DISEASES OF THE LIVER
ACUTE HEPATITIS A
ESSENTIALS
OF DIAGNOSIS
v Prodromal
of anorexia, nausea, vomiting, malaise, aversion to smoking.
v Fever,
enlarged and tender liver, jaundice.
v Normal
to low white cell count; markedly elevated aminotransferases.
General Considerations
The hepatitis A virus
(HAV) causes hepatitis A, an inflammation of the liver. The virus spreads mainly through the consumption of food or water contaminated with an infected person's excrement by an uninfected (and unvaccinated) person. Oral-anal sex, poor personal hygiene, inadequate sanitation, and contaminated food or water are all strongly linked to the disease.
The five hepatotropic
viruses (A, B, C, D, and E), as well as numerous medications and toxic
substances, can cause hepatitis; the clinical signs and symptoms may be similar
regardless of the source. The 27-nm RNA hepatovirus known as the Hepatitis A
virus (HAV) is a member of the picornavirus family and can cause hepatitis in
epidemics or in isolated individuals. The fecal-oral pathway is how the virus
is disseminated, and crowded conditions and inadequate cleanliness contribute
to its transmission. International travel has become the primary risk factor,
accounting for more than 40% of cases, and the incidence rate of HAV infection
has decreased from 14 to 1.3 cases per 100,000 people since the introduction of
the HAV vaccine in the United States in 1995. This has resulted in a 32%
decrease in the mortality rate.
According to WHO
estimates, 7134 people died from hepatitis A globally in 2016 (which represents
0.5% of the deaths from viral hepatitis). With a propensity for cyclical
recurrences, hepatitis A occurs both sporadically and in epidemics around the
globe. As demonstrated by the 1988 pandemic in Shanghai that afflicted over
300,000 people, epidemics linked to tainted food or water can explode. They
can also spread from person to person, impacting communities for months at a
time. Hepatitis A viruses can survive food production procedures that are
frequently employed to inactivate or eliminate bacterial diseases because they
are persistent in the environment [1].
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Distribution by geography
Hepatitis A virus
infection levels can be classified as high, intermediate, or low in geographic
distribution areas. However, since infected young infants do not exhibit any
obvious symptoms, infection does not always equate to disease.
In low- and
middle-income nations with inadequate sanitation and hygiene standards,
infection is prevalent, and 90% of children have contracted the hepatitis A
virus before turning ten years old, usually with no symptoms (2). High-income
nations with clean and sanitary conditions have low infection rates.
Adolescents and adults in high-risk groups, such as injecting drug users
(PWID), men who have sex with men (MSM), travelers to high-endemicity areas,
and secluded populations, like closed religious groups, may contract the
disease. There have been significant epidemics among homeless people in the
United States of America.
An additional 18% of
cases are linked to exposure to foreign visitors. Contaminated food or water,
especially undercooked seafood, can still cause common source outbreaks. HAV
has been identified as a reemerging food-borne public health concern in Europe,
and an epidemic in the United States in 2013 was caused by frozen pomegranate
arils imported from Turkey. There have also been documented incidences among
international adoptees and their connections, as well as outbreaks among
injecting drug users.
On average, the
incubation phase lasts 30 days. Rarely, HAV is eliminated in feces beyond the
first week of sickness, but it can occur up to two weeks before the onset of
clinical illness. Hepatitis A has a low death rate, and fulminant hepatitis A
is rare, except a few unusual cases where it develops in a
patient who already has chronic hepatitis C. A chronic carrier status does not
exist. Approximately 30% of people in the US have serologic indications of
prior HAV infection.
Clinical Findings
A. Symptoms and Signs
While clinical disease is typically
asymptomatic in youngsters, but more severe in adults. The symptoms, which
include anorexia, upper respiratory symptoms, myalgia, arthralgia, easy
fatigability, and malaise, might appear suddenly or gradually. Similar to
anorexia, a dislike of smoking may develop early. In addition to diarrhea or
constipation, nausea and vomiting are common. Except in rare instances where systemic
toxicity may develop, fever is typically low-grade but prevalent. Jaundice
frequently begins with effervescence and a decrease in pulse rate.
Abdominal pain is usually mild and constant in the right upper quadrant or epigastrium, often aggravated by jarring or exertion, and rarely may be severe enough to simulate cholecystitis.
Jaundice could appear
concurrently with the early symptoms, but it usually takes 5–10 days to appear.
Jaundice never appears in a large number of patients. Prodromal symptoms
frequently get worse when jaundice first appears, and then there is a gradual
improvement in the condition. During this stage, alcoholic stools may be
present.
Usually, the acute
illness goes away in two to three weeks, and by nine weeks, all clinical and
laboratory symptoms have recovered. Recovery is common, but in few instances,
one or two relapses may occur after clinical, biochemical, and serologic
recovery. Sometimes the course of acute hepatitis A is complicated by acute
cholecystitis.
Hepatomegaly-rarely
marked-is present in over half of cases. Liver tenderness is usually present.
Splenomegaly is reported in 15% of patients, and soft, enlarged lymph nodes
especially in the cervical or epitrochlear areas-may occur.
Who is in danger?
Hepatitis A can infect
someone who has not had a vaccination or has already contracted the virus. The
majority of hepatitis A infections in regions with high epidemics happen in
young children. Risk factors consist of:
Ø Living
in a home with an infected person,
Ø using
recreational drugs,
Ø having
sex with someone who has an acute hepatitis A infection,
Ø having
inadequate sanitation,
Ø not
having access to safe water,
Ø Visiting
high-endemicity areas without getting vaccinated.
B. Laboratory Findings
During the preicteric
period, the white blood cell count is typically low to normal. There may
occasionally be large atypical lymphocytes seen. Bilirubinuria frequently occurs
before jaundice manifests, and mild proteinuria is usual. Elevations of
bilirubin and alkaline phosphatase accompany remarkably high ALT or AST values,
and in a small percentage of cases, the latter continue to rise after
aminotransferase levels have returned to normal. Sometimes cholestasis is
noticeable. Early in the illness, anti-body to hepatitis A (anti-HAV) develops
(Figure 16-1). Serum levels of IgM and IgG anti-HAV can be found shortly after
the beginning. The first week of clinical illness is when peak IgM anti-HAV
titers arise, and they go away in three to six months. Although IgM anti-HAV
detection is a great test for identifying acute hepatitis A, it is not advised
for evaluating asymptomatic individuals with consistently high blood aminotransferase
levels due to the possibility of false-positive results. One patient receiving
rituximab for rheumatoid arthritis has reported experiencing false-negative
results. IgG anti-HAV titers increase one month into the illness and can last
for years. IgG anti-HAV (without IgM anti-HAV) signifies immunity,
noninfectivity, and prior HAV exposure.
Differential Diagnosis
Other viruses that
cause hepatitis, especially hepatitis B and C, as well as illnesses like
infectious mononucleosis, cytomegalovirus infection, herpes simplex virus
infection, Middle East respiratory syndrome, and infections from numerous other
viruses, such as influenza and Ebola virus, are included in the differential
diagnosis. Other illnesses include brucellosis, rickettsia diseases, such as Q
fever and drug-induced liver injury, and ischemic hepatitis (shock liver).
Sometimes the acute onset of autoimmune hepatitis can be mistaken for acute
viral hepatitis. Rarely, leukemia, lymphoma, or liver cancer that has spread
may show symptoms similar to hepatitis.
The prodromal phase of
viral hepatitis must be distinguished from another infectious diseases, such as the
exanthematous diseases. Cholestasis may mimic obstructive jaundice.
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Prevention
Strict isolation of
patients is not necessary, but hand washing after bowel movements is required.
Unvaccinated per-sons who are exposed to HAV are advised to receive post
exposure prophylaxis with a single dose of HAV vaccine or immune globulin (0.02
mL/kg) as soon as possible. The vaccine is preferred in healthy persons ages 1
year to 40 years, whereas immune globulin is preferred in those who are younger
than I year or older than 40 years or who are immunocompromised or who have
chronic liver disease.
In the United States,
there are two effective inactivated hepatitis A vaccines that are advised for
everyone who lives in or visits endemic areas (including military personnel),
people with chronic liver disease after being prescreened for immunity (though
it has been questioned whether it is cost-effective to vaccinate all patients
with concurrent chronic hepatitis C), people with clotting-factor disorders
receiving concentrate treatment, men who have sex with men, people who handle
animals, people who use illegal drugs, people who work in sewage systems,
people who handle food, close personal contacts of international adoptees, and
children and caregivers in daycare facilities and institutions. A single dose
of the vaccine given at any point prior to departure can offer sufficient
protection for healthy travelers. The Centers for Disease Control and
Prevention's (CDC) Advisory Committee on Immunization Practices has approved
the routine vaccination for use in all children in the United States between
the ages of one and two, and it is recommended for all children in states where
the incidence of hepatitis A is at least twice the national average. The HAV
vaccination is also successful in preventing secondary transmission to primary
cases' home contacts. One milliliter (1440 ELISA units) of Havrix
(GlaxoSmithKline) or one milliliter (50 units) of Vaqta (Merck) should be
administered intramuscularly to adults, with a booster dose at six to eighteen
months. There is a vaccination called Twinrix, made by GlaxoSmithKline, that
combines the hepatitis A and B viruses. The response to the HAV vaccine is
hampered by HIV infection, particularly in those whose CD4 count is less than
200/mcLl.
Treatment
Bed rest is advised
only in cases where symptoms are noticeable. Intravenous 10% glucose is
recommended if there is significant nausea and vomiting or if oral intake is
significantly reduced.
The goal of dietary
control is to eat tasty meals as directed without going overboard; breakfast is
typically the meal that is most tolerated. Avoid hepatotoxic substances,
alcohol, and strenuous physical activity. Because oxazepam metabolism is not
hepatic, small doses are safe; morphine sulfate should be avoided.
Patients with viral
hepatitis, even those with fulminant illness, do not benefit from corticosteroids.
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Prognosis
In most patients,
clinical recovery is generally complete within 3 months. Laboratory evidence of
liver dysfunction
may persist for a
longer period, but most patients recover completely. Hepatitis A does not cause
chronic liver dis-ease, although it may persist for up to 1 year, and clinical
and biochemical relapses may occur before full recovery.
The mortality rate is
less than 0.6%.
When to Admit
Ø Encephalopathy
is present.
Ø INR
greater than 1.6.
Ø The
patient is unable to maintain hydration.
References
1. Collier
MG et al; Hepatitis A Outbreak Investigation Team. Out-break of hepatitis A in
the USA associated with frozen pome-granate arils imported from Turkey: an
epidemiological case study. Lancet Infect Dis. 2014 Oct;14(10):976-81. [PMID:
25195178]
2. Wenzel
JJ et al. Hepatitis A as a foodborne infection. Lancet Infect Dis. 2014
Oct;14(10):907-8. [PMID: 25195177]
3. WHO,
Hepatitis
A report 12 February 2025 .
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