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Statin Continuation After an Index Hospitalization for Hepatic Decompensation in MASLD Cirrhosis
Mohammad Alabbas1,2, Akram Alnounou3, EzzElDien A Ibrahim4
1Department of Gastroenterology, Hepatology and Nutrition, Cleveland Clinic Foundation, Cleveland, OH, USA. alabbam@ccf.org.
Background:
Whether established statin therapy should be continued after hospitalization for hepatic decompensation in metabolic dysfunction-associated steatotic liver disease (MASLD) cirrhosis remains uncertain.
Methods:
We performed a retrospective multicenter cohort study in the TriNetX Research network. Adults aged 18-75 years with MASLD cirrhosis, a qualifying inpatient decompensation event, and a statin record before index were classified by whether a statin was recorded from the index date through day 30. Propensity score matching was used to improve balance across demographics, comorbidities, liver-related features, medications, and laboratory values. Outcomes were evaluated through 1 year using platform-generated survival analyses.
Results:
The matched analysis included 1,108 patients (554 per group). At 1 year, statin continuation was not associated with the subsequent decompensation composite (62.1% vs 61.6%; HR 1.08, 95% CI 0.93-1.26) or all-cause mortality (19.7% vs 19.5%; HR 1.04, 95% CI 0.80-1.36). Subsequent ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, the cardiovascular composite, and the muscle and laboratory liver injury composites also did not differ. Liver transplantation was less frequent (2.3% vs 6.1%; HR 0.38, 95% CI 0.20-0.73), whereas all-cause hospitalization was more frequent (62.6% vs 57.8%; HR 1.20, 95% CI 1.03-1.40). Exploratory high-intensity analyses showed higher decompensation, hepatic encephalopathy, and hospitalization.
Conclusions:
Among prevalent statin users with MASLD cirrhosis, continuation after an index decompensation hospitalization was not associated with lower 1-year decompensation or mortality. Isolated secondary and intensity findings are exploratory. Residual confounding, exposure misclassification, competing risk, and overlap between exposure classification and early follow-up limit causal interpretation; prospective and time-aligned studies are needed.
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