Adipokine profiles reflect metabolic dysfunction but not fibrosis in patients with primary biliary cholangitis

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.

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.

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.

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).

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.