Correlations of indices of systemic endotoxinemia with lipid profile in patients without clinical manifestation of atherosclerosis

Abstract

Background. Atherosclerosis is a manifestation of chronic systemic inflammation, the induction of which may be associated with endotoxin aggression (EA) as a pathogenic form of systemic endotoxemia (SEE). Objective: to identify correlations of the lipid profile with SEE depending on severity of the atherosclerotic process. Materials and methods. Patients were interviewed using the SCORE risk assessment scale. All patients underwent a triplex ultrasound examination of extracranial brachiocephalic arteries using MedisonSA9900 (South Korea) including evaluation of the intima-media complex (TIM) structure and thickness. The ECST method was used to quantify arterial stenosis. Indices of the lipid profile (total cholesterol, LDL, HDL, TG, atherogenic index (AI)) and SEE were estimated; the micro-LAL test was used to measure the lipopolysaccharide (LPS) concentration; and the AEI activity was measured using SOISELISA. Results. Using the SCORE scale patients were assigned to the group of intermediate risk for development of cardiovascular complications. Based on ultrasound data the patients were divided into three subgroups: first subgroup, TIM thickening; second subgroup, atherosclerotic plaques; third subgroup, no signs of disturbed structure of the arterial wall but abnormal lipid profile. There were no significant differences between subgroups in indices of the lipid profile but patients significantly differed from the control group in concentrations of LDL, cholesterol, and AI. Statistically significant differences in SEE indices between the subgroups and the control group were absent. However, multiple regression showed a significant effect of the ET level and the ratio of antibodies to the hydrophilic/hydrophobic parts of the LPS molecule on the level of total cholesterol and AI (p < 0.001). Conclusion. The observed direct relationship between concentrations of LPS in the systemic circulation and total cholesterol may be due to a higher affinity of the ET molecule to HDL and the competitive binding in transport of molecules. This explains the found direct correlations of SEE indices with the lipid profile.