ArticleCell communication and signaling : CCS2026
HBV re-activation is associated with increased mortality and dysregulation of oxidative and polyamine metabolism in pre-acute-on-chronic liver failure.
Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Chinese Chronic Liver Failure Consortium Acute-on-Chronic Liver Disease and Failure Study --a Prospective Multi-center Study in China, the Largest Hepatitis B Virus High-endemic Region.
A Prospective Multi-center Validating Cohort for ACLF Diagnosis and Prognosis From Ch-CANONIC Study
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsAcute-on-chronic liver failure (ACLF) is one of the deadliest complications of chronic liver disease yet treatment options are sparse. In Asia, HBV-reactivation (HBVr) is one of the most common triggers. Recently, HBV-associated ACLF was associated with distinct changes in the metabolome. Here, metabolic impacts of HBVr were analysed in-depth in non-ACLF, pre-ACLF and ACLF.
methodsClinical and metabolic data of 1024 Chinese patients (CATCH-LIFE studies) with chronic HBV mono-infection were analyzed. ACLF was diagnosed according to COSSH criteria. Metabolites in plasma were quantified using LC-MS, compared to non-ACLF and subjected to enrichment and pathway analyses using the database SMPDB via MetaboAnalyst v6.
resultsIn 1024 patients (611: non-ACLF, 72: pre-ACLF, 341: ACLF), HBVr was present in 20.2% (ACLF) or 33.3% (pre-ACLF) of patients. HBVr increased 28-day mortality in pre-ACLF patients (2.1% in HBVnr vs. 25% in HBVr). Energy metabolism generating reactive oxygen species (ROS) was highly induced in the absence of ROS-detoxifying pathways in pre-ACLF. Urea cycle, thus nitric oxide (NO) build-up, the polyamine metabolism and related pathways were highly increased in both HBVr pre-ACLF and ACLF, shifting pre-ACLF close to mature ACLF. Specific metabolites could be identified as putative markers and key-regulators herein.
conclusionHBV reactivation induces inflammation, hepatic injury and mortality especially in pre-ACLF patients. Metabolic disruption in the ROS/NO/polyamine axis favors stress and hinders liver regeneration. Findings help identifying and alleviating HBVr-driven progression towards ACLF via pharmacological or biopharmaceutical intervention.
trial registrationAnalyses were based on the CATCH-LIFE studies. The CATCH-LIFE studies were registered at Clinical. TRIALS: gov (Clinical Trial Number: NCT02457637, first registered 2015-01-31 and NCT03641872, first registered 2018-08-14).
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.