Quantificação do HBsAg : uma nova alternativa para o monitoramento da hepatite B crônica?

Abstract

Although the level of HBsAg is determined only qualitatively in routine clinical practice, recent data suggest that its quantification can assist or replace the viral load of HBV DNA in monitoring of HBV replication, which would be an easier and more economical alternative. Thus, the aim of this study was to correlate the levels of HBsAg with viral load of HBV DNA and other laboratory (HBeAg, ALT and AST) and histological (activity and fibrosis) findings in patients with chronic hepatitis B. A prospective, observational, cross-sectional study was performed on 128 patients with chronic hepatitis B, aged over 18 years, from the Hepatology Service of the University Hospital of Sergipe. Categorical variables were presented as frequencies and percentages with range of 95% where applicable. For the correlation analysis we used the Spearman test. It was considered that the correlations had statistical significance when ρ≤ 0.05. The overall correlation between HBV viral load and quantitative HBsAg was weak (ρ= 0.197, ρ= 0.026), and this same correlation was also weak and not statistically significant in HBeAg-positive patients (ρ= 0.233, ρ= 0.263). However, a strong correlation between HBsAg and HBV DNA >20,000 in HBeAgpositive patients was found. A regular correlation between HBsAg and HBV DNA in patients who were not on treatment (*ρ= 0394; ρ<0.001) was found and there was no significant correlation in patients receiving treatment (*ρ= -0.061; ρ= 0.673). No statistically significant association was observed between the levels of HBsAg and HBeAg, even when considering only the positive HBeAg (ρ: 0.121; ρ=0.565) and even not only the negative HBeAg (ρ =-0.067; ρ=0.501). The correlation between HBV DNA and HBeAg positive was fair (ρ =0.444; ρ=0.026). There was no statistical correlation between the levels of HBsAg and aminotransferases (ALT and AST). The distribution of HBsAg values did not differ between the degree of activity (ρ= 0.17) and fibrosis (ρ= 0.20). Conclusion: Our results show that, in general, the correlation between levels of HBsAg and HBV DNA exists, but it proved to be weak. Also, they suggest that HBsAg better reflects HBV DNA in the initial replicative phase of chronic hepatitis B, when patients present HBV reagent and high titers of HBeAg viral load. They also show that there is no association of HBsAg with aminotransferases or with the degree of activity and liver fibrosis.