Aug 2026· Journal of Personalized Medicine· Vol 16, pp. 429· 0 citations· 37 references
Medicine
TL;DR
Patients with definite FH exhibited persistently higher circulating Lp-PLA2 and TNF-α concentrations despite maximally tolerated lipid-lowering therapy, suggesting ongoing activation of specific inflammatory pathways.
Abstract
Background: Familial hypercholesterolemia (FH) is associated with accelerated atherosclerosis and an increased risk of cardiovascular disease. Aims: To evaluate circulating biomarkers of inflammation and atherosclerosis in patients with clinically suspected FH stratified according to the Dutch Lipid Clinic Network (DLCN) criteria. Methods: This cross-sectional study included 80 patients (mean age, 53.4 [13.2] years; 58% women) receiving maximally tolerated lipid-lowering therapy (statins ± ezetimibe). Serum concentrations of lipoprotein-associated phospholipase A2 (Lp-PLA2), tumor necrosis factor-α (TNF-α), apolipoprotein B (ApoB), oxidized low-density lipoprotein (oxLDL), and monocyte chemoattractant protein-1 (MCP-1) were measured. Participants were classified as definite FH (DLCN score > 8; n = 45) or non-definite FH (DLCN score ≤ 8; n = 35). Biomarker concentrations were analyzed according to the above subgroups and sex. Results: Patients with definite FH had significantly higher serum Lp-PLA2 concentrations (62.2 [33.8] vs. 46.5 [19.9] ng/mL; p = 0.03) and TNF-α concentrations (6.94 [4.53] vs. 4.51 [2.93] pg/mL; p = 0.02) compared to non-definite FH, whereas ApoB, oxLDL, and MCP-1 concentrations did not differ significantly between the subgroups. Women had significantly higher TNF-α concentrations compared to men (6.57 [4.74] vs. 4.60 [2.20] pg/mL; p = 0.04) with no differences among other cytokines. Conclusions: Patients with definite FH exhibited persistently higher circulating Lp-PLA2 and TNF-α concentrations despite maximally tolerated lipid-lowering therapy, suggesting ongoing activation of specific inflammatory pathways. These findings support further investigation of Lp-PLA2 and TNF-α as candidate biomarkers for cardiovascular risk assessment in FH.
Triangulating evidence across approaches, Mendelian randomization analyses supported inverse associations of genetically predicted total cholesteryl esters and sphingomyelins with IPF risk, and highlights cholesterol and sphingolipid metabolism as potential contributors to IPF susceptibility.
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