Evaluation of hepatitis B viraemia levels in patients with HBeAg-negative chronic hepatitis B virus infection.

OBJECTIVES: To evaluate patients with chronic hepatitis B virus (HBV) infection and low-level viraemia in terms of determining HBV DNA cut-off values and levels of alanine aminotransferase (ALT) and other possible markers for discriminating between chronic hepatitis B e-antigen (HBeAg)-negative patients and hepatitis B surface antigen (HBsAg) inactive carriers. METHODS: HBV-infected patients who were HBeAg-negative with undetectable HBV DNA by standard hybridization assay and high (HBeAg-negative group, n = 81) or normal (HBsAg inactive carrier group, n = 77) ALT levels were enrolled. Quantitative polymerase chain reaction assay using a COBAS Amplicor HBV monitor test was performed to detect low HBV DNA levels. RESULTS: The HBV DNA level was found to be significantly higher in the HBeAg-negative chronic HBV group (mean ± SD 94,477 ± 167,528 copies/ml) compared with the HBsAg inactive carrier group (mean ± SD 19,215 ± 57,970 copies/ml). CONCLUSIONS: A low level of viral replication may persist in chronic HBV-infected patients who are HBeAg-negative, and the level of HBV DNA was higher in the HBeAg-negative group than in the inactive HBsAg carrier group. Necroinflammation also persisted in the HBeAg-negative group and these patients had a higher level of ALT than the inactive HBsAg carriers.

Hepatitis B surface antigen seroconversion is associated with favourable long-term clinical outcomes during lamivudine treatment in HBeAg-negative chronic hepatitis B patients.

The aims of this study were to assess hepatitis B surface antigen (HBsAg) seroconversion and to determine its impact on the natural course of the disease in patients with HBeAg-negative chronic hepatitis B (CHB) during lamivudine (LMV) treatment. A total of 183 consecutive patients with HBeAg-negative CHB who were treated with LMV were included in the study. Data were retrospectively collected from outpatient visit charts. The primary endpoint was HBsAg seroconversion to anti-HBs. The secondary endpoint was to determine the development of cirrhosis. Loss of HBsAg was confirmed in 10 patients and seroconversion to anti-HBs in nine patients during LMV treatment or after its discontinuation. HBsAg seroconversion was achieved on-treatment in four patients after a median treatment duration of 30 months and off-treatment in the remaining five patients in a median 61 months after LMV discontinuation. The cumulative probability of HBsAg seroconversion increased from 0.6% at 1 year and 1.9% at 5 years to 21.5% at 10 years of LMV during and after LMV treatment. HBsAg clearance was preceded by undetectable serum hepatitis B virus (HBV) DNA. The majority of the patients responding to treatment had undetectable HBV DNA levels at 24 weeks of treatment. The cumulative probability of LMV resistance increased from 2.2% at 1 year to 37.3% at 5 years. No baseline parameter predicting either HBsAg seroconversion or the emergence of LMV resistance was identified. None of the patients with HBsAg seroconversion experienced virological breakthrough or disease progression during the follow-up period. These results indicate that HBsAg seroclearance can occur in patients with HBeAg-negative CHB under LMV therapy and predicts better clinical outcome.