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Impact of Obeticholic acid Exposure on Decompensation and Mortality in Primary Biliary Cholangitis and Cirrhosis
Hepatol Commun. 2021 May 6;5(8):1426-1436. doi: 10.1002/hep4.1720. eCollection 2021 Aug.
Binu V John12, Kaley Schwartz1, Cynthia Levy2, Bassam Dahman3, Yangyang Deng3, Paul Martin2, Tamar H Taddei45, David E Kaplan67
1Division of Hepatology Bruce W Carter VA Medical Center Miami FL USA.
2Division of Digestive Health and Liver Diseases University of Miami Miller School of Medicine Miami FL USA.
3Department of Health Behavior and Policy Virginia Commonwealth University Richmond VA USA.
4Section of Digestive Diseases Yale School of Medicine New Haven CT USA.
5Division of Gastroenterology and Hepatology VA Connecticut Healthcare System West Haven CT USA.
6Division of Gastroenterology and Hepatology University of Pennsylvania Philadelphia PA USA.
7Division of Gastroenterology and Hepatology Corporal Michael J. Crescenz VA Medical Center Philadelphia PA USA.
Obeticholic acid (OCA) is approved for the treatment of patients with primary biliary cholangitis (PBC) who are partial responders or intolerant to ursodeoxycholic acid. Reports of serious liver injury have raised concerns about its safety in cirrhosis. We investigated the effects of treatment with OCA on hepatic decompensation and liver-related mortality or transplantation in a cohort with compensated PBC cirrhosis. This was a retrospective cohort study using national data of US veterans with PBC and cirrhosis. We performed a propensity score model using variables associated with OCA prescription to control for baseline risk of decompensation. New OCA users were matched to nonusers. We identified 509 subjects with compensated PBC cirrhosis. We developed a propensity score model using variables associated with OCA prescription; 21 OCA users were matched with 84 nonusers. Over 569 and 3,847 person-months, respectively, of follow-up, 5 (23.8%) OCA users and 22 (26.2%) OCA nonusers decompensated. The C-statistic of the propensity score model was 0.87. On multivariable analysis, after adjusting for potential confounders, OCA use was associated with an increased risk of hepatic decompensation (adjusted hazard ratio, 3.9; 95% confidence interval, 1.33-11.57; P = 0.01). There was no association between OCA use and liver-related mortality or transplantation (adjusted hazard ratio, 1.35; 95% confidence interval, 0.35-5.21; P = 0.66). Conclusion: OCA use was associated with an increase in hepatic decompensation but not liver-related mortality or transplantation in patients with compensated PBC cirrhosis. Additional studies are recommended to prospectively investigate these findings.