BACKGROUND AND OBJECTIVES: Little is known about hepatitis B surface antigen (HBsAg) level during the natural course of hepatitis B virus (HBV) infection. The aims of this study were to determine the HBsAg titer in the different phases of HBV infection and to evaluate for the presence of a correlation between HBsAg titers and HBV DNA levels. STUDY DESIGN: 272 HBV patients were analyzed in a cross-sectional study. The patients were classified into 4 categories: immune tolerant phase (IT, n=9), immune clearance phase (IC, n=26), low-replicative phase (LR, n=131), and HBeAg-negative hepatitis (ENH, n=106). RESULTS: Median HBsAg titers were different between each phase of CHB (p<0.001): IT (4.31log(10)IU/ml), IC (4.42log(10)IU/ml), LR (3.32log(10)IU/ml) and ENH (3.71log(10)IU/ml). Correlation of HBsAg and HBV DNA was strong in IT patients (r=0.74) and the whole group (r=0.83), moderate in the ENH phase (r=0.44) and poor in the IC (r=0.14) and the LR phases (r=0.080). CONCLUSIONS: This large study demonstrates that in HBV patients, HBsAg levels are significantly different in the different stages of the disease. A correlation between serum HBV DNA and HBsAg titers does not exist except in the IT and ENH phases. Three other studies have addressed the same issue on different genotypes and we notice that there is no concordance between the 4 studies. This leads to conclude that measurement of HBsAg level, for the time being, will not replace the serum HBV DNA as a marker of replication.
BACKGROUND AND OBJECTIVES: Little is known about hepatitis B surface antigen (HBsAg) level during the natural course of hepatitis B virus (HBV) infection. The aims of this study were to determine the HBsAg titer in the different phases of HBV infection and to evaluate for the presence of a correlation between HBsAg titers and HBV DNA levels. STUDY DESIGN: 272 HBVpatients were analyzed in a cross-sectional study. The patients were classified into 4 categories: immune tolerant phase (IT, n=9), immune clearance phase (IC, n=26), low-replicative phase (LR, n=131), and HBeAg-negative hepatitis (ENH, n=106). RESULTS: Median HBsAg titers were different between each phase of CHB (p<0.001): IT (4.31log(10)IU/ml), IC (4.42log(10)IU/ml), LR (3.32log(10)IU/ml) and ENH (3.71log(10)IU/ml). Correlation of HBsAg and HBV DNA was strong in IT patients (r=0.74) and the whole group (r=0.83), moderate in the ENH phase (r=0.44) and poor in the IC (r=0.14) and the LR phases (r=0.080). CONCLUSIONS: This large study demonstrates that in HBVpatients, HBsAg levels are significantly different in the different stages of the disease. A correlation between serum HBV DNA and HBsAg titers does not exist except in the IT and ENH phases. Three other studies have addressed the same issue on different genotypes and we notice that there is no concordance between the 4 studies. This leads to conclude that measurement of HBsAg level, for the time being, will not replace the serum HBV DNA as a marker of replication.