BACKGROUND AND AIM: Liver macrophages are activated in chronic hepatitis B virus (CHB) infection and play a pivotal role in hepatic inflammation and fibrosis. However, their role during anti-viral treatment is unclear. The soluble (s) macrophage activation markers, sCD163 and mannose receptor (sMR), are released during liver damage and their serum levels reflect liver disease severity and portal hypertension. We aimed to investigate associations between sCD163 and sMR and histopathological activity and fibrosis, and changes in sCD163, sMR and hepatic CD163-expression following anti-viral treatment in CHB patients.

METHODS: We assessed Ishak histological necroinflammatory activity and fibrosis scores in liver biopsies from 254 CHB patients, and serially in 71 patients before and after nucleoside-analogue treatment. Liver CD163-expression was semi-quantitatively determined by immunohistochemistry and serum sCD163 and sMR measured by ELISA.

RESULTS: Before treatment, the mean levels of sCD163 and sMR were 3.57 (SD 1.72) mg L(-1) and 0.35 (0.12) mg L(-1) . sCD163 and sMR increased with histological inflammatory activity (sCD163: r=0.46, p<0.00001; sMR: r=0.48, p<0.00001) and correlated positively with fibrosis (sCD163: OR 1.16, 95%CI:1.03-1.31; sMR: OR 1.34, 95%CI:1.13-1.59); both were markers of fibrosis independent of other biochemical parameters and risk factors. Anti-viral treatment significantly reduced sCD163 (3.76 (1.46) vs. 2.31 (0.95), p<0.00001), sMR (0.37 (0.1) vs. 0.29 (0.07), p<0.00001) and hepatic CD163-expression (p=0.0002).

CONCLUSIONS: The macrophage activation markers sCD163 and sMR were associated with activity and fibrosis in liver biopsies from CHB patients. Both serum markers decreased with anti-viral treatment, along with decreased hepatic CD163 expression.