Assessment of laboratory indicators of inflammatory, infection and indicators of subclinical atherosclerosis in patients with systemic lupus erythematosus

The aim of the study was to reveal the relationship between the activity of inflammation, the infectious component, platelet function and dyslipidemia, in the development of subclinical atherosclerosis in patients with systemic lupus erythematosus (SLE). Material and methods. Fifty women with SLE at the age of 52.0 [48.0–58.0] years and disease duration – 11.5 [6.0– 22.0] years were examined. The control group consisted of 21 healthy women. The concentration of high-sensitivity C-reactive protein (hsCRP), interleukin 6 (IL-6), IgG antibodies to Chlamydia pneumonia (at IgG CP), the level of Toll-like receptor (TLR2), platelet factor 4 (PF4) and antibodies to oxidized high-density lipoproteins (at oxLDL) were determined by enzyme immunoassay. Platelet aggregation indices, lipid spectrum, intima-media thickness (IMT) of common carotid arteries were investigated. Results. A significant increase in IMT of the common carotid artery (1.00 [0.80–1.10] and 0.80 [0.70–0.90] mm, respectively; p <0.01) and TKIM of the carotid bifurcation (1.10 [1.00–1.20] and 0.80 [0.70–1.10] mm, respectively; p <0.01), increased hsCRP concentration (3.67 [2.17–5.92] and 0.74 [0.30–1.26] mg/L, respectively; p <0.01), IL-6 (1.72 [1.39–2.68] and 0.60 [0.22–0.75] pg/mL, respectively; p <0.01). Significant platelet activation was noted in SLE: significant increase in TF4 concentration (21.5 [19.80–23.28] and 18.30 [13.88–20.46] ng/mL, respectively; p <0.01), marked dyslipidemia, increased concentration of oxLDL (3.16 [1.45–4.60] and 1.39 [1.26–2.04] kp, respectively; p <0.01). At IgG CP concentration and TLR2 values in patients with SLE did not differ from controls. Conclusion. In addition to traditional risk factors for the development of cardiovascular disease, the association between SLE and subclinical atherosclerotic lesions of the vascular wall can be explained by additional risk factors – inflammation and autoimmune processes. The role of the infectious component is for further study.