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
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