DYSLIPIDEMIA, MEDIATED BY METABOLIC ENDOTOXEMIA, MAY ACT AS A DRIVER OF JOINT DAMAGE IN RHEUMATOID ARTHRITIS
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Abstract
Rheumatoid arthritis (RA) is characterized by progressive joint destruction, the mechanisms of which are not fully explained by the level of clinical disease activity.
The aim of this study was to evaluate the role of dyslipidemia in the development of metabolic endotoxemia and its contribution to radiographic disease progression.
Materials and methods. The study included 81 patients with rheumatoid arthritis and 17 healthy controls. Lipid profile parameters, markers of endotoxemia, and angiogenesis (vascular endothelial growth factor A, VEGF) were assessed; structural joint damage was evaluated using the Sharp-van der Heijde scoring method.
Results. A significant positive correlation was found between triglyceride (TG) levels and lipopolysaccharide (LPS) concentration (ρ = 0.451; p < 0.001), supporting the role of lipid transport in the development of metabolic endotoxemia. The absence of an association with zonulin suggests the predominance of a metabolic rather than barrier-related mechanism of endotoxin translocation. Mediation analysis demonstrated a significant indirect effect of triglycerides on erosive joint damage through the cascade «TG → LPS → VEGF → erosions», in the absence of a direct effect. LPS levels were associated with increased VEGF, which was identified as a strong predictor of bone destruction.
Conclusion. These findings indicate that dyslipidemia acts as an independent risk factor for radiographic progression in rheumatoid arthritis, exerting its effects through endotoxin-induced angiogenesis.
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