ArticleGut and liver2025
Serial Liver Stiffness Measurement and Serum Biomarkers Are Not Strong Predictors of the Regression of Fibrosis among Chronic Hepatitis B Patients Receiving Antiviral Therapy Based on Triple Liver Biopsies.
Article in Gut and liver, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02849132 (Effect of Entecavir Treatment on Regression and Long-term Disease Outcome in Patients With HBV-induced Liver Fibrosis and Cirrhosis), which is not on this map. Cited by 1 paper.
What it found
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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.
Effect of Entecavir Treatment on Regression and Long-term Disease Outcome in Patients With HBV-induced Liver Fibrosis and Cirrhosis (Regress Extension Study)
Who cites it
1 citing paper in PubMed.
- Liver fibrosis: Pathogenesis and innovative nanoparticle-based therapeutic strategies.International journal of pharmaceutics: X · 2026Review
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/Aims: Noninvasive indexes can be used to diagnose and stage liver fibrosis caused by chronic hepatitis B (CHB). We aimed to evaluate whether changes in the liver stiffness measurement (LSM) and serum biomarkers can predict liver fibrosis regression in CHB patients based on triple liver biopsies. Methods: This multicenter cohort study was based on triple liver biopsies and lasted for 260 weeks. Liver fibrosis regression was defined as Ishak decreased ≥1 stage or predominantly regressive by P-I-R classification with stable Ishak stage. Twelve noninvasive models were validated externally and yielded area under the receiver operating characteristic curve (AUROC) values ≥0.700 for predicting significant fibrosis in the training set. Results: A total of 175 CHB patients were included (median age: 38 years, 76.6% male). A total of 69.2% (117/169) and 79.6% (78/98) patients achieved liver fibrosis regression at week 78 and week 260, respectively. The mixed effects model revealed significant group×time interactions between the regression and non-regression groups for aminotransferase to platelet ratio index (APRI; p=0.041), new algorithm attributed to age, alanine aminotransferase, gamma-glutamyl transferase algorithm (p=0.022), and King's score (p=0.016) from baseline to week 78 as well as for APRI (p=0.046) from baseline to week 260. The AUROC values for model changes were all <0.750 for predicting liver fibrosis regression. Additionally, the changes in the LSM and most noninvasive models were significantly correlated with the changes of Ishak-histology activity index score. Conclusions: Changes in the LSM and noninvasive models were not strong predictors of liver fibrosis regression after 78 weeks and 260 weeks of treatment among CHB patients. It is critical to develop a dynamic noninvasive model for assessing liver fibrosis regression (ClinicalTrials.gov identifier NCT02849132).
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