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Abstract

have remained below 100 IU/mL in most cases. On the other hand, one of our recent nonresponders vaccinated while receiving lamivudine, developed positive serum hepatitis B surface antigen and HBV DNA 9 months after the failure of vaccination despite the uninterrupted administration of oral lamivudine. Although we currently have no data regarding lamivudine resistance in this patient, the case appears to be similar to the one described by Pruett 3 and suggests that, at least in nonresponders to HBV vaccination, hepatitis B immune globulin may be a safer prophylactic regimen than lamivudine.Differences in the definition of response to vaccination, however, do not seem to account for the divergent results reported. The presence in our series of 8 patients transplanted for HBV-induced fulminant hepatitis could be a more likely explanation, though we did not observe in our study statistically significant differences in the distribution of these 8 patients among responders and nonresponders. Finally, our failure to induce seroconversion in patients receiving lamivudine suggests that this may also be a critical difference between the 2 studies. Pruett 3 also describes no durable anti-HBs responses to vaccination in liver transplant recipients converted to oral lamivudine, whereas anecdotic reports from other centers 4,5 mention rates of anti-HBs seroconversion after HBV vaccination similar to ours in the absence of lamivudine administration. Certainly, this issue merits further investigation because it is not evident at present why lamivudine should be responsible for a decreased response to HBV vaccination.Altogether we believe that our data still supports a role for HBV vaccination in the prophylaxis of HBV infection recurrence in a selected group of patients.