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Objective To investigate the characteristics of liver tissue pathology and immunohistochemistry in HBeAg negative hepatitis B virus infection and provide a reference for the diagnosis and treatment.Methods Liv-er biopsy was carried out on the 63 HBeAg negative HBV infections,then liver tissue inflammation,fibrosis and immu-nohistochemistry were detected.Results In HBeAg negative and HBV DNA negative patients,both the male and female,ALT normal and mildly abnormal group had no significant difference in liver inflammation and fibrosis(all P >0.05).Among the patients with fibrosis stage ≥S2,the ratio(30 /41,73.2%)of patients above 30 years old was higher than that below 30 years old (6 /14,46.2%)(P =0.041).There were no differences in liver tissue inflamma-tion(5 /34,14.7% vs.9 /29,31.0%)and fibrosis (8 /34,23.5% vs.8 /29,27.6%)between HBV DNA negative group and HBV DNA positive patients(all P >0.05).Only 2 cases of HBcAg positive in those 63 cases of liver tissue immunohistochemistry.Conclusion The liver tissues of HBeAg negative HBV DNA negative or positive patients have obvious liver inflammation and fibrosis,and the necessary treatment measures should be taken.HBcAg positive is extremely low in those liver tissue immunohistochemistry,which lead to the pathogenesis of liver inflammation needs further research.
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<p><b>OBJECTIVE</b>To explore the changes in HBsAg titer and HBV DNA load and their correlation in patients with chronic hepatitis B (CHB) and HBV-related liver cirrhosis (HBV-LC).</p><p><b>METHODS</b>Forty-six patients with mild to moderate CHB (CHB-LM), 24 patients with severe CHB (CHB-S), and 28 patients with HBV-LC at admission, and 51 patients with HBV-LC at 4.08 ± 3.06 months during antiviral treatment were tested for serum HBsAg titer and HBV DNA load using Abbott chemiluminescence and fluorescence quantitative PCR, respectively.</p><p><b>RESULTS</b>The serum HBsAg titer and HBV DNA load gradually decreased with increased disease severity (from CHB-LM, CHB-S to HBV-LC; χ(2)=12.537 and 8.381, respectively, P<0.05). HBsAg titer and HBV DNA load were significantly higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05), but comparable between CHB-LM and CHB-S groups (Z=-0.649 and 0.032, respectively, P>0.05). Among HBeAg-positive patients, HBsAg titer and HBV DNA load tended to decrease with increased disease severity (from CHB-LM, CHB-S to HBV-LC; χ(2)=6.146, P=0.046 and χ(2)=1.017, P>0.05; respectively), and CHB-LM group had significantly higher HBsAg titer than HBV-LC group (Z=-2.247, P=0.025). Among the HBeAg-negative patients, serum HBsAg and HBV DNA load gradually declined with the disease severity (χ(2)=8.660 and 13.581, respectively, P<0.05), and were obviously higher in CHB-LM and CHB-S groups than in HBV-LC group (P<0.05). Positive correlations were found between serum HBsAg and HBV DNA levels in CHB-LM (r=0.389, P=0.009) and HBV-LC groups (r=0.431, P=0.022), but not in CHB-S group (r=0.348, P=0.104). After antiviral therapy, the serum HBsAg titer was slightly decreased (Z=-1.050, P=0.294) while HBV DNA load markedly reduced (Z=-5.415, P<0.001), showing no correlation between them (r=0.241, P=0.111) or between the measurements before and after treatment (r=0.257, P=0.085).</p><p><b>CONCLUSION</b>Serum HBsAg titer and HBV DNA load decreases progressively from CHB-LM to CHB-S and HBV-LC in both HBeAg- positive and -negative patients. The serum HBsAg titer is positively correlated with HBV DNA load, but their levels are not consistently parallel.</p>