Virologic Response at 12 Months of Treatment Predicts Sustained Antiviral Efficacy in Patients with Adefovir-Treated Lamivudine-Resistant Chronic Hepatitis B
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Background/Aims: The aim of our study was to define the potential role of virologic response at 12months of treatment (VR12) in predicting subsequent virologic and clinical outcomes in adefovir (ADV)-treated lamivudine-resistant chronic hepatitis B. Methods: Two hundred and four patients with lamivudine-resistant chronic hepatitis B virus (HBV) treated with ADV monotherapy were included. Serum HBV DNA was quantified by real-time polymerase chain reactions. VR12was defined as a HBV DNA level of less than 4 log10copies/mL after 12 months of ADV treatment. Results: VR12 was observed in 110 of the 204 patients (54%). The mean HBV DNA reductions from baseline after 12 months of ADV treatment were 3.8and 1.9 log10 copies/mL in patients with and without VR12, respectively (p<0.001). The hepatitis B “e” antigen (HBeAg) seroconversion rates in patients with and without VR12 were 32% and 14% at 12 months treatment,respectively (p=0.018), and 40% and 27% at 24months of treatment (p=0.032). The genotypic mutation rates to ADV in patients with and without VR12were 0% and 6% at 12 months of treatment, respectively (p=0.033), and 21% and 42% at 24 months (p=0.012). The rates of viral breakthrough in patients with and without VR12 were 0% and 7% at 12 months of treatment, respectively (p=0.072), and 9% and 25% at 24 months (p=0.006). Conclusions: Patients without VR12 may need to switch to or add on other potent antiviral drugs in their medical regimens.
Abstract
Background/Aims: The aim of our study was to define the potential role of virologic response at 12months of treatment (VR12) in predicting subsequent virologic and clinical outcomes in adefovir (ADV)-treated lamivudine-resistant chronic hepatitis B. Methods: Two hundred and four patients with lamivudine-resistant chronic hepatitis B virus (HBV) treated with ADV monotherapy were included. Serum HBV DNA was quantified by real-time polymerase chain reactions. VR12was defined as a HBV DNA level of less than 4 log10copies/mL after 12 months of ADV treatment. Results: VR12 was observed in 110 of the 204 patients (54%). The mean HBV DNA reductions from baseline after 12 months of ADV treatment were 3.8and 1.9 log10 copies/mL in patients with and without VR12, respectively (p<0.001). The hepatitis B “e” antigen (HBeAg) seroconversion rates in patients with and without VR12 were 32% and 14% at 12 months treatment,respectively (p=0.018), and 40% and 27% at 24months of treatment (p=0.032). The genotypic mutation rates to ADV in patients with and without VR12were 0% and 6% at 12 months of treatment, respectively (p=0.033), and 21% and 42% at 24 months (p=0.012). The rates of viral breakthrough in patients with and without VR12 were 0% and 7% at 12 months of treatment, respectively (p=0.072), and 9% and 25% at 24 months (p=0.006). Conclusions: Patients without VR12 may need to switch to or add on other potent antiviral drugs in their medical regimens.
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