C h a p t e r 3 0
Disorders of Hepatobiliary and Exocrine Pancreas Function
733
Antibodies to HAV (anti-HAV) appear early in the
disease and tend to persist in the serum (Fig. 30-7). The
immunoglobulin M (IgM) antibodies (see Chapter 15)
usually appear during the first week of symptomatic dis-
ease and begin to decline in a few months.
3
Their pres-
ence coincides with a decline in fecal shedding of the
virus. Peak levels of IgG antibodies occur after 1 month
of illness and may persist for years; they provide long-
term protective immunity against reinfection. The pres-
ence of IgM anti-HAV is indicative of acute hepatitis A,
whereas IgG anti-HAV merely documents past infection.
A HAV vaccine is available for persons at high risk for
HAV exposure.
9
These include international travelers to
regions where sanitation is poor and endemic HAV infec-
tions are high, children living in communities with high
rates of HAV infection, homosexually active men, and
users of illicit drugs. A public health benefit also may be
derived from vaccinating persons with increased poten-
tial for transmitting the disease (e.g., food handlers). The
Centers for Disease Control and Prevention (CDC) has
recently recommended vaccination of children in states,
counties, and communities with high rates of infection.
9
Persons who have been exposed to HAV are advised to
receive postexposure prophylaxis with a single dose of
HAV vaccine or immune globulin (IgG) as soon as possible.
The immune globulin is preferred for persons older than
40 years or younger than 1 year of age and for those who
are immunocompromised or have chronic liver disease.
Hepatitis B.
Hepatitis B is caused by a hepatotropic
deoxyribonucleic acid (DNA)-containing
Hepadnavirus
.
The complete hepatitis B virion, also called a
Dane par-
ticle,
consists of an outer envelope and an inner nucleo-
capsid that contains the viral DNA and viral polymerase
that exhibits both DNA polymerase and reverse tran-
scriptase activity (Fig. 30-8). HBV infection can produce
acute hepatitis, chronic hepatitis, hepatocellular carci-
noma, and fulminant hepatic failure. It also participates
in the development of hepatitis D (delta hepatitis).
3,4,10
The virus usually is transmitted through inoculation
with infected blood or serum. However, the viral anti-
gen can be found in most body secretions and can be
spread by oral or sexual contact.
Hepatitis B has a longer incubation period and rep-
resents a more serious health problem than hepatitis A.
More than 2 billion people—one third of the world’s
population—alive today have been infected with HBV,
and of these more than 240 million remain infected.
3,11
The incidence of acute hepatitis B in the United States
has dramatically declined since 1990, with the greatest
declines in children and adolescents, coincident with
HBV vaccination.
Worldwide, perinatal (vertical) transmission is the
predominant mode of HBV transmission, whereas intra-
venous drug use and unprotected sexual intercourse are
the main routes of transmission in low-prevalence areas
such as the United States. Although the virus can be
spread through transfusion or administration of blood
products, routine screening methods have appreciably
reduced transmission through this route.
12
Three well-defined antigens are associated with the
HBV virus: a core antigen, HBcAg; HBeAg, a precore pro-
tein; and a surface antigen, HBsAg. These HBV antigens
evoke specific antibodies: anti-HBc, anti-HBe, and anti-
HBs. The antigens and their antibodies serve as serologic
markers for following the natural course of the disease
3,4
(see Fig. 30-8). HBsAg is the viral antigen measured most
Incubation
period
Acute
illness
Convalescence
Exposure
Fecal
HAV
HAV
IgG
anti-HAV
IgM
anti-HAV
0
4
8
12
16
20
Weeks after exposure
FIGURE 30-7.
The sequence of fecal shedding of the hepatitis
A virus (HAV), HAV viremia, and HAV antibody (IgM and IgG
anti-HAV) changes in hepatitis A.
HBsAg
(envelope)
Viral coat
Double-stranded
circular DNA
(HBV genome)
HBcAg/HBeAg
(nucleocapsid)
DNA
polymerase
Onset
symptoms Onset recovery
HBsAg
HBeAg
HBV DNA
Exposure
IgG anti-HBc
Anti-HBs
IgM anti-HBc
0 4 8 12 16 20 24 28 32 36 40 52
Weeks
A
B
FIGURE 30-8.
(A)
The hepatitis B virus.
(B)
The sequence of
hepatitis B virus (HBV) viral antigens (HBsAg, HBeAg), HBV
DNA, and HBV antibody (IgM, IgG, anti-HBc, and anti-HBs)
changes in acute resolving hepatitis B.
