Kotlyarov S. Metabolic links between metabolic dysfunction-associated steatotic liver disease and primary biliary cholangitis. World J Hepatol 2026; 18(6): 118902 [DOI: 10.4254/wjh.118902]
Corresponding Author of This Article
Stanislav Kotlyarov, PhD, Department of Nurse, Ryazan State Medical University, Vysokovoltnaya 9, Ryazan 390005, Russia. skmr1@yandex.ru
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
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 19.2 Hours
Abstract
Primary biliary cholangitis (PBC) and metabolic dysfunction-associated steatotic liver disease (MASLD) increasingly coexist in the same patient against the backdrop of a global epidemic of metabolic disorders. A growing body of evidence points to profound pathogenetic intersections between autoimmune damage to the biliary tract and systemic metabolic dysfunction. These interactions involve key mechanisms: Immune regulation, lipid metabolism, adipokine profile, and gut microbiota function. In comorbid cases, these processes do not simply add up, but may give rise to a qualitatively distinct clinical-pathogenetic variant. A recent study conducted by Koky et al published in World Journal of Hepatology provides important information about this comorbidity, demonstrating that patients with PBC and concomitant MASLD have a specific adipokine imbalance characterized by decreased adiponectin and increased leptin levels, resulting in an elevated leptin/adiponectin ratio. This editorial summarizes current understanding of the pathogenetic links between PBC and MASLD and discusses the implications for clinical practice and future research.
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.