Serum hepatitis B virus surface antigen (HBsAg) levels have been suggested to predict interferon response in chronic hepatitis B. A few data are available on the role of HBsAg measurement in nucleos(t)ide analogues (NA) treatment. We retrospectively investigated the relation between HBsAg changes and main treatment outcomes during long-term lamivudine treatment in hepatitis e antigen (HBeAg)-negative chronic hepatitis B. A total of 42 HBeAg-negative patients were consecutively enrolled in an open-label study on long-term lamivudine monotherapy (150 mg/die). Serum HBsAg levels were quantified every 6 months by Architect assay (Abbott Diagnostics). HBV-DNA was quantified quarterly by real-time PCR (Roche Diagnostics). The median duration of lamivudine treatment was 66 months (20-153). One patient (2%) was a primary nonresponder, 35 (83%) developed virological breakthrough (VB) and the remaining six patients (14%) were classified as long-term on-treatment responders. During treatment, HBsAg levels decreased only in long-term on-treatment responders, while no changes were observed in resistant patients. Failure to achieve a decrease of 0.7 log(10) IU/mL in serum HBsAg at month six of lamivudine had a positive predictive value of developing VB of 90% and a negative predictive value of 100%. These high predictive values were also maintained in the subgroup of patients negative for HBV-DNA at month six. The results of this study with a small sample size suggest a role of on-treatment HBsAg quantification in the management of lamivudine-treated patients. If validated prospectively in a larger patient cohort, HBsAg measurements would be a useful adjunct to optimize antiviral therapy.

Gramenzi A, Loggi E, Micco L, Cursaro C, Fiorino S, Galli S, et al. (2011). Serum hepatitis B surface antigen monitoring in long-term Lamivudine-treated hepatitis B virus patients. JOURNAL OF VIRAL HEPATITIS, 18(10), e468-e474 [10.1111/j.1365-2893.2011.01473.x].

Serum hepatitis B surface antigen monitoring in long-term Lamivudine-treated hepatitis B virus patients

GRAMENZI, ANNAGIULIA;LOGGI, ELISABETTA;MICCO, LORENZO;GITTO, STEFANO;BERNARDI, MAURO;ANDREONE, PIETRO
2011

Abstract

Serum hepatitis B virus surface antigen (HBsAg) levels have been suggested to predict interferon response in chronic hepatitis B. A few data are available on the role of HBsAg measurement in nucleos(t)ide analogues (NA) treatment. We retrospectively investigated the relation between HBsAg changes and main treatment outcomes during long-term lamivudine treatment in hepatitis e antigen (HBeAg)-negative chronic hepatitis B. A total of 42 HBeAg-negative patients were consecutively enrolled in an open-label study on long-term lamivudine monotherapy (150 mg/die). Serum HBsAg levels were quantified every 6 months by Architect assay (Abbott Diagnostics). HBV-DNA was quantified quarterly by real-time PCR (Roche Diagnostics). The median duration of lamivudine treatment was 66 months (20-153). One patient (2%) was a primary nonresponder, 35 (83%) developed virological breakthrough (VB) and the remaining six patients (14%) were classified as long-term on-treatment responders. During treatment, HBsAg levels decreased only in long-term on-treatment responders, while no changes were observed in resistant patients. Failure to achieve a decrease of 0.7 log(10) IU/mL in serum HBsAg at month six of lamivudine had a positive predictive value of developing VB of 90% and a negative predictive value of 100%. These high predictive values were also maintained in the subgroup of patients negative for HBV-DNA at month six. The results of this study with a small sample size suggest a role of on-treatment HBsAg quantification in the management of lamivudine-treated patients. If validated prospectively in a larger patient cohort, HBsAg measurements would be a useful adjunct to optimize antiviral therapy.
2011
Gramenzi A, Loggi E, Micco L, Cursaro C, Fiorino S, Galli S, et al. (2011). Serum hepatitis B surface antigen monitoring in long-term Lamivudine-treated hepatitis B virus patients. JOURNAL OF VIRAL HEPATITIS, 18(10), e468-e474 [10.1111/j.1365-2893.2011.01473.x].
Gramenzi A; Loggi E; Micco L; Cursaro C; Fiorino S; Galli S; Gitto S; Galli C; Furlini G; Bernardi M; Andreone P.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11585/105922
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