Serum Galectin-3 in Hepatitis B e-Antigen-Negative Chronic Hepatitis B Virus Infection: Clinical and Histological Correlations

<b><i>Background and aims:</i></b> 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. <b><i>Methods:</i></b> 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. <b><i>Results:</i></b> 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; <i>p</i> < 0.001). Although Gal-3 levels were higher in CHB than CHI, the difference was not significant (<i>p</i> = 0.08). Median Gal-3 levels in CHB patients decreased from 567 U/L to 288 U/L after 12 months of antiviral therapy (<i>p</i> = 0.043 after excluding an outlier). Gal-3 levels showed weak correlations with HBV DNA (Spearman's rho = 0.32, <i>p</i> = 0.12), ALT (rho = 0.28, <i>p</i> = 0.17), and fibrosis scores (rho = 0.35, <i>p</i> = 0.09). <b><i>Conclusions:</i></b> 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.