Background Systemic inflammation has been postulated to be an independent cardiovascular risk factor, particularly in patients with autoimmune rheumatic disorders (ARD), such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), and is associated with accelerated atherosclerosis. There is some evidence to suggest that antiphospholipid antibodies (aPL) may also play a role in the development of atherosclerosis. However, it is few data about the relationship between these autoantibodies and inflammatory mediators in the development of atherosclerosis.
Objectives To clarify the involvement of inflammatory mediators and aPL in the atherosclerotic process in patients with ARD.
Methods The study included 87 female patients with ARD (RA (n=47), mean age 45,0 (33,0; 51,0) years old, disease duration 9,0 (3,0; 14,0) years, disease activity (DAS28=5,37 (4,69; 5,86) points); SLE (n=40), mean age 33,5 (27,5; 44,5) years old, disease duration 8,0 (5,0; 14,5) years, disease activity SLEDAI-2K 7,0 (4,0; 11,5) points). Sixty healthy women (mean age 40,5 (36,0; 47,0) years old) formed the control group.
The levels of high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor - α (TNF-α), LA, IgG/IgM antibodies to cardiolipin (aCL), β2-glucoprotein-1(aβ2-GP1), annexin V (aAnV) and prothrombin (aPT)) were determined with ELISA. Intima-media thickness (IMT) of the carotid artery wall and the presence of atherosclerotic plaques were revealed ultrasonographically according to the described ESH/ESC Guidelines.
Results The levels of hs-CRP, IL-6, TNF-α were significantly higher in ARD patients than in the control group, which indicates the disease activity. Furthermore, the patients with SLE had a significant correlation between IL-6 and SLEDAI-2K (r=0,471, p=0,002), TNF-α and SLEDAI-2K (r=0,499, p=0,001), whereas the patients with RA had only significant correlation between hs-CRP and DAS28 (r=0,355, p=0,031).
The concentration of IgG aCL, IgG and IgM aβ2-GP1, IgM aAnV, IgG aPT, LA were higher in patients with SLE than in the control group, and the levels of IgG and IgM aCL, IgM aβ2-GP1, IgG and IgM aAnV, LA were higher in patients with RA v.s. the control group.
We revealed a correlation between IgG aCL, IgG aβ2-GP1, IgG aAnV and TNF-α, IgG aCL and IL-6 in SLE patients, and only one between IgG aAnV and hs-CRP in RA patients. There wasn't any correlation between aPL and inflammatory mediators in the control group.
Univariate analysis has demonstrated an association of IgG aAnV with IMT (r=0,320, p=0,044) in SLE patients and positive association between TNF-α and IMT (r=0,362, p=0,028) in RA patients. Furthermore, we found an association between IL-6 and IgG aPT (r=0,426, p=0,038), TNF-α and IgG aCL (r=0,419, p=0,042) in SLE patients with carotid atherosclerosis. There wasn't any association between investigated parameters in the control group.
Conclusions The association between inflammatory mediators and disease activity has been confirmed in ARD patients. Increased autoimmune activity has been verified both in patients with SLE and RA. It has been determined that IgG aAnV had more significance for IMT in patients with SLE, TNF-α - in RA patients. Our data can suggest that inflammatory mediators and antiphospholipid antibodies are involved in the atherosclerotic process in patients with ARD.
Disclosure of Interest None declared