A 72-week clinical study involving patients with chronic hepatitis B and liver fibrosis found that early decreases in liver stiffness measurements were primarily caused by reduced inflammation rather than actual regression of fibrosis.
At baseline and again after 72 weeks of treatment, researchers assessed the liver biopsies and liver stiffness measurements (LSM) of 82 treatment-naive patients with chronic hepatitis B and liver fibrosis who received entecavir combined with Biejia-Ruangan, a traditional antifibrotic herbal therapy.
By the end of the study period, liver enzymes such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST) significantly decreased. Most of the patients also experienced reductions in LSM values. Histologic activity index (HAI) scores, used to assess liver inflammation, improved in 61% of patients, whereas fibrosis scores improved in only 38%. The difference was statistically significant (P = .003).
Correlation analysis revealed that LSM was more strongly associated with inflammation compared with fibrosis. The correlation between LSM and HAI dropped from r = 0.526 at baseline to r = 0.286 after 72 weeks, while correlation with fibrosis remained relatively stable (r = 0.677 to r = 0.587).
A key finding from the study was the result of a logistic regression analysis. The researchers found that improvement in inflammation significantly influenced the drop in LSM values (odds ratio [OR] = 1.018, 95% confidence interval = 1.002–1.031, P = .023), while fibrosis improvement didn't (OR = 0.994, P = .414). The results suggested that the early improvements seen in noninvasive stiffness measurements likely reflected inflammation control rather than a reversal of scarring in the liver.
Virologic suppression was achieved in most of the patients, with 87.8% of them reaching undetectable hepatitis B DNA levels. Liver function markers normalized, and noninvasive fibrosis indices such as FIB-4 and APRI decreased significantly. However, liver biopsy confirmed that fibrosis regression lagged behind improvements in inflammation.
The researchers emphasized that liver inflammation can affect LSM readings and should be considered when interpreting early changes. Prior to treatment, LSM values increased with higher HAI scores, a trend that weakened after inflammation was reduced. This pattern suggested that active inflammation can elevate LSM independently of fibrosis severity.
The researchers noted that while LSM is widely used as a noninvasive surrogate for liver fibrosis, early treatment-related reductions may reflect inflammation resolution rather than structural changes in liver tissue.
The findings called for long-term, multicenter studies to validate the results and to refine strategies for monitoring fibrosis progression and treatment response in patients with chronic hepatitis B.
The authors reported no conflicts of interest.