Predicting response to peginterferon alfa-2a, lamivudine and the two combined for HBeAg-negative chronic hepatitis B
- Ferruccio Bonino ( )
- Published Online First 24 November 2006
Background and aims: In a trial of patients with hepatitis B e antigen (HBeAg)-negative chronic hepatitis B, 24-week post-treatment biochemical and virologic response rates with peginterferon alfa-2a ± lamivudine were significantly higher than with lamivudine alone. The effect of pre-treatment factors on post-treatment responses has been investigated.
Patients and methods: Multivariate analyses were performed using available data from 518 patients treated with peginterferon alfa-2a monotherapy ± lamivudine, or lamivudine monotherapy. A post-treatment response was defined as alanine aminotransferase (ALT) normalisation and hepatitis B virus (HBV) DNA <20,000 copies/mL.
Results: In logistic regression analyses across all treatment arms, peginterferon alfa-2a (± lamivudine) therapy, younger age, female gender, high baseline ALT, low baseline HBV DNA and HBV genotype were identified as significant predictors of combined response 24 weeks post-treatment. In the peginterferon alfa-2a and lamivudine monotherapy arms, patients infected with genotypes B or C had a higher chance of response than genotype D infected patients (p<0.001), the latter responding better to combination than peginterferon alfa-2a monotherapy (p=0.015). At 1 year post-treatment, response rates by intention-to-treat analysis were 19.2% for peginterferon alfa-2a, 19.0% for combination, and 10.0% for lamivudine-treatment groups, with genotypes B or C associated with a sustained combined response to peginterferon alfa-2a ±lamivudine therapy.
Conclusions: Baseline ALT and HBV DNA levels, patient age, gender, and infecting HBV genotype significantly influenced combined response 24 weeks post-treatment, in patients treated with peginterferon alfa-2a and/or lamivudine. At 1 year post-treatment HBV genotype was significantly predictive of efficacy for patients treated with peginterferon alfa-2a ±lamivudine.