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U N I T 8
Gastrointestinal and Hepatobiliary Function
Hepatitis
Hepatitis refers to the acute or chronic inflammation of
the liver. Although hepatitis viruses account for many
cases of chronic hepatitis, there are many other causes
including chronic alcoholism, drug toxicities, and auto-
immune disorders. The discussion in this section focuses
on viral and autoimmune hepatitis.
Viral Hepatitis
Viral hepatitis refers to hepatic infections due to a group
of viruses known as
hepatotropic viruses
(hepatitis A
[HAV], hepatitis B [HBV], hepatitis C [HCV], hepatitis
D [HDV], and hepatitis E [HEV]) that have a particular
affinity for the liver.
3,4
Although all of the hepatotropic
viruses cause hepatitis, they differ in terms of their mode
of transmission and incubation period; mechanism,
degree, and chronicity of liver damage; and ability to
evolve to a carrier state. Acute hepatitis may also occur
in the course of other viral infections such as infectious
mononucleosis, caused by the Epstein-Barr virus; and
cytomegalovirus infection, particularly in newborn or
immunosuppressed persons. These other forms of hepa-
titis must be distinguished from those caused by hepa-
totropic viruses.
Syndromes of Viral Hepatitis.
The clinical course
of viral hepatitis can involve a number of syndromes,
including acute asymptomatic hepatitis with only sero-
logic evidence of infection, acute symptomatic hepatitis,
and chronic hepatitis, which can produce a carrier state.
Fulminant hepatic failure, a syndrome of hepatic insuf-
ficiency with rapid progression to liver failure, occurs in
a small percentage of persons with hepatitis B.
3
The manifestations of
acute symptomatic viral hepa-
titis
can be divided into three phases: the prodromal or
preicterus period, the icterus period, and the convales-
cent period. The onset of the
prodromal period
may vary
from abrupt to insidious, with general malaise, myalgia,
arthralgia, easy fatigability, and severe anorexia out
of proportion to the degree of illness. Gastrointestinal
symptoms such as nausea, vomiting, and diarrhea or
constipation may occur. Abdominal pain is usually mild
and felt on the right side. Chills and fever may mark
an abrupt onset. In persons who smoke, there may be
distaste for smoking that parallels the anorexia. Serum
levels of AST and ALT show variable increases during
the preicterus phase and precede a rise in bilirubin that
accompanies the onset of the icterus or jaundice phase
of infection. The
icterus phase
, if it occurs, usually fol-
lows the prodromal phase within 5 to 10 days. The pro-
dromal symptoms may become worse with the onset of
jaundice, followed by progressive clinical improvement.
Severe pruritus and liver tenderness are common during
the icterus period. The
convalescent phase
is character-
ized by an increased sense of well-being, return of appe-
tite, and disappearance of jaundice. The acute illness
usually subsides gradually over a 2- to 3-week period,
with complete clinical recovery by approximately
9 weeks in hepatitis A and 16 weeks in uncomplicated
hepatitis B.
Chronic hepatitis is defined as symptomatic, bio-
chemical, or serological evidence of continuing or
relapsing disease that has persisted for more than 6
months.
3
The clinical features of chronic hepatitis are
extremely variable and not predictive of outcome. In
many people the only manifestation is a persistent ele-
vation of serum aminotransferases. If there are symp-
toms, the most frequently reported ones are fatigue,
abdominal discomfort, and joint or muscle aches.
However, even asymptomatic persons with normal
serum aminotransferase levels are at risk for develop-
ing liver damage.
Infection with HBV/HDV, and HCV, can produce a
carrier state
in which the person does not have symp-
toms but harbors the virus and can therefore transmit
the disease. There is no carrier state for HAV infec-
tion. There are two types of carriers: healthy carriers
who have few or no ill effects, and those with chronic
disease who may or may not have symptoms. Factors
that increase the risk of becoming a carrier are age at
time of infection and immune status. The carrier state
for infections that occur early in life, as in infants of
HBV-infected mothers, may be as high as 90% to 95%,
compared with 1% to 10% of infected adults.
3
Hepatitis A.
Hepatitis A is usually a benign and self-
limited disease caused by a small, nonenveloped, single-
stranded ribonucleic acid (RNA) picornavirus. Lack of
a lipid envelope confers resistance to lysis by bile acids
in the intestine. Infection is contracted primarily by the
fecal–oral route.
8
Hepatitis A occurs throughout the world and is
endemic in countries with poor sanitation. At special
risk of infection are persons traveling abroad who have
not been vaccinated or previously exposed to the virus.
HAV has a brief incubation period, with an average of
25 to 30 days. The virus replicates in the liver, is excreted
in the bile, and is shed in the stool. The fecal shedding
of HAV occurs for 2 to 3 weeks before the development
of symptoms and ends about 1 week after the onset of
jaundice.
3
Because young children are asymptomatic,
they play an important role in the spread of the disease.
Oral behavior and lack of toilet training promote viral
spread among children attending day care centers, who
then carry the virus home to older siblings and parents.
Infected workers in food industries may also be a source
of spread. HAV usually is not transmitted by transfusion
of blood or plasma derivatives, presumably because its
short period of viremia usually coincides with clinical
illness, so that the disease is apparent and blood dona-
tions are not accepted.
The onset of symptoms usually is abrupt and includes
fever, malaise, nausea, anorexia, abdominal discom-
fort, dark urine, and jaundice. The likelihood of hav-
ing symptoms is related to age. Children younger than
6 years often are asymptomatic. The illness in older
children and adults usually is symptomatic and jaundice
occurs in approximately 70% of cases.
9
Symptoms usu-
ally last approximately 2 months. HAV infection does
not cause chronic hepatitis or induce a carrier state, and
only rarely causes acute fulminant hepatitis.
3,8