In patients with HBeAg-positive chronic hepatitis B, peginterferon alfa-2a offers superior efficacy over lamivudine, on the basis of HBeAg seroconversion, HBV DNA suppression, and HBsAg seroconversion.

We investigated the relationship between hepatitis B virus surface antigen (HBsAg) serum level decline and posttreatment response in patients with hepatitis B e antigen (HBeAg)-negative chronic hepatitis B from a large multinational study of pegylated interferon alfa-2a (peginterferon alfa-2a), with or without lamivudine, versus lamivudine alone. Serum HBsAg was quantified using the Architect assay (Abbott Diagnostics) at pretreatment, end of treatment (week 48), and 6 months after the end of treatment (week 72) in sera from 386 of the 537 patients who participated in the multinational study (peginterferon alfa-2a, 127; peginterferon alfa-2a plus lamivudine, 137; lamivudine monotherapy, 122). Pretreatment HBsAg levels varied according to genotype, with the highest levels present in patients infected with genotypes A (median, 4.11 log 10 IU/mL) and D (median, 3.85 log 10 IU/mL). Significant on-treatment decline in HBsAg was observed during treatment with peginterferon alfa-2a (alone or combined with lamivudine; mean decline at week 48, ؊0.71 and ؊0.67 log 10 IU/mL, respectively, P < 0.001), but not during treatment with lamivudine alone (؊0.02 log 10 IU/mL). Significantly more patients treated with peginterferon alfa-2a (21%) or peginterferon alfa-2a plus lamivudine (17%) achieved HBsAg levels <100 IU/mL at the end of treatment compared with lamivudine (1%) (both P < 0.001 versus lamivudine). End-of-treatment HBsAg level correlated strongly with HBV DNA suppression to <400 copies/mL 6 months posttreatment. An HBsAg level <10 IU/mL at week 48 and on-treatment decline >1 log 10 IU/mL were significantly associated with sustained HBsAg clearance 3 years after treatment (both P < 0.0001). Conclusion: On-treatment quantification of HBsAg in patients with HBeAg-negative chronic hepatitis B treated with peginterferon alfa-2a may help identify those likely to be cured by this therapy and optimize treatment strategies. C hronic hepatitis B is a global health problem accounting for 1 million deaths each year. 1 Ageadjusted death rates are 3 to 3.6 times higher in carriers of hepatitis B virus (HBV) surface antigen (HBsAg) than in persons without HBV infection. 2 The aim of treatment for patients with chronic hepatitis B (CHB) is to decrease progression of liver disease to cirrhosis and hepatocellular carcinoma, with the ultimate aim of improving survival. This can be pursued by maintaining constant inhibition of viral replication through a longterm treatment with nucleos(t)ide analogs or by inducing, through the combined antiviral and immunomodulatory Abbreviations: ALT, alanine aminotransferase; CART, classification and regression tree; CHB, chronic hepatitis B; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B virus surface antigen; HBV, hepatitis B virus;

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