Abstract

Chronic inflammatory rheumatic diseases are associated with an increased risk of cardiovascular disease. In this group of patients, inflammation causes various changes in lipid metabolism, which in a chronic course may contribute to an increased risk of atherosclerosis. The most frequent abnormality is decreased serum high-density lipoprotein cholesterol (HDL–C) and increased triglyceride (TG) levels. This imbalance may be due to increased production and secretion of very low-density lipoprotein cholesterol (VLDL–С) in the liver and decreased clearance of TG-rich lipoproteins. The mechanisms by which inflammation lowers HDL–C levels are still unclear. Additionally, there is a persistent increase in lipoprotein (a) (Lp[a]) due to its increased synthesis. Thus, systemic inflammation negatively affects lipoprotein function: LDL–C oxidation becomes more active since there is the decreased ability of HDL–C to prevent this pathway. Moreover, chronic inflammation adversely affects the reverse cholesterol transport mechanism. The greater the severity of the underlying disease is associated with the more pronounced disorders in lipid metabolism. In general, approaches to the correction of lipid metabolism in patients with inflammatory rheumatic diseases are similar to those in patients from the general population.

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