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7
Hepatitis A Vaccine
INTRODUCTION
Hepatitis A virus (HAV) is a 27-nm spherical RNA virus that replicates
in the liver of the infected individual (Fiore et al., 2008). HAV incubates
for an average of 28 days, but this period can range from 15 to 50 days
(CDC, 2006; Fiore et al., 2008). Prior to the onset of typical hepatitis
symptoms such as darkening urine, pale stools, and jaundice, individuals
may experience less specific symptoms including abdominal pain, anorexia,
fatigue, fever, malaise, myalgia, nausea, or vomiting (Lemon, 1985; Tong
et al., 1995). The illness lasts several weeks before the virus is eliminated
from the body; recovery is virtually 100 percent (Fiore et al., 2008; Tong
et al., 1995).
The severity of illness with HAV infection is directly correlated to the
age of the individual at the time of infection. Fifty to 90 percent of infec-
tions in persons less than 5 years of age are asymptomatic, while 70–95
percent of adults experience some symptoms (Fiore et al., 2008). Although
11–22 percent of cases require hospitalization (CDC, 2006), serious or
permanent complications from HAV infection are rare (Fiore et al., 2008).
Atypical manifestations, which may occur in 7–11 percent of patients,
include relapse, a prolonged cholestatic phase that occurs with itching
and jaundice, and rash (Fiore et al., 2008; Tong et al., 1995). Itching and
arthralgia are not uncommon during the prodromal phase before jaundice
appears (Tong et al., 1995). A very rare occurrence is type I autoimmune
chronic hepatitis (Tong et al., 1995). It is not known whether this is caused
by hepatitis A infection, or whether the infection triggers a condition al-
421
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422 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
ready present (Tong et al., 1995). This condition resolves with prednisone
treatment (Tong et al., 1995). Very rarely fulminant hepatitis associated
with coma and occasionally death may occur (Wasley et al., 2010). In
most cases of hepatitis A infection, all symptoms and the infection resolve
completely (Gordon et al., 1984; Tong et al., 1995).
The fecal-oral route is the most common mode of transmission for
hepatitis A. An individual with HAV is most infectious, with highest stool
HAV concentrations, during the 2 weeks prior to appearance of jaundice
(Fiore et al., 2008). Transmission from a person with active infection may
occur through food preparation, household contact, and sexual contact
(Fiore et al., 2008). Because children with HAV are frequently asymptom-
atic, they may serve as reservoirs of disease in households and close-contact
environments such as day care (Smith et al., 1997; Staes et al., 2000). HAV
has been transmitted through blood transfusion; however, screening has
greatly reduced this risk (Soucie et al., 1998). Finally, HAV is resistant to
most organic solvents, detergents, and heat, and can survive in the environ-
ment (Fiore et al., 2008; Murphy et al., 1993; Peterson et al., 1983). As a
result, HAV can be transmitted by food and water contamination, as well as
through contact with infected soil and marine sediment (Fiore et al., 2008).
Food and waterborne hepatitis is generally associated with contamination
by HAV-infected workers, sewage contamination, and inadequate water
treatment (Bergeisen et al., 1985; Bloch et al., 1990; Dalton et al., 1996;
De Serres et al., 1999; Fiore, 2004).
From 1980 through 1995, reports of hepatitis A to the Centers for
Disease Control and Prevention (CDC) numbered between 22 and 36 thou-
sand cases per year (CDC, 2006). Approximately 33 percent of reported
cases were in children less than 15 years old (CDC, 2008), and outbreaks
of hepatitis A were reported among injection and noninjection drug users
and men who have sex with men (Cotter et al., 2003; Harkess et al., 1989;
Hutin et al., 1999; Schade and Komorwska, 1988).
Prior to the development and licensure of a vaccine, immune globulin,
a sterile solution of antibodies collected and purified from a large group
of donors, was used to prevent hepatitis A in those likely to be exposed
or recently exposed to the virus (Fiore et al., 2008). In 1995–1996, in-
activated vaccines for hepatitis A became available, and since 1999 the
CDC has reported a significant decrease in HAV infection in the United
States—markedly a 76 percent decrease in 2003 when compared to 1990–
1997 (Wasley et al., 2005). Currently, three inactivated vaccines—Havrix
(GlaxoSmithKline Biologicals), VAQTA (Merck & Co., Inc.), and Twinrix
(GlaxoSmithKline)—are available in the United States. In these vaccines,
the virus is grown in MRC-5 cell cultures and harvested by cell lysis (Fiore
et al., 2008). From there, the virus is inactivated and purified through vari-
ous methods before being packaged with (Havrix and Twinrix) or without
(VAQTA) a preservative (Fiore et al., 2008).
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423
HEPATITIS A VACCINE
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 for-
mulations 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 vac-
cine 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).
ACUTE DISSEMINATED ENCEPHALOMYELITIS
Epidemiologic Evidence
No studies were identified in the literature for the committee to evalu-
ate 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.
Mechanistic Evidence
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 pos-
sible mechanisms involved (Huber et al., 1999; Rogalewski et al., 2007).
Rogalewski et al. (2007) reported the concomitant administration of vac-
cines, 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 develop-
ment 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 con-
sistent with those leading to a diagnosis of ADEM. Autoantibodies, T cells,
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424 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
and molecular mimicry may contribute to the symptoms of ADEM; how-
ever, the publications did not provide evidence linking these mechanisms
to hepatitis A vaccine.
The committee assesses the mechanistic evidence regarding an as-
sociation between hepatitis A vaccine and ADEM as weak based
on knowledge about the natural infection.
Causality Conclusion
Conclusion 7.1: The evidence is inadequate to accept or reject a
causal relationship between hepatitis A vaccine and ADEM.
TRANSVERSE MYELITIS
Epidemiologic Evidence
No studies were identified in the literature for the committee to evalu-
ate the risk of transverse myelitis 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 transverse myelitis.
Mechanistic Evidence
The committee did not identify literature reporting clinical, diagnostic,
or experimental evidence of transverse myelitis after the administration of
hepatitis A vaccine.
Weight of Mechanistic Evidence
While rare, hepatitis A infection has been associated with the develop-
ment of transverse myelitis (Wasley et al., 2010). The committee considers
the effects of natural infection one type of mechanistic evidence.
Autoantibodies, T cells, and molecular mimicry may contribute to the
symptoms of transverse myelitis; however, the committee did not identify
literature reporting evidence of these mechanisms after administration of
hepatitis A vaccine.
The committee assesses the mechanistic evidence regarding an as-
sociation between hepatitis A vaccine and transverse myelitis as
weak based on knowledge about the natural infection.
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425
HEPATITIS A VACCINE
Causality Conclusion
Conclusion 7.2: The evidence is inadequate to accept or reject
a causal relationship between hepatitis A vaccine and transverse
myelitis.
MULTIPLE SCLEROSIS
Epidemiologic Evidence
No studies were identified in the literature for the committee to evalu-
ate the risk of multiple sclerosis (MS) 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 MS.
Mechanistic Evidence
The committee identified one publication reporting symptoms of MS
after administration of hepatitis A vaccine. Rogalewski et al. (2007) did
not provide evidence beyond a temporal relationship between vaccination
against hepatitis B, diphtheria and tetanus toxoids, poliovirus, and hepatitis
A and development of symptoms. The concomitant administration of vac-
cines make it difficult to determine which vaccine, if any, could have been
the precipitating event. The publication did not contribute to the weight of
mechanistic evidence.
Weight of Mechanistic Evidence
The symptoms described above are consistent with those leading to a
diagnosis of MS. Autoantibodies, T cells, and molecular mimicry may con-
tribute to the symptoms of MS; however, the publication did not provide
evidence linking these mechanisms to hepatitis A vaccine.
The committee assesses the mechanistic evidence regarding an as-
sociation between hepatitis A vaccines and MS as lacking.
Causality Conclusion
Conclusion 7.3: The evidence is inadequate to accept or reject a
causal relationship between hepatitis A vaccine and MS.
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426 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
GUILLAIN-BARRÉ SYNDROME
Epidemiologic Evidence
No studies were identified in the literature for the committee to evalu-
ate the risk of Guillain-Barré syndrome (GBS) 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 GBS.
Mechanistic Evidence
The committee identified four publications reporting the development
of GBS after the administration of hepatitis A vaccine. The publications
did not provide evidence beyond temporality, some too short based on the
possible mechanisms involved (Blumenthal et al., 2004; Huber et al., 1999;
Pritchard et al., 2002; Uriondo San Juan et al., 2004). One publication also
reported the concomitant administration of vaccines, making it difficult to
determine which, if any, vaccine could have been the precipitating event
(Uriondo San Juan et al., 2004). In addition, the patient described in Hu-
ber et al. (1999) had a concomitant Campylobacter jejuni infection. These
publications did not contribute to the weight of mechanistic evidence.
Weight of Mechanistic Evidence
While rare, hepatitis A infection has been associated with the develop-
ment of GBS (Wasley et al., 2010). The committee considers the effects of
natural infection one type of mechanistic evidence.
The symptoms described in the publications referenced above are con-
sistent with those leading to a diagnosis of GBS. Autoantibodies, comple-
ment activation, immune complexes, T cells, and molecular mimicry may
contribute to the symptoms of GBS; however, the publications did not
provide evidence linking these mechanisms to hepatitis A vaccine.
The committee assesses the mechanistic evidence regarding an as-
sociation between hepatitis A vaccine and GBS as weak based on
knowledge about the natural infection.
Causality Conclusion
Conclusion 7.4: The evidence is inadequate to accept or reject a
causal relationship between hepatitis A vaccine and GBS.
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427
HEPATITIS A VACCINE
CHRONIC INFLAMMATORY DISSEMINATED POLYNEUROPATHY
Epidemiologic Evidence
No studies were identified in the literature for the committee to evalu-
ate the risk of chronic inflammatory disseminated polyneuropathy (CIDP)
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 CIDP.
Mechanistic Evidence
The committee did not identify literature reporting clinical, diagnostic,
or experimental evidence of CIDP after the administration of hepatitis A
vaccine.
Weight of Mechanistic Evidence
Autoantibodies, T cells, and molecular mimicry may contribute to
the symptoms of CIDP; however, the committee did not identify literature
reporting evidence of these mechanisms after administration of hepatitis A
vaccine.
The committee assesses the mechanistic evidence regarding an as-
sociation between hepatitis A vaccine and CIDP as lacking.
Causality Conclusion
Conclusion 7.5: The evidence is inadequate to accept or reject a
causal relationship between hepatitis A vaccine and CIDP.
BELL’S PALSY
Epidemiologic Evidence
No studies were identified in the literature for the committee to evalu-
ate the risk of Bell’s palsy 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 Bell’s palsy.
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428 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
Mechanistic Evidence
The committee did not identify literature reporting clinical, diagnostic,
or experimental evidence of Bell’s palsy after the administration of hepatitis
A vaccine.
Weight of Mechanistic Evidence
The committee assesses the mechanistic evidence regarding an as-
sociation between hepatitis A vaccine and Bell’s palsy as lacking.
Causality Conclusion
Conclusion 7.6: The evidence is inadequate to accept or reject a
causal relationship between hepatitis A vaccine and Bell’s palsy.
ANAPHYLAXIS
Epidemiologic Evidence
No studies were identified in the literature for the committee to evalu-
ate the risk of anaphylaxis 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 anaphylaxis.
Mechanistic Evidence
The committee identified two publications identifying the development
of anaphylaxis posthepatitis A vaccination (Bohlke et al., 2003; Peng and
Jick, 2004). Bohlke et al. (2003) used records from participants in the
Vaccine Safety Datalink to study the development of anaphylaxis postvac-
cination. The authors did not observe a single case of anaphylaxis postvac-
cination out of 23,185 doses of hepatitis A vaccine administered. Peng and
Jick (2004) used computer records from general practitioners in the United
Kingdom to study the incidence, cause, and severity of anaphylaxis. The
authors reviewed 120 cases, out of 897, in detail. One report of anaphylaxis
developing after vaccination against hepatitis A was identified.
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429
HEPATITIS A VACCINE
Weight of Mechanistic Evidence
The publications described above did not present evidence sufficient
for the committee to conclude the vaccine may be a contributing cause of
anaphylaxis after the administration of hepatitis A vaccine. A temporal
relationship was established between the administration of a hepatitis A
vaccine and the development of anaphylaxis in one case; however, clinical
details were not presented. Also, while it was presumed the patient had
experienced an IgE-mediated reaction, no data were reported to establish
the mechanism of action.
The committee assesses the mechanistic evidence regarding an asso-
ciation between hepatitis A vaccine and anaphylaxis as weak based
on one case presenting temporality consistent with anaphylaxis.
Causality Conclusion
Conclusion 7.7: The evidence is inadequate to accept or reject a
causal relationship between hepatitis A vaccine and anaphylaxis.
AUTOIMMUNE HEPATITIS
Epidemiologic Evidence
No studies were identified in the literature for the committee to evalu-
ate the risk of autoimmune hepatitis 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 autoimmune hepatitis.
Mechanistic Evidence
The committee identified two publications reporting the development
of autoimmune hepatitis after the administration of hepatitis A vaccine.
The publications did not provide evidence beyond temporality, one too
short based on the possible mechanisms involved (Berry and Smith-Laing,
2007; Veerappan et al., 2005). One publication reported the concomitant
administration of vaccines making it difficult to determine which, if any,
vaccine could have been the precipitating event (Veerappan et al., 2005). In
addition, the patient described by Berry and Smith-Laing (2007) presented
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430 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
with acute hepatitis 5 months before vaccination. The publications did not
contribute to the weight of mechanistic evidence.
Weight of Mechanistic Evidence
Active autoimmune hepatitis is a recognized complication of infection
with hepatitis A (Wasley et al., 2010). The committee considers the effects
of natural infection one type of mechanistic evidence.
The symptoms described in the publications referenced above are con-
sistent with those leading to a diagnosis of autoimmune hepatitis. Autoanti-
bodies, T cells, and complement activation may contribute to the symptoms
of autoimmune hepatitis; however, the publications did not provide evi-
dence linking these mechanisms to hepatitis A vaccine.
The committee assesses the mechanistic evidence regarding an as-
sociation between hepatitis A vaccine and autoimmune hepatitis as
weak based on knowledge about the natural infection.
Causality Conclusion
Conclusion 7.8: The evidence is inadequate to accept or reject a
causal relationship between hepatitis A vaccine and autoimmune
hepatitis.
CONCLUDING SECTION
Table 7-1 provides a summary of the epidemiologic assessments, mech-
anistic assessments, and causality conclusions for hepatitis A vaccine.
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TABLE 7-1 Summary of Epidemiologic Assessments, Mechanistic Assessments, and Causality Conclusions for
Hepatitis A Vaccine
Studies Cases
Contributing to Contributing to
Epidemiologic the Epidemiologic Mechanistic the Mechanistic Causality
Vaccine Adverse Event Assessment Assessment Assessment Assessment Conclusion
Hepatitis A Acute Disseminated Encephalomyelitis Insufficient None Weak None Inadequate
Hepatitis A Transverse Myelitis Insufficient None Weak None Inadequate
Hepatitis A Multiple Sclerosis Insufficient None Lacking None Inadequate
Hepatitis A Guillain-Barré Syndrome Insufficient None Weak None Inadequate
Hepatitis A Chronic Inflammatory Disseminated Insufficient None Lacking None Inadequate
Polyneuropathy
Hepatitis A Bell’s Palsy Insufficient None Lacking None Inadequate
Hepatitis A Anaphylaxis Insufficient None Weak 1 Inadequate
Hepatitis A Autoimmune Hepatitis Insufficient None Weak None Inadequate
431
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432 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY
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