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Editorial
Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Hepatol. Jun 27, 2026; 18(6): 118902
Published online Jun 27, 2026. doi: 10.4254/wjh.118902
Metabolic links between metabolic dysfunction-associated steatotic liver disease and primary biliary cholangitis
Stanislav Kotlyarov
Stanislav Kotlyarov, Department of Nurse, Ryazan State Medical University, Ryazan 390005, Russia
Author contributions: Kotlyarov S contributed to the conceptualization, methodology, validation, resources, data curation, preparation of the original draft, review and editing, supervision, and project administration.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Stanislav Kotlyarov, PhD, Department of Nurse, Ryazan State Medical University, Vysokovoltnaya 9, Ryazan 390005, Russia. skmr1@yandex.ru
Received: January 14, 2026
Revised: January 26, 2026
Accepted: March 6, 2026
Published online: June 27, 2026
Processing time: 155 Days and 20.9 Hours
Core Tip

Core Tip: The increase in metabolic disorders has led to the comorbidity of primary biliary cholangitis (PBC) and metabolic dysfunction-associated steatotic liver disease (MASLD) becoming increasingly common. Beyond simple comorbidity, these conditions cause complex immunometabolic cross-talk involving common pathways of immune dysregulation, lipid metabolism alterations, adipokine imbalance, and gut microbiota dysfunction. Recent data suggest that in patients with PBC, concomitant MASLD disrupts the characteristic hyperadiponectinemia associated with cholestasis, leading to a specific adipokine profile with an elevated leptin/adiponectin ratio. This Editorial summarizes current understanding of the pathogenetic relationships between PBC and MASLD, analyzes new clinical data on their bidirectional effects, and identifies critical gaps in knowledge. Understanding these interactions is important for developing personalized therapeutic approaches and improving treatment outcomes for patients with this increasingly recognized dual pathology.

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