Havrix and VAQTA are single-antigen vaccines and are available in two formulations for individuals between 12 months and 18 years of age, and those who are 18 years of age and older (Fiore et al., 2008). The child formulations of both vaccines are prepared with half the concentration of the adult dose (Fiore et al., 2008). Havrix and VAQTA are given on a two-dose schedule at least 6 months apart (Fiore et al., 2008). Twinrix is approved for adults and contains antigens for HAV and hepatitis B virus (HBV). Twinrix is given on the same schedule commonly used for single-antigen HBV vaccine and includes three doses of the vaccine given at 0, 1, and 6 months after the initial inoculation (CDC, 2006). By 2009 46.6 percent of children aged 19 to 35 months were vaccinated against HAV (CDC, 2010).
No studies were identified in the literature for the committee to evaluate the risk of acute disseminated encephalomyelitis (ADEM) after the administration of hepatitis A vaccine.
Weight of Epidemiologic Evidence
The epidemiologic evidence is insufficient or absent to assess an association between hepatitis A vaccine and ADEM.
The committee identified two publications reporting the development of ADEM after administration of hepatitis A vaccine. The publications did not provide evidence beyond temporality, one too short based on the possible mechanisms involved (Huber et al., 1999; Rogalewski et al., 2007). Rogalewski et al. (2007) reported the concomitant administration of vaccines, making it difficult to determine which, if any, vaccine could have been the precipitating event. In addition, the patient described in Huber et al. (1999) had a concomitant Campylobacter jejuni infection. The publications did not contribute to the weight of mechanistic evidence.
Weight of Mechanistic Evidence
While rare, hepatitis A infection has been associated with the development of ADEM (Yiu and Kornberg, 2010). The committee considers the effects of natural infection one type of mechanistic evidence.
The symptoms described in the publications referenced above are consistent with those leading to a diagnosis of ADEM. Autoantibodies, T cells,