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Published on: March 25, 2022
Steatotic Liver Disease at Primary Biliary Cholangitis Diagnosis: Association With Ursodeoxycholic Acid Response and
María Del Barrio1, Margarita Sala2, Judith Gómez3
1Gastroenterology and Hepatology Department, Clinical and Translational Research in Digestive Diseases, Valdecilla Research Institute (IDIVAL), Marqués de Valdecilla University Hospital, Santander, Spain.
Background And Aim:
Steatotic liver disease (SLD) is becoming increasingly prevalent, leading to a higher frequency of primary biliary cholangitis (PBC) cases coexisting with SLD. However, data on its impact in patients with PBC remain scarce. The aim is to assess the impact of SLD on treatment response and prognosis in patients with PBC receiving ursodeoxycholic acid (UDCA).
Methods:
A retrospective, multicenter cohort study including patients diagnosed with PBC enrolled in the Spanish ColHai registry.
Results:
A total of 469 patients with available data required for the study were included. Among them, 158 (33.7%) had SLD, and 124 (78.5%) met the diagnostic criteria for MASLD. Patients with PBC and SLD had lower baseline levels of alkaline phosphatase and higher liver stiffness at diagnosis. Regarding treatment response, no significant differences were observed across the different response criteria (Paris II, GLOBE, UK-PBC, deep response and complete normalization). Additionally, the presence of SLD was not associated with UDCA response at 1-year (Paris II: OR 1.04 [0.69-1.56]; GLOBE: OR 0.91 [0.58-1.44]; deep response: OR 1.08 [0.72-1.63]; complete normalization: OR 0.82 [0.52-1.30]). Baseline SLD was not associated with an increased risk of liver related-events in either the univariate analysis (HR 1.19, 95% CI 0.71-2.02) or in the different multivariate models evaluated. After inverse probability of treatment weighting (IPTW) using propensity scores, SLD still showed no significant impact on hepatic event development (HR 1.62; 95% CI 0.92-2.83).
Conclusion:
Although SLD is frequently observed in PBC, it does not appear to adversely affect UDCA response or long-term hepatic outcomes.
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