Small dense low-density lipoprotein in primary biliary cholangitis: Independent association with metabolic syndrome

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BACKGROUND Primary biliary cholangitis (PBC) is frequently associated with cholestasis-driven hypercholesterolemia characterized by lipoprotein X accumulation. Despite markedly elevated cholesterol levels, cardiovascular risk in PBC is not consistently increased, suggesting that conventional lipid parameters may inadequately reflect true atherogenic burden. Small dense low-density lipoprotein (sdLDL), a highly atherogenic low-density lipoprotein (LDL) subfraction closely linked to insulin resistance and metabolic syndrome (MetS), has not been systematically evaluated in PBC. AIM To evaluate determinants of sdLDL levels in PBC, focusing on MetS, metabolic dysfunction-associated steatotic liver disease (MASLD), liver fibrosis, and biochemical response, and assess whether sdLDL reflects metabolic dysfunction rather than cholestatic disease severity. METHODS In this cross-sectional study, 148 consecutive patients with PBC were recruited from a tertiary hepatology center. sdLDL was quantified using the Lipoprint® LDL System. MetS was defined according to International Diabetes Federation criteria. Hepatic steatosis and fibrosis were assessed using vibration-controlled transient elastography. Multivariable linear and logistic regression analyses were performed to evaluate independent determinants of sdLDL. RESULTS MetS was present in 39.2% of patients. sdLDL levels were significantly higher in patients with MetS (P = 0.004). In multivariable analysis, MetS remained independently associated with ln-transformed sdLDL levels [B = 0.76; 95% confidence interval (CI): 0.26-1.26; P = 0.003] and with the presence of detectable sdLDL (odds ratio 2.10; 95%CI: 1.02-4.35; P = 0.045), independent of age, sex, adiposity, and lipid-lowering therapy. In contrast, MASLD, advanced fibrosis, and cholestatic activity were not independently associated with sdLDL. Notably, LDL-C levels were lower in patients with MetS, whereas sdLDL and sdLDL/largeLDL ratio were significantly increased, suggesting discordance between conventional LDL-C and qualitative lipoprotein remodeling. CONCLUSION In PBC, sdLDL appears to reflect superimposed metabolic dysfunction rather than cholestatic liver disease severity. Advanced lipoprotein profiling may therefore help distinguish metabolically driven atherogenic dyslipidemia from cholestatic hypercholesterolemia in contemporary PBC cohorts.

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