Koky T, Drazilova S, Janicko M, Harhovsky M, Hubkova B, Tothova I, Rabajdova M, Marekova M, Jarcuska P. Small dense low-density lipoprotein in primary biliary cholangitis: Independent association with metabolic syndrome. World J Hepatol 2026; 18(8): 124436 [DOI: 10.4254/wjh.124436]
Corresponding Author of This Article
Sylvia Drazilova, MD, PhD, Associate Professor, 2nd Department of Internal Medicine, PJ Safarik University, Faculty of Medicine and L Pasteur University Hospital, Trieda SNP 1, Kosice 04011, Slovakia. sylvia.drazilova@upjs.sk
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Koky T, Drazilova S, Janicko M, Harhovsky M, Hubkova B, Tothova I, Rabajdova M, Marekova M, Jarcuska P. Small dense low-density lipoprotein in primary biliary cholangitis: Independent association with metabolic syndrome. World J Hepatol 2026; 18(8): 124436 [DOI: 10.4254/wjh.124436]
World J Hepatol. Aug 27, 2026; 18(8): 124436 Published online Aug 27, 2026. doi: 10.4254/wjh.124436
Small dense low-density lipoprotein in primary biliary cholangitis: Independent association with metabolic syndrome
Tomas Koky, Sylvia Drazilova, Martin Janicko, Martin Harhovsky, Beata Hubkova, Ivana Tothova, Miroslava Rabajdova, Maria Marekova, Peter Jarcuska
Tomas Koky, Sylvia Drazilova, Martin Janicko, Martin Harhovsky, Peter Jarcuska, 2nd Department of Internal Medicine, PJ Safarik University, Faculty of Medicine and L Pasteur University Hospital, Kosice 04011, Slovakia
Beata Hubkova, Ivana Tothova, Miroslava Rabajdova, Maria Marekova, Department of Medical and Clinical Biochemistry, PJ Safarik University, Faculty of Medicine, Kosice 04011, Slovakia
Author contributions: Koky T wrote the paper and contributed to the analysis; Drazilova S designed, conducted and supervised the study; Harhovsky M, Janicko M and Hubkova B and Tothova I contributed to the analysis; Rabajdova M and Marekova M provided clinical advice; Jarcuska P supervised the study.
AI contribution statement: Portions of this manuscript were edited using AI tools for language refinement. The authors were responsible and agree to accountability for all scientific content.
Institutional review board statement: This study was reviewed and approved by the Ethics Committee of Faculty of Medicine of Pavol Jozef Šafárik University, Košice.
Informed consent statement: Each patient provided written informed consent for the examinations and inclusion in the study.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
STROBE statement: The authors have read the STROBE Statement-checklist of items, and the manuscript was prepared and revised according to the STROBE Statement-checklist of items.
Data sharing statement: Technical appendix, statistical code, and dataset are available from the corresponding author at sylvia.drazilova@upjs.sk.
Corresponding author: Sylvia Drazilova, MD, PhD, Associate Professor, 2nd Department of Internal Medicine, PJ Safarik University, Faculty of Medicine and L Pasteur University Hospital, Trieda SNP 1, Kosice 04011, Slovakia. sylvia.drazilova@upjs.sk
Received: June 15, 2026 Revised: July 13, 2026 Accepted: July 27, 2026 Published online: August 27, 2026 Processing time: 64 Days and 13.2 Hours
Abstract
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.
Core Tip: Hypercholesterolemia in primary biliary cholangitis (PBC) is largely driven by cholestasis and lipoprotein X, making conventional lipid parameters difficult to interpret. In this study, small dense low-density lipoprotein (LDL) was independently associated with metabolic syndrome but not with liver fibrosis, cholestatic activity, metabolic dysfunction-associated steatotic liver disease, or biochemical response. These findings suggest that small dense LDL reflects superimposed metabolic dysfunction rather than intrinsic cholestatic liver disease and may help identify a metabolically driven atherogenic phenotype in contemporary PBC cohorts.
