Abstract
Background and aims:
Chronic hepatitis B (CHB) drives liver fibrosis, contributing to chronic liver disease. Galectin-3 (Gal-3), a lectin linked to inflammation and fibrosis, was investigated for its association with liver injury severity in HBeAg-negative CHB and chronic hepatitis B virus (HBV) infection (CHI) patients.
Methods:
We enrolled 25 CHB, 25 CHI, and 25 healthy controls. Serum Gal-3 levels were measured in all subjects, with liver biopsies performed in CHB patients. Gal-3 and HBV DNA levels were monitored at 0, 1, 3, 6, and 12 months during antiviral therapy in CHB patients.
Results:
Serum Gal-3 levels were significantly higher in CHI (median: 422 U/L, interquartile range [IQR]: 144–900) and CHB (median: 567 U/L, IQR: 196–1093) patients than controls (median: 179 U/L, IQR: 79–350; p < 0.001). Although Gal-3 levels were higher in CHB than CHI, the difference was not significant (p = 0.08). Median Gal-3 levels in CHB patients decreased from 567 U/L to 288 U/L after 12 months of antiviral therapy (p = 0.043 after excluding an outlier). Gal-3 levels showed weak correlations with HBV DNA (Spearman’s rho = 0.32, p = 0.12), ALT (rho = 0.28, p = 0.17), and fibrosis scores (rho = 0.35, p = 0.09).
Conclusions:
Elevated Gal-3 levels correlate with HBeAg-negative CHB and CHI, with a significant decline posttreatment in CHB. If validated, Gal-3 could serve as a noninvasive marker for fibrosis and treatment response.
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