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Trends in the etiology of acute insult and underlying chronic liver disease in patients with acute-on-chronic liver failure: A retrospective study in Southwest China (2020-2023).

Created on 18 Jul 2026

Authors

Yi Fang, Haifeng Dai, Qiufen Li, Danni Wang, Jianwen Liu, Yanan Liu

Published in

Medicine. Volume 105. Issue 29. Pages e49420. Jul 17, 2026.

Abstract

The etiology of acute insults and underlying chronic liver disease in acute-on-chronic liver failure has evolved in recent years. This study examined etiological patterns and trends from 2020 to 2023 in Southwest China. This study is a retrospective analysis that included 346 patients diagnosed with acute-on-chronic liver failure according to the Asian pacific association for the study of liver criteria at our hospital from 2020 to 2023. The etiology of acute insult and chronic liver disease and changing trends from 2020 to 2023 were analyzed. The top 5 etiologies of acute insult were spontaneous hepatitis B virus (HBV) reactivation (45.4%), HBV reactivation due to nucleot(s)ide analog withdrawal (16.2%), drug-induced liver injury (16.2%), unknown (6.1%), and alcoholic hepatitis (4.6%). The top 5 etiologies of chronic liver disease were chronic hepatitis B (53.2%), HBV-associated cirrhosis (22.00%), chronic hepatitis B plus alcoholic hepatitis (6.6%), HBV plus alcoholic hepatitis-associated cirrhosis (6.4%), and alcoholic hepatitis-associated cirrhosis (3.8%). From 2020 to 2023, the percentage of patients with viral hepatitis initially declined and then increased. The percentage of patients with alcoholic hepatitis showed a slight declining trend. The proportion of HBV-associated cirrhosis increased from 18.8% to 29.9%. The percentage of patients with chronic hepatitis B plus alcoholic hepatitis decreased from 11.8% to 2.6%, respectively. Viral hepatitis, especially chronic hepatitis B, remains the leading cause of acute insult and underlying chronic liver disease in Southwest China. These findings underscore the need for targeted HBV management strategies.

PMID:
42470051
Bibliographic data and abstract were imported from PubMed on 18 Jul 2026.

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