Background Antiviral therapy is recommended for patients with immune-active chronic hepatitis B (CHB) to decrease the risk of liver-related complications. However, the outcomes of the pegylated IFN-α (PEG-IFN-α) therapy vary among CHB patients. We aimed to identify factors that can influence the outcomes in CHB patients who received antiviral PEG-IFN-α monotherapy. Methods Thirty-two CHB patients who received PEG-IFN-α monotherapy were enrolled in this study. All of the patients underwent two liver biopsies at baseline and 6 months after the initiation of the therapy. CD8 + T cells, CD4 + T cells, CD68 + mononuclear cells, and PD-1 levels in the 64 liver biopsy specimens were examined via immunofluorescence. Results The overall median frequency of CD8 + T cells in the liver tissues of 32 CHB patients significantly decreased at 6 months after the therapy initiation ( p < 0.01). In the FIER (fibrosis and inflammation response with HBeAg seroconversion) group, CD8 + PD-1 + T cells significantly decreased at 6 months ( p < 0.05), while CD8 + PD-1 − T cells had no significant difference. On the contrary, in the FIENR (no fibrosis and inflammation response and HBeAg seroconversion) group, CD8 + PD-1 − T cells significantly decreased after 6 months of PEG-IFN-α treatment ( p < 0.05), while CD8 + PD-1 + T cells had no significant difference. In addition, the levels of CD68 + mononuclear cells in the FIER group showed an overall increasing trend after treatment ( p < 0.05). Conclusions The changes in the levels of CD8 + PD-1 + T cells and CD68 + mononuclear cells may be related to the response to PEG-IFN-α therapy.
Several hepatitis B virus (HBV) serum markers have been identified as risk factors for liver fibrosis in patients with chronic HBV infection, and several noninvasive fibrosis tests based on serum indexes are now used to identify the severity of liver fibrosis. We aimed to identify the relationship between hepatitis B core‐related antigen (HBcrAg) serum levels and liver fibrosis in treatment‐naive chronic HBV infection patients. A total of 246 treatment‐naive chronic HBV infection patients were enrolled in this study. All of the patients underwent liver biopsies at baseline. Using the METAVIR fibrosis stages, there were 15, 140, 50, 26 and 15 patients in the F0, F1, F2, F3 and F4 stages (METAVIR scoring system), respectively. The biochemical, serological and virological parameters were measured using standard laboratory procedures. The HBcrAg serum levels of the patients were examined via ELISA. HBcrAg serum levels of F2, F3 and F4 stage patients were significantly higher than those of nonsignificant liver fibrosis patients (METAVIR F0‐F1), but there were no significant differences among F2, F3 and F4 stage patients. Serum HBcrAg (OR, 2.18; 95% confidence interval [CI], 1.51–3.16), albumin (ALB) (OR, 0.60; 95% CI, 0.41–0.87), prothrombin activity (PTA) (OR, 0.58; 95% CI, 0.40–0.83) and platelet (PLT) counts (OR, 0.38; 95% CI, 0.25–0.57) were associated with significant liver fibrosis (METAVIR F2‐F4). The serum HBcrAg value enabled the correct identification of patients with significant fibrosis, with an area under the receiver operating characteristic curve of 0.81 (95% CI, 0.75–0.88). The APRI, FIB‐4 index and ALBI score can identify significant liver fibrosis with an area under the ROC curve of 0.74 (95% CI, 0.66–0.81), 0.73 (95% CI, 0.65–0.80) and 0.63 (95% CI, 0.55–0.72), respectively. Compared with these three indexes, the accuracy rate of diagnosis of significant fibrosis based on HBcrAg was higher than that of the FIB‐4 index (p = 0.0479) and ALBI score (p = 0.0030). HBcrAg, ALB, PTA serum levels and PLT counts were associated with significant liver fibrosis in treatment‐naive chronic HBV infection patients. HBcrAg serum levels enabled the correct identification of patients with significant fibrosis (METAVIR F2–F4), and HBcrAg was more effective than the FIB‐4 index and ALBI score.
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