BACKGROUND:Serum HBV DNA level is crucial in the management of chronic hepatitis B (CHB); however, the assay is expensive and cannot be used widely. Therefore, we explored the possibility of hepatitis B surface antigen (HBsAg) quantification as a surrogate marker for HBV DNA level in CHB patients. METHODS: A total of 289 CHB patients were enrolled, 251 were evaluated at baseline and 75 of them were also evaluated during anti-HBV treatment. Another 38 on-treatment patients were used for validation. Serum HBsAg titre was quantified by an immunoassay and HBV DNA level by a PCR-based method. Baseline and on-treatment data were analysed. RESULTS: In parallel to log(10) HBV DNA, the log(10) HBsAg was high in both immune tolerance and immune clearance phases, and significantly decreased in the inactive carrier state and was again increased in the reactivation phase of the CHB infection. There was a positive correlation between log(10) HBsAg and log(10) HBV DNA, which was greater in patients with chronic hepatitis, hepatitis B e antigen-positivity, greater alanine aminotransferase or HBsAg levels at baseline and during pegylated interferon treatment. Log(10) HBsAg could predict log(10) HBV DNA independently. An HBsAg titre of >900 IU/ml at baseline or >1,500 IU/ml within the first year of treatment could predict an HBV DNA level of >20,000 IU/ml, especially in subgroups of chronic hepatitis with alanine aminotransferase levels >40 IU/l. The dynamics of HBsAg might also predict serial HBV DNA changes. In the validation group, 64% of patients with on-treatment HBV DNA levels >20,000 IU/ml could be correctly predicted. CONCLUSIONS: Serum HBsAg concentration might serve as a surrogate marker of HBV DNA level in CHB patients.
RCT Entities:
BACKGROUND: Serum HBV DNA level is crucial in the management of chronic hepatitis B (CHB); however, the assay is expensive and cannot be used widely. Therefore, we explored the possibility of hepatitis B surface antigen (HBsAg) quantification as a surrogate marker for HBV DNA level in CHB patients. METHODS: A total of 289 CHB patients were enrolled, 251 were evaluated at baseline and 75 of them were also evaluated during anti-HBV treatment. Another 38 on-treatment patients were used for validation. Serum HBsAg titre was quantified by an immunoassay and HBV DNA level by a PCR-based method. Baseline and on-treatment data were analysed. RESULTS: In parallel to log(10) HBV DNA, the log(10) HBsAg was high in both immune tolerance and immune clearance phases, and significantly decreased in the inactive carrier state and was again increased in the reactivation phase of the CHB infection. There was a positive correlation between log(10) HBsAg and log(10) HBV DNA, which was greater in patients with chronic hepatitis, hepatitis B e antigen-positivity, greater alanine aminotransferase or HBsAg levels at baseline and during pegylated interferon treatment. Log(10) HBsAg could predict log(10) HBV DNA independently. An HBsAg titre of >900 IU/ml at baseline or >1,500 IU/ml within the first year of treatment could predict an HBV DNA level of >20,000 IU/ml, especially in subgroups of chronic hepatitis with alanine aminotransferase levels >40 IU/l. The dynamics of HBsAg might also predict serial HBV DNA changes. In the validation group, 64% of patients with on-treatment HBV DNA levels >20,000 IU/ml could be correctly predicted. CONCLUSIONS: Serum HBsAg concentration might serve as a surrogate marker of HBV DNA level in CHB patients.
Authors: Jeyamani Ramachandran; Ashrafali Mohamed Ismail; Gaurav Chawla; Gnanadurai John Fletcher; Ashish Goel; C E Eapen; Priya Abraham Journal: Indian J Gastroenterol Date: 2013-09-20