Background The main causes of death in Rheumatoid Arthritis (RA) are cardiovascular events related to early atherosclerosis, myocardial infarction and congestive heart failure. The risk for cardiovascular disease it it not completely explained by the traditionally accepted cardiovascular risk factors. Inflammatory pathways of RA might be involved in the pathogenesis of subclinical atherosclerosis. Objectives To evaluate the relationship of anti-CCP antibody titers, serum IL-6, TNFa and high sensitivity c-Reactive Protein with increased carotid intima-media thickness (cIMT) in patients with RA without cardiovascular risk factors. Methods Sixty patients with RA, 27 anti-CCP positive and 33 anti-CCP negative, and 62 controls (HC) matched by age and gender. All groups were assessed for comorbidities, demographics, clinical evaluations, and cardiovascular risk calculated by atherogenic index of plasma (AIP). The cIMT was performed by high-resolution B-mode ultrasound by a single operator. Serum titers of anti-CCP, hs-cRP, levels of TNFα and IL-6 were measured by ELISA. Results The anti-CCP positive RA patients showed increased cIMT compared to HC and anti-CCP negative patients (p<0.001). Anti-CCP positive vs. Anti-CCP negative patients, had increased disease activity (DAS28) (p=0.05), increased AIP (p<0.001), higher TNFα (20.54±5.38 vs 32.77±12.30, p=0.002) and IL-6 (18.54±14.09 vs 65.07±34.95, p<0.001). The cIMT correlated with titers of anti-CCP (r=0.539, p<0.001), TNFα (r=0.791, p<0.001) and IL-6 (p=0.794, p<0.001). In multiple regression analysis, cIMT was associated with hs-cRP (p=0.05) and anti-CCP levels (p=0.006). Conclusions High levels of anti-CCP and hs-cRP are useful markers of an increased cIMT and cardiovascular risk supporting a clinical role of the preventive measurement of cIMT in RA Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.5947
Background Rheumatoid arthritis (RA) patients have a higher risk for atherosclerosis mainly as a consequence of chronic systemic inflammation, notwithstanding, the implicated pathways have not been completely understood. CD36 is a scavenger receptor relevant for atherogenesis, there are still controversies about its role in this process and there is no clinical information about CD36 and subclinical atherosclerosis in human patients with RA. Objectives To Evaluate the relation between the membrane expression of CD36 in peripheral blood monocyte cells and carotid intima media thickness (cIMT) in patients with RA. Methods We included 37 patients with RA (ACR 1987) attending the rheumatology department of Hospital Civil “Dr. Juan I. Menchaca” Guadalajara, Jalisco, Mexico. The cIMT was assessed by high definition mode B ultrasound and patients were grouped as increased cIMT if >0.6 mm or as no increased cIMT if <0.6 mm. Disease activity was evaluated with the DAS28-cRP. Total cholesterol (TC), triglycerides (Tg), high density lipoprotein cholesterol (HDL-c) and low density lipoprotein cholesterol (LDL-c) were measured. The atherogenic index of plasma (AIP) was calculated. Anti-CCP antibodies, serum IL-6 and TNFa were measured by ELISA. Membrane expression of CD36 was measured by immunofluorescence flow cytometry in PMBC. Data was analyzed with the software WinMDI 2.9 and SPSS v. 22 IBM, Inc. Results Of the studied patients, 24 (65%) had increased cIMT, this group showed higher serum TC (p<0.001), Tg (p=0.006), oxLDL (p<0.001) and AIP (p<0.001) and lower serum HDL-c (p=0.005). Titers of hs-cRP, TNFα, IL-6 and anti-CCP also were higher in the increased cIMT group. Mean fluorescence intensity (MFI) for CD36 was lower in the increased cIMT compared with the no increased cIMT (46.84±40.46 vs. 122.70±34.71, p<0.001). The cIMT was negatively correlated with CD36 MFI. We observed negative correlations between CD36 and TNFa (-0.729, p<0.001) and IL-6 (-0.822, p<0.001). Conclusions Low membrane expression of CD36 is observed in RA patients with subclinical atherosclerosis, Further, studies are needed to validate our findings and clarify the regulation and role CD36 in subclinical atherosclerosis in RA Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.6032
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