and obesity (BMI ≥25; 63%), DLP (38.8%), HTN (31.5%), chronic kidney disease (32.3%; 6.9% ≥Stage III) and chronic lung disease (23.8%). Other diseases included TD (18.5%), OP (17.7%), diabetes mellitus (9.2%) and liver disease (9.2%). Five patients with a history of tumour (2 metastases) and 2 lymphomas in the last 5 years. Four patients had a heart disease, in 3 as an ischaemic event.According to CCI, 20.8% of the patients had a Charlson 0, 43.8% Charlson 1–2, and 35.4% Charlson ≥3.ConclusionsIn our cohort, despite being a relatively young population, the presence of comorbidities and cardiovascular risk factors is relatively high, in agreement with what has been observed in other studies. 1 out of 3 patients has a severe comorbidity burden.Disclosure of InterestNone declared

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Background:Seronegative (sero-) and seropositive (sero+) Rheumatoid Arthritis (RA) have different genetic, immunopathological and vascular morphology features, but no previous studies have analyzed if US characteristics differ between sero+ or sero- RA. Our preliminary studies suggest that sero+ RA is associated with an expansive synovitis pattern that we have called “proliferative synovitis” (PS)Objectives:To analyze potential differences between patients with RA according to their autoantibody status by using ultrasonography (US). We aimed to assess whether PS is associated with ACPA+ ptsMethods:We collected clinical, epidemiological data and bilateral carpal and hand US images of pts with RA. Synovial hypertrophy (SH), Power Doppler signal (PD) and total score (sum of scores of SH and PD) in wrist and hand (1-5 metacarpophalangeal) were assessed. We evaluated the presence of PS, defined as expansive synovial growth encompassing the concepts of synovial SH grade II and III. We performed synovial biopsies of a subgroup of pts using arthroscopy or US guided in order to see immunohistochemistry differences between “proliferative” and “flat” (non-proliferative) synovitis. Serum levels of angiogenic and inflammatory biomarkers were performedResults:Two hundred and five RA patients were collected. Overall, 173 (84.8%) pts were sero+ for RF (68.7%) or ACPA (74.6%), general characteristics are summarized in Table. No significant differences between sero+ and sero- pts in terms of disease activity or therapy were found. PS was present in 55.5% of sero+ pts (55.3% in RF+ and 58.2% in ACPA+ pts) and 16.1% of sero- pts (p=0.0001). Globally, 101 pts (49.2%) had PS. Ninety-six (95.0%) were RF or ACPA positive. Only 5 pts with sero- RA had PS (p=0.001). In the univariate analysis, significantly more pts with PS had erosive disease (72.3% vs 35.0% p=0.0001), higher US scores (p=0.0001) and more of them were taking conventional synthetic Disease-modifying anti-rheumatic drugs (csDMARD) (81.8% vs 69.6% p=0.05). No differences regarding disease activity were found.In the multivariate analysis erosions [OR 4.90 CI 95% (2.17-11.07) p=0.0001] and ACPA [OR 3.5 CI 95% (1.39-10.7) p=0.09] but not RF status [OR 0.74 CI 95% (0.31-1.71) p=0.483] were independently associated with the presence of PS.We immunostained synovial biopsies from 23 pts with PS (13 pts) or non-PS (10 pts). PS was significantly associated with higher density of vessels (p=0.042) and a strong trend to a higher density of B, T, Mast cells and macrophages (figure 1). Significantly higher serum levels of angiogenic (Activin A, bFGF, IL18, IL20, PIGF, SDF-1 and VEGF-D) and pro-inflammatory (IL23) cytokines were found in patients with PS (figure 2).Conclusion:The presence of “proliferative Synovitis” was significantly associated with ACPA and erosive disease in patients with RA. PS pattern also was associated with higher density of synovial vessels and higher serum levels of angiogenic and inflammatory mediatorsTable .Total US pattern p valueN=205Proliferative (N=101)Non proliferative (N=104)Female, n (%)162 (79.4)79 (78.2)83 (80.6)0.57Age, mean (SD) years57.1 (± 14,1)56.3 (± 12.0)58.0 (± 15.9)0.40Current Smoker, n (%)47 (26.9)22 (25.6)25 (28.1)0.73Disease duration, mean (SD) months113.3 (± 105.7)127.7 (± 111.1)99.3 (± 99.3)0.05Erosion, n (%)108 (53.7)73 (72.3)35 (35.0)0.00ACPA, n (%)153 (75.4)89 (89)64 (62.1)0.00RF, n (%)99 (68.3)78 (78)63 (61.2)0.01DAS 28–CRP, mean (SD)2.55 (±1.03)2.66 (±1.04)2.44 (±1.02)0.17GC, n (%)99 (49.3)45 (45.5)54 (52.9)0.32cDMARDs, n (%)152 (75.6)81 (81.8)71 (69.6)0.05bDMARD, n (%)69 (34.3)35 (35.4)34 (33.3)0.76Total US score14.9 (± 11.5)18.8 (± 11.8)11.1 (± 9.9)0.00*ACPA anti-citrullinated protein antibodies, RF rheumatoid factor, DAS28-CRP Disease Activity Score 28-joint count, CRP C-reactive protein, GC glucocorticoids, bDMARD biological disease-modifying antirheumatic drugsDisclosure of Interests:Ana Belén Azuaga-Piñango: None declared, Beatriz Frade-Sosa: None declared, Roberto Gumucio: None declared, Katherine Cajiao: None declared, Andrea Cuervo: None declared, Raquel Celis: None declared, Jose A. Gómez-Puerta Speakers bureau: Abbvie, BMS, GSK, Lilly, Pfizer, Roche, Raimón Sanmartí Speakers bureau: Abbvie, Eli Lilly, BMS, Roche and Pfizer, Juan de Dios Cañete: None declared, Julio Ramirez: None declared