Synergistic effects of ursodeoxycholic acid, and quercetin on liver function and systemic inflammation in non-alcoholic fatty liver disease and atrial fibrillation patients

Abstract

Background. Non-alcoholic fatty liver disease (NAFLD) and atrial fibrillation (AF) co-occur with signifi­cant clinical implications, necessitating therapeutic strategies that address the multifaceted nature of these conditions. This study evaluated the efficacy of standard treatment alone versus combined treatments with ursodeoxycholic acid (UDCA) and quercetin in patients with NAFLD and AF, focusing on improvements in liver function, lipid profile, systemic inflammation, and fibrosis markers. Aim: to evaluate and compare the efficacy of standard treatment alone versus standard treatment combined with ursodeoxycholic acid with and without quercetin in patients with non-alcoholic fatty liver disease and concurrent atrial fibrillation. Materials and methods. In a prospective, randomi­zed, controlled trial, 127 patients with diagnosed NAFLD and concurrent AF were enrolled. They were divided into three groups: group 1 — standard treatment (n = 42), group 2 — standard treatment plus UDCA (n = 44), and group 3 — standard treatment plus UDCA and quercetin (n = 41). The primary outcomes included changes in liver function tests (alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase, alkaline phosphatase), lipid profile (total cholesterol, low- and high-density lipoprotein cholesterol (HDL-C), triglycerides), and non-invasive liver fibrosis scores (NFS, FIB-4). Secondary outcomes focused on systemic inflammation markers (C-reactive protein, galectin-3, soluble ST2) and fibronectin levels. Results. All treatment groups showed significant improvements in liver function tests and lipid profiles. Group 3 exhibited the most substantial reductions in ALT, AST, and improvements in HDL-C, indicating enhanced hepatoprotective and lipid-modulating effects. Systemic inflammation markers and fibronectin levels decreased significantly in groups receiving UDCA and quercetin, with the most pronounced effects observed in group 3, suggesting potent anti-inflammatory and anti-fibrotic action. Additionally, significant improvements in NFS and FIB-4 scores in group 3 highlight the anti-fibrotic potential of combining UDCA and quercetin with standard treatment. Conclusions. The addition of UDCA and quercetin to standard treatment for patients with NAFLD and AF significantly improves liver function, lipid metabolism, and reduces systemic inflammation and fibrosis, compared to standard treatment alone. These findings suggest a synergistic effect of UDCA and quercetin, offering a promising therapeutic strategy for managing the complex interplay between NAFLD and AF.