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MORE POTENT HBV DNA SUPPRESSION DOES NOT RESULT IN A HIGHER SUPPRESSION OF HEPATITIS B e ANTIGEN LEVEL

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Background: Despite more potent anti-hepatitis B virus (HBV) activity of newer agents, there appears to be a “ceiling” effect with regards to hepatitis B e antigen (HBeAg) seroconversion in HBeAg-positive chronic HBV patients after 48-weeks of therapy. Aim: This study aims to determine the effect of viral suppression on HBeAg suppression. Methods: One-hundred-and-seventy-one consecutive HBeAg-positive patients treated with adefovir (n=59), entecavir (n=58) or lamivudine (n=54) for 48 weeks (end-of-follow-up) without drug resistance were included into this study. HBeAg was retrospectively quantied with a microparticle enzyme-immunoassay. Results: The entecavir group had the lowest HBV DNA at end-of-follow-up [mean±standard error of mean (SEM) 2.18±0.16 logIU/ml] followed by the lamivudine group (mean±SEM 3.74±0.22 log IU/ml) and the adefovir group (mean±SEM 5.16±0.25 logIU/ml, p<0.001). However, there was no signicant difference in the end-of-followup HBeAg level in the entecavir group (mean±SEM 2.13±1.31 log PEIU/ml) when compared w ith the lamivudine (mean±SEM 2.40±1.76 log PEIU/ml) and the adefovir groups (mean±SEM 2.17±1.63 log PEIU/ml), (p=0.10). HBeAg level below the lower-limit-of-detection at end-offollow-up was not higher in the entecavir group when compared with the adefovir group [26/58 (44.8%) vs. 25/59 (42.4%), p=0.79] Conclusion: Potent HBV DNA suppression during therapy does not result in higher HBeAg suppression.
Title: MORE POTENT HBV DNA SUPPRESSION DOES NOT RESULT IN A HIGHER SUPPRESSION OF HEPATITIS B e ANTIGEN LEVEL
Description:
Background: Despite more potent anti-hepatitis B virus (HBV) activity of newer agents, there appears to be a “ceiling” effect with regards to hepatitis B e antigen (HBeAg) seroconversion in HBeAg-positive chronic HBV patients after 48-weeks of therapy.
Aim: This study aims to determine the effect of viral suppression on HBeAg suppression.
Methods: One-hundred-and-seventy-one consecutive HBeAg-positive patients treated with adefovir (n=59), entecavir (n=58) or lamivudine (n=54) for 48 weeks (end-of-follow-up) without drug resistance were included into this study.
HBeAg was retrospectively quantied with a microparticle enzyme-immunoassay.
Results: The entecavir group had the lowest HBV DNA at end-of-follow-up [mean±standard error of mean (SEM) 2.
18±0.
16 logIU/ml] followed by the lamivudine group (mean±SEM 3.
74±0.
22 log IU/ml) and the adefovir group (mean±SEM 5.
16±0.
25 logIU/ml, p<0.
001).
However, there was no signicant difference in the end-of-followup HBeAg level in the entecavir group (mean±SEM 2.
13±1.
31 log PEIU/ml) when compared w ith the lamivudine (mean±SEM 2.
40±1.
76 log PEIU/ml) and the adefovir groups (mean±SEM 2.
17±1.
63 log PEIU/ml), (p=0.
10).
HBeAg level below the lower-limit-of-detection at end-offollow-up was not higher in the entecavir group when compared with the adefovir group [26/58 (44.
8%) vs.
25/59 (42.
4%), p=0.
79] Conclusion: Potent HBV DNA suppression during therapy does not result in higher HBeAg suppression.

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