The aims of this study are to assess the efficacy of hepatitis B virus (HBV
) vaccination using an accelerated schedule and double dose of recombinant
vaccine in liver transplant recipients and identify factors associated with
seroconversion and persistence of antibody to hepatitis B surface antigen
(anti-HBs). Three hundred fifty-six patients were enrolled. Exclusion crite
ria were previous HBV infection, fulminant liver failure, or less than 2 ye
ars of follow-up after orthotopic liver transplantation (OLT). The vaccinat
ion schedule was 0, 2 weeks, 4 weeks, and 6 months using double-dose recomb
inant vaccine. Seroconversion was evaluated prospectively by measuring anti
-HBs on the day of OLT and 1 and 2 years after OLT. Quantitative analyses o
f anti-HBs were performed retrospectively on stored sera Geometric mean con
centrations (GMCs) were calculated using a standard formula. All patients c
ompleted the full vaccination schedule, and 129 patients (36%) completed th
e schedule before OLT. The overall prevalence of anti-HBs was 128 of 356 pr
e-OLT samples (36%) compared with 41 of 353 (11.6%) and 26 of 325 post-OLT
samples (8%) 1 and 2 years after OLT, respectively (both P = .001). The pre
-OLT GMC was 86.7 compared with 0.32 and 0.33 at 1 and 2 years after OLT, r
espectively (P = .001). Patients with high titers of anti-HBs before OLT we
re more likely to have persistence of antibodies 1 or 2 years after OLT. Yo
unger age (P = .02), low Child-Pugh score (P =.02), underlying chronic hepa
titis C (P = .03), and specific host HLA subtypes were most strongly associ
ated with seroconversion and/or persistence of anti-HBs. Thus, (I) seroconv
ersion before or after OLT using double-dose accelerated-schedule vaccinati
on against HBV is low, (2) there is a rapid, significant decrease in antibo
dy titer after OLT, (3) pre-OLT anti-HBs titer potentially may be useful in
predicting persistence of protective antibodies after OLT, and (4) several
factors (age, genetic predisposition, severity of liver disease, and under
lying liver disease) may have a role in poor vaccine responsiveness.