AB0807 VITAMIN D ROLE IN VASCULAR DAMAGE PROGRESSION IN PATIENTS WITH PSORIATIC ARTHRITIS

Abstract

Background: Psoriatic arthritis (PsA) is associated with insufficent levels of vitamin D (25OHD) and an increased cardiovascular risk. Several studies, have shown an inverse relationship between 25OHD levels and cardiovascular damage. Objective(s): To study the relationship between 25OHD and vascular damage, as well as its possible influence on its progression, in patients with PsA. Method(s): Pre-post longitudinal study with analytical components. PsA patients with peripheral joint involvement were included. Demographic (sex, age), clinical [follow-up time, DAPSA, current treatment, body mass index (BMI), classic vascular risk factors, vascular events] and analytical variables [atherogenic index, glomerular filtration (GF-MDRD), glycosylated hemoglobin (HbA1c), CRP, ESR, 25OHD] were collected. We considered deficient level of 25OHD <20 ng/ml and insufficient <30 ng/ml. Basal vascular risk was estimated through SCORE tool. Extracranial carotid artery was explored with an Esaote MyLab70XVG ultrasound with linear probe (7-12mHz) and an automated program that measures intima media thickness (IMT) by radiofrequency, and the presence of atheroma plaques was evaluated following Mannheim consensus. Pulse wave velocity (PWV) was measured through Mobil o graphR dispositive. IMT>=900 mu and PWV>= 10m/s were considered as pathological values. We repeat vascular study 3 years later. Vascular damage progression was defined as the appearance of atheroma plaques during the follow-up and/or an increase in their number. Statistical analysis was performed using SPSS 22.0 program. Result(s): 78 patients were included. Eighteen patients were excluded due to high vascular risk [previous event, diabetes type II or type I with target organ injury and/or GF-MDRD< 60 ml/min]. 57.5% were women with a mean age of 54.2 (SD 10.9) years. The mean follow-up time was 96.8 (SD 163.6) months and mean DAPSA was 10.2 (SD 8.3). 96.2% of patients had received DMARDs and 42.3% biologicals, and 42.3% took calcium and 25OHD supplements. Mean BMI was 27.5 (SD 4.7) kg/m2. 42.3% had tobacco exposure, 29.5% were hypertensive and 32% dyslipidemic. Mean SCORE was 1.6 (SD 1.8) and mean 25OHD was 27.6 (DSD 11.6) ng/ml. 28.2% patients had 25OHD deficit and 60.3 % insufficiency. At the beginning, 32.1 % of patients had atheromatous plaques with a number of plaques around 1.7 (SD 1.2), and 6.7% and 19.7% had a pathological IMT or PWV, respectively. Baseline, we had not observed any association between 25OHD and the presence of atheroma plaques, IMT or PWV. Three years later, we detected progression of vascular damage in 31.2% patients. In these patients, the existence of hypovitaminosis D was associate with the appearance of atheroma plaques (p=0.043). This association desappeared in the multivariate analysis, in which only the CRP influenced the appearance of atherome plaques (OR: 1.4, IC 95% 1.04-1.98, p=0.025). Conclusion(s): Low 25OHD levels are not related to vascular damage or influence a posible progression of it in our serie. As might be expected, the progression of vascular damage depends on the inflammatory load in these patients.