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Copyright ©The Author(s) 2026. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Feb 27, 2026; 18(2): 113685
Published online Feb 27, 2026. doi: 10.4254/wjh.v18.i2.113685
Adipokine profiles reflect metabolic dysfunction but not fibrosis in patients with primary biliary cholangitis
Tomas Koky, Sylvia Drazilova, Slavomira Komarova, Marian Macej, Dominika Toporcerova, Martin Janicko, Ivana Spakova, Miroslava Rabajdova, Maria Marekova, Peter Jarcuska
Tomas Koky, Sylvia Drazilova, Slavomira Komarova, Marian Macej, Dominika Toporcerova, Martin Janicko, Peter Jarcuska, 2nd Department of Internal Medicine, L Pasteur University Hospital, Kosice 04190, Slovakia
Tomas Koky, Sylvia Drazilova, Slavomira Komarova, Marian Macej, Martin Janicko, Peter Jarcuska, PJ Safarik University, Faculty of Medicine, Kosice 04011, Slovakia
Ivana Spakova, Miroslava Rabajdova, Maria Marekova, Department of Medical and Clinical Biochemistry, Faculty of Medicine, PJ Safarik University, Kosice 04011, Slovakia
Author contributions: Koky T participated in formal analysis and writing-original draft; Koky T, Drazilova S, Janicko M, and Jarcuska P contributed to the methodology; Koky T, Drazilova S, Komarova S, Macej M, Spakova I, Rabajdova M, and Marekova M contributed to the investigation; Koky T, Drazilova S, Komarova S, Macej M, Toporcerova D, Janicko M, Spakova I, Rabajdova M, Marekova M, and Jarcuska P contributed to data curation; Drazilova S and Jarcuska P contributed to the conceptualization; Drazilova S contributed to supervision; Drazilova S, Janicko M, and Jarcuska P involved in writing-review and editing; Janicko M contributed to analysis. All authors have read and approved the final manuscript.
Institutional review board statement: This study was reviewed and approved by the Ethics Committee of Louis Pasteur University Hospital in Košice (approval No. 2020/EK/10076).
Informed consent statement: All study participants, or their legal guardian, provided informed written consent prior to study enrollment.
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 available from the corresponding author at sylvia.drazilova@upjs.sk.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Sylvia Drazilova, MD, PhD, Associate Professor, Faculty of Medicine, PJ Safarik University, Trieda SNP 1, Kosice 04011, Slovakia. drazilovasylvia@gmail.com
Received: September 1, 2025
Revised: October 22, 2025
Accepted: December 24, 2025
Published online: February 27, 2026
Processing time: 165 Days and 0.5 Hours
Abstract
BACKGROUND

Primary biliary cholangitis (PBC) is a rare, nonsuppurative cholestatic disease that affects the small intrahepatic bile ducts. If not adequately managed, it may progress to liver cirrhosis and hepatocellular carcinoma. Only a few studies have explored the impact of cardiometabolic risk factors on liver fibrosis progression in PBC. Relevant data on the role of adipokines in these processes are also limited.

AIM

To compare leptin and adiponectin levels in PBC patients stratified by the presence of metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic syndrome (MetS), fibrosis, and biochemical response.

METHODS

We conducted a cross-sectional study involving 81 PBC patients diagnosed according to European Association for the Study of the Liver guidelines, all followed at a tertiary care center in Košice, Slovakia. Patients were included consecutively from the patient database in hepatology clinic in a prospective manner. Data on biochemical, clinical and anthropometric variables and their associations with MASLD, MetS, fibrosis, and biochemical response were evaluated using statistical methods including logistic regression and receiver operating characteristic analysis.

RESULTS

Patients with PBC/MASLD had significantly lower adiponectin levels (1698.24 pg/mL vs 2042.08 pg/mL, P = 0.015) and higher leptin levels (1.89 ng/mL vs 0.62 ng/mL, P < 0.001) compared with those without MASLD. The leptin-to-adiponectin (L/A) ratio was also significantly elevated (1.63 vs 0.27, P < 0.001). Similar patterns were observed in patients with MetS: Adiponectin (1208.41 pg/mL vs 2086.10 pg/mL, P = 0.002), leptin (1.51 ng/mL vs 0.79 ng/mL, P = 0.002), and L/A ratio (1.28 vs 0.41, P = 0.009). By contrast, no significant differences in adipokine levels were observed between patients with and without advanced fibrosis or complete biochemical response (all P > 0.05).

CONCLUSION

Adipokines reflect metabolic status in PBC. The L/A ratio is promising biomarker for MASLD. No significant association between leptin and adiponectin levels and advanced fibrosis was detected within the limited sample size of this study.

Keywords: Primary biliary cholangitis; Adipokines; Liver fibrosis; Metabolic dysfunction-associated steatotic liver disease; Metabolic syndrome

Core Tip: Our results show that primary biliary cholangitis (PBC) patients with metabolic dysfunction-associated steatotic liver disease or metabolic syndrome as comorbidities exhibit significantly lower adiponectin levels, higher leptin levels, and an elevated leptin-to-adiponectin ratio within the limited sample size of this study. Thus, adipokines may serve as potential biomarkers for identifying metabolic conditions in PBC. By contrast, no significant associations were observed between adipokine levels and fibrosis severity or biochemical response. Our findings indicate that adipokines, particularly leptin-to-adiponectin ratio may become a promising biomarker for identifying metabolic dysfunction-associated steatotic liver disease in PBC patients.