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CASE PRESENTATION

HEPATITIS A

Mentor :
dr. Ulynar Marpaung, Sp. A

Written by :
Rizkie Arianti Putri Noor 1102010254

Faculty of Medicine Yarsi


Pediatric Department
Rumah Sakit Bhayangkara tk.I R.S. Sukanto-Jakarta
Periode 21 December 2015 28 February 2016

Contents
IDENTITY............................................................................................................................................
PHYSICAL EXAMINATION (April 5th 2015)......................................................................................
General Status....................................................................................................................................
Antropometry Status..........................................................................................................................
Head to Toe Examination...................................................................................................................
Neurological Examination...............................................................................................................
Meningeal Sign............................................................................................................................
Motoric Examination...................................................................................................................
Autonom Examination.................................................................................................................
Laboratory Investigation..............................................................................................................
FOLLOW UP..................................................................................................................................
LITERATURE REVIEW.....................................................................................................................
DEFINITION..................................................................................................................................

ETIOLOGY...........................................................................................................
...............16

PATHOPHYSIOLOGY.........................................................................................
...............17
CLINICAL MANIFESTATIONS....................................................................................................
DIAGNOSIS....................................................................................................................................
TREATMENT.................................................................................................................................
PREVENTION................................................................................................................................
REFERENCES....................................................................................................................................

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IDENTITY
Patient
Name
: Ms. CZ
Birth Date
: June 30th 2010
Age
: 10 years
Gender
: Female
Address
: Bidara Cina, Jatinegara
Nationality : Indonesia
Religion
: Islam
Date of admission: August 3rd 2016
Date of examination: August 4th 2016

Father

Mother

Name

Mr. P

Mrs. D

Age

38 years old

35 years old

Job

Enployee

Housewife

Nationality

Javanese

Javanese

Religion

Islam

Islam

Education

High School (graduated)s

High School (graduated)s

Earning/month

Approximately Rp.3.500.000,-

Address

Bidara Cina, Jatinegara

ANAMNESIS
The anamnesis was taken on August 3rd 2016, by autoanamnesis.
Chief complain : Icteric since 5 days before admission to the hospital.
Additional complains : Vomit and abdominal pain.

History Of Present Ilness


A girl age 10 years old came to Raden Said Sukanto Police Center Hospital
emergency room suffering from Icteric since 5 days before admission the hospital.

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Patient also complaining to keep vomiting, loss of appetite, pain on the lower side
of abdomen, and passing dark coloured urine.
On the day she went to the emergency room, no fever showed. There was no
past history of jaundice, blood transfusion or surgical procedures.

History Of Past Illness


Pharyngitis/Tonsilitis

Bronchitis

Pneumonia

Morbilli

Pertussis

Varicella

Diphteria

Malaria

Polio

Enteritis

Bacillary Dysentry

Amoeba Dysentry

Diarrhea

Thypoid

Worms

Surgery

Brain Concussion

Fracture

Drug Reaction

Birth History
Mothers Pregnancy History

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The mother routinely checked her pregnancy to the doctor in the hospital. She
denied any problem noted during her pregnancy. She took vitamins routinely
given.
Childs Birth History
Labor

: Hospital

Birth attendants

: Doctor

Mode of delivery

: pervaginam

Gestation

: 38 weeks

Infant state

: healthy

Birth weight

: 3100 grams

Body length

: 46 cm

According to the mother, the baby started to cry and the baby's skin is red,
no congenital defects were reported
Development History
First dentition: 6 months
Psychomotor development

Head Up

: 1 month old

Smile

: 1 month old

Laughing

: 1- 2 month old

Slant

: 3 months old

Speech Initation

: 5 months old

Prone Position

Food Self

Sitting

: 5 months old
: 5-6 months old
: 6 months old

Mental Status: Normal


Conclusion: Growth and development status is still in the normal limits
and was appropriate according to the patients age

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History of Eating

Breast Milk : Exclusively 1 year.

Formula milk : -

Baby biscuits : Biscuits regal

Fruit and vegetables : Banana, papaya

Solid foods and side dishes : White rice, Egg, Chicken

Immunization History
Immunization

Frequency

Time

BCG

1 time

1 month old

Hepatitis B

3 times

0, 1, 6 months old

DPT

3 times

2, 4, 6 months old

Polio

4 times

Hib

0, 2, 4, 6 months old

4 times

2, 4, 6, months old

Family History

There is no one living around their home known for having the same
condition as the patient.

History of her brothers


Childbirth
Spontan pervaginam,
gestation aterm

Gender

Age

Boy

Age Died

Sumption Died

7 years old

Born died : ( - )
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Child dies : ( - )
Miscarriage : ( - )
History of Disease in Other Family Members / Around the House
There is no one living around their home known for having the same condition as
the patient.

Sosial and Economic History

The patient lived at the house together with father, mother, and brother.
There are 3 rooms and 1 toilet. There are some windows inside the house.
The windows are occasionally opened during the day.
Hygiene:
o The patient changes his clothes everyday with clean clothes.
o Bed sheets changed every two weeks.

PHYSICAL EXAMINATION (April 5th 2015)


General Status
- General condition

: mild ill

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Awareness
Pulse
Breathing rate
Temperature

: Compos Mentis
: 123 x/min, regular, full, strong.
: 36x/min
: 36,8oC (per axilla)

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Antropometry Status
- Weight
- Height

: 40 kilogram
: 150 cm

Nutritional Status based NCHS (National Center for Health Statistics) year 2000:

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WFA (Weight for Age): 40/33 x 100 % = 121 % ( good nutrition)


HFA (Height for Age): 150/138 x 100 % = 108 % (good nutrition)
WFH (Weight for Height): 40/41 x 100 % = 97 % (good nutrition)
Conclusion: The patient has good nutritional status.

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Head to Toe Examination

Head
Normocephaly, hair (black, normal distributon, not easily removed ) sign of
trauma (-), sunken fontanelle (-).
Eyes
Icteric sclera +/+, pale conjunctiva -/-, hyperaemia conjunctiva -/- ,
lacrimation -/-, sunken eyes -/-,

pupils 3mm/3mm isokor, Direct and

indirect light response ++/++


Ears
Normal shape, no wound, no bleeding ,secretion or serumen
Nose
Normal shape, midline septum, secretion -/Mouth

Lips: moist
Teeth: no caries
Mucous: moist
Tongue: Not dirty, yellow
Tonsils: T1/T1, No hyperemia
Pharynx: hyperemia (-)

Neck
Lymph node enlargement (-), scrofuloderma (-)
Thorax
:
i. Inspection
: symmetric when breathing , no retraction, ictus cordis is
ii.
iii.
iv.
1.
2.

i.

not visible
Palpation
: mass (-), tactile fremitus +/+
Percussion
: sonor on left lungs
Auscultation :
Cor
: regular S1-S2, murmur (-), gallop (-)
Pulmo : vesicular +/+, Wheezing -/- , Rhonchy -/Abdomen
:
Inspection
: Convex, epigastric retraction (-), there is no a widening of the
veins, no spider nevi.

ii. Palpation

: supple, liver palpable, spleen not palpable, fluid wave

(-),abdominal mass (-)


iii. Percussion
: The entire field of tympanic abdomen, shifting dullness (-)
iv. Auscultation : normal bowel sound, bruit (-)

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Vertebra

not look any mass along the line of the vertebral


Ekstremities : warm, capillary refill time < 2 second, edema(-)
Skin
: Good turgor.

: There does not appear scoliosis, kyphosis, and lordosis, do

Neurological Examination
Meningeal Sign

Motoric Examination
Power
Hand
Feet
Tonus
Hand
Feet
Trophy
Hand
Feet
Physiologic Reflex
Upper extrimities
Biceps
Triceps
Lower extrimities
Patella
Achilles
Pathologic Reflex
Upper extrimities
Hoffman
Trommer

5 5 5 5/ 5 5 5 5
5 5 5 5/ 5 5 5 5
Normotonus / Normotonus
Normotonus / Normotonus
Normotrophy / Normotrophy
Normotrophy / Normotrophy
+/+
+/+
+/+
+/+

-/-/-

Lower extrimities

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Babinsky
Chaddock
Oppenheim
Gordon
Schaeffer

-/-/-/-/-/-

Clonus
Patella
Achilles

-/-/-

Autonom Examination

Defecation
Urination
Sweating
Laboratory Investigation

Normal
Normal ( 4-5 times daily )
Normal

Hematology August 02th 2016


Hematology

Results

Normal Value

Haemoglobin

13,5 g/dL

13-16 g/dL

Leukocytes

7.500/L

5,000 10,000/L

Hematocrits
Trombocytes

39 %
408.000/ L

40 48 %
150,000 400,000/L

Chemical Clinic August 02nd 2016


Hematology

Results

Normal Value

SGOT

253,0 U/L

< 30 U/L

SGPT

635,0 U/L

<35 U/L

Chemical Clinic January 08th 2016


Hematology

Results

Normal Value

SGOT

30 U/L

< 30 U/L

SGPT

32 U/L

<35 U/L

Serologi/Immunologi
Hematology

Results

Normal Value

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Hbs Ag

Non Reactive

Non Reactive

Anti HCV

Non Reactive

Non Reactive

WORKING DIAGNOSIS
Type A Hepatitis
MANAGEMENT
IVFD RL 1400 cc / 24 hours
Inj. Rantin 2x1/2 a
HP Pro 2x1 cap
PROGNOSIS

Quo ad vitam
: bonam
Quo ad functionam : bonam
Quo ad sanactionam : bonam

FOLLOW UP August 3th 2015 - August 8th 2015.


August 3rd 2016. Second day of hospitalization, 6th day of illness
S

Fever (-)
Icteric (+)
Nausea (+)

General condition: Compos mentis.


Heart rate
= 97 x/min
Respiratory rate = 24x/min
Temperature
= 37,3C
Cardio : S1/S2, reguler, no murmur, no gallop
Pulmonary : vesiculer +/+, rhonchi- /-, wheezing -/Abdomen : Hepatomegali (+)

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A
P

Hepatitis A
IVFD RL 1400 cc / 24 hours
Inj. Rantin 2x1/2 a
HP Pro 2x1 cap

August 4th 2016. Third day of hospitalization, 7th day of illness


S

Fever (-)
Icteric (+)
Nausea (+)

General condition: Compos Mentis


Heart rate
= 95 x/min
Respiratory rate = 24x/min
Temperature
= 37.5C
Cardio : S1/S2, reguler, no murmur, no gallop
Pulmonary : retraction (+) vesiculer +/+, rhonchi -/-, wheezing -/Abdomen : Hepatomegali (+)

Hapatitis A

IVFD RL 1400 cc / 24 hours


Inj. Rantin 2x1/2 a
HP Pro 2x1 cap

August 5th 2016, Fourth days of hospitalization, 8th day of illness


S

Fever (-)
Icteric (+)
Nausea (-)

General condition: Compos mentis.


Heart rate
= 99x/min
Respiratory rate = 29x/min

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Temperature
= 37,2C
Cardio : S1/S2, reguler, no murmur, no gallop
Pulmonary : vesiculer +/+, rhonchi -/-, wheezing -/Abdomen : Hepatomegali (+)
A
P

Hapatitis A
IVFD RL 1400 cc / 24 hours
Inj. Rantin 2x1/2 a
HP Pro 2x1 cap

August 6th 2015. Fifth of hospitalization, 9th day of illness


S

Fever (-)
Icteric (+)
Nausea (-)

General condition: Compos mentis (+)


Heart rate
= 96 x/min
Respiratory rate = 26x/min
Temperature
= 36,8C
Cardio : S1/S2, reguler, no murmur, no gallop
Pulmonary : vesiculer +/+, rhonchi -/-, wheezing -/Abdomen : Hepatomegali (+)

Hapatitis A

IVFD RL 1400 cc / 24 hours


Inj. Rantin 2x1/2 a
HP Pro 2x1 cap

August 7th 2015. Sixth day of hospitalization, 10th day of illness


S

Fever (-)
Icteric (+)

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Nausea (-)
O

General condition: Compos Mentis


Heart rate
= 97 x/min
Respiratory rate = 30x/min
Temperature
= 37C
Cardio : S1/S2, reguler, no murmur, no gallop
Pulmonary : retraction (+) vesiculer +/+, rhonchi -/-, wheezing -/Abdomen : Hepatomegali (-)

Hapatitis A

IVFD RL 1400 cc / 24 hours


Inj. Rantin 2x1/2 a
HP Pro 2x1 cap

January 8th 2016. Ninth day of hospitalization, 13th day of illness


S

Fever (-)
Icteric (-)
Nausea (-)

General condition: Compos Mentis


Heart rate
= 120 x/min
Respiratory rate = 30x/min
Temperature
= 38.5C
Cardio : S1/S2, reguler, no murmur, no gallop
Pulmonary : retraction (+) vesiculer +/+, rhonchi -/-, wheezing -/-

Hapatitis A

IVFD RL 1400 cc / 24 hours


Inj. Rantin 2x1/2 a
HP Pro 2x1 cap
Patient went home

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LITERATURE REVIEW
DEFINITION
Hepatitis A is a liver disease caused by the hepatitis A virus. The virus is primarily
spread when an uninfected (and unvaccinated) person ingests food or water that is
contaminated with the faeces of an infected person. The disease is closely
associated with unsafe water, inadequate sanitation and poor personal hygiene.
Unlike hepatitis B and C, hepatitis A infection does not cause chronic liver disease
and is rarely fatal, but it can cause debilitating symptoms and fulminant hepatitis
(acute liver failure), which is associated with high mortality.
Hepatitis A occurs sporadically and in epidemics worldwide, with a tendency for
cyclic recurrences. The hepatitis A virus is one of the most frequent causes of
foodborne infection. Epidemics related to contaminated food or water can erupt
explosively, such as the epidemic in Shanghai in 1988 that affected about 300 000
people1. Hepatitis A viruses persist in the environment and can withstand foodproduction processes routinely used to inactivate and/or control bacterial
pathogens.
The disease can lead to significant economic and social consequences in
communities. It can take weeks or months for people recovering from the illness
to return to work, school or daily life. The impact on food establishments
identified with the virus, and local productivity in general, can be substantial.
The hepatitis A virus HAV
HAV, first identified in 1973, is a nonenveloped, spherical, positive stranded RNA
virus, classified within the genus hepatovirus of the picornavirus family.
HAV infection does not lead to chronic or persistent hepatitis.

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HAV strains recovered from widely separated regions of the world are
antigenically similar. In humans, a single serotype of HAV exists.
HAV is known to produce disease in humans and non-human primates. In vitro,
the wild type virus is generally difficult to grow and no cytopathic effect is
observed. Attenuated HAV strains adapted to cell culture have been used to
develop vaccines.
HAV infection induces lifelong protection against reinfection.

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Geographical distribution

Geographical distribution areas can be characterized as having high, intermediate


or low levels of hepatitis A infection.
Areas with high levels of infection
In developing countries with very poor sanitary conditions and hygienic practices,
most children (90%) have been infected with the hepatitis A virus before the age
of 10 years2. Those infected in childhood do not experience any noticeable
symptoms. Epidemics are uncommon because older children and adults are
generally immune. Symptomatic disease rates in these areas are low and outbreaks
are rare.
Areas with intermediate levels of infection
In developing countries, countries with transitional economies and regions where
sanitary conditions are variable, children often escape infection in early
childhood. Ironically, these improved economic and sanitary conditions may lead

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to a higher susceptibility in older age groups and higher disease rates, as


infections occur in adolescents and adults, and large outbreaks can occur.
Areas with low levels of infection
In developed countries with good sanitary and hygienic conditions, infection rates
are low. Disease may occur among adolescents and adults in high-risk groups,
such as injecting-drug users, men who have sex with men, people travelling to
areas of high endemicity, and in isolated populations, such as closed religious
communities.
Transmission
The hepatitis A virus is transmitted primarily by the faecal-oral route; that is when
an uninfected person ingests food or water that has been contaminated with the
faeces of an infected person. Waterborne outbreaks, though infrequent, are usually
associated with sewage-contaminated or inadequately treated water.
The virus can also be transmitted through close physical contact with an infectious
person, although casual contact among people does not spread the virus.
Symptoms
The incubation period of hepatitis A is usually 1428 days.
Symptoms of hepatitis A range from mild to severe, and can include fever,
malaise, loss of appetite, diarrhoea, nausea, abdominal discomfort, dark-coloured
urine and jaundice (a yellowing of the skin and whites of the eyes). Not everyone
who is infected will have all of the symptoms.
Adults have signs and symptoms of illness more often than children, and the
severity of disease and mortality increases in older age groups. Infected children
under 6 years of age do not usually experience noticeable symptoms, and only
10% develop jaundice. Among older children and adults, infection usually causes
more severe symptoms, with jaundice occurring in more than 70% of cases.
The Stage
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The course of acute hepatitis A can be divided into four clinical phases:18, 21-23,
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an incubation or preclinical period,
ranging from 10 to 50 days, during which the patient remains asymptomatic
despite active replication of the virus. In this phase, transmissibility is of greatest
concern.
a prodromal or preicteric phase
ranging from several days to more than a week, characterised by the appearance
of symptoms like loss of appetite, fatigue, abdominal pain, nausea and vomiting,
fever, diarrhoea, dark urine and pale stools, followed by
an icteric phase,
during which jaundice develops at total bilirubin levels exceeding 20 - 40 mg/l.
Patients often seek medical help at this stage of their illness. The icteric phase
generally begins within 10 days of the initial symptoms. Fever usually improves
after the first few days of jaundice. Viremia terminates shortly after hepatitis
develops, although faeces remain infectious for another 1 - 2 weeks. Extrahepatic
manifestations of hepatitis A are unusual. Physical examination of the patient by
percussion can help to determine the size of the liver and possibly reveal massive
necrosis. The mortality rate is low (0.2% of icteric cases) and the disease
ultimately resolves. Occasionally, extensive necrosis of the liver occurs during the
first 6 - 8 weeks of illness. In this case, high fever, marked abdominal pain,
vomiting, jaundice and the development of hepatic encephalopathy associated
with coma and seizures, are the signs of fulminant hepatitis, leading to death in 70
- 90% of the patients. In these cases mortality is highly correlated with increasing
age, and survival is uncommon over 50 years of age. Among patients with chronic
hepatitis B or C or underlying liver disease, who are superinfected with HAV, the
mortality rate increases considerably.
a convalescent period,
where resolution of the disease is slow, but patient recovery uneventful and
complete. Relapsing hepatitis occurs in 3 - 20% of patients 4 to 15 weeks after the
initial symptoms have resolved. Cholestatic hepatitis with high bilirubin levels
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persisting for months is also occasionally observed. Chronic sequelae with


persistence of HAV infection for more than 12 months are not observed.
Who is at risk?
Anyone who has not been vaccinated or previously infected can contract hepatitis
A. In areas where the virus is widespread (high endemicity), most hepatitis A
infections occur during early childhood. Risk factors include:

poor sanitation;

lack of safe water;

injecting drugs;

living in a household with an infected person;

being a sexual partner of someone with acute hepatitis A infection; and

travelling to areas of high endemicity without being immunized.

Diagnosis
Cases of hepatitis A are not clinically distinguishable from other types of acute
viral hepatitis. Specific diagnosis is made by the detection of HAV-specific IgM
and IgG antibodies in the blood. Additional tests include reverse transcriptase
polymerase chain reaction (RT-PCR) to detect the hepatitis A virus RNA, but may
require specialised laboratory facilities.
Treatment
There is no specific treatment for hepatitis A. Recovery from symptoms following
infection may be slow and may take several weeks or months. Therapy is aimed at
maintaining comfort and adequate nutritional balance, including replacement of
fluids that are lost from vomiting and diarrhoea.

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Prevention
Improved sanitation, food safety and immunization are the most effective ways to
combat hepatitis A.
The spread of hepatitis A can be reduced by:

adequate supplies of safe drinking water;

proper disposal of sewage within communities; and

personal hygiene practices such as regular hand-washing with safe water.

Several hepatitis A vaccines are available internationally. All are similar in terms
of how well they protect people from the virus and their side-effects. No vaccine
is licensed for children younger than 1 year of age.
Nearly 100% of people develop protective levels of antibodies to the virus within
1 month after a single dose of the vaccine. Even after exposure to the virus, a
single dose of the vaccine within 2 weeks of contact with the virus has protective
effects. Still, manufacturers recommend two vaccine doses to ensure a longer-term
protection of about 5 to 8 years after vaccination.
Millions of people have been immunized worldwide with no serious adverse
events. The vaccine can be given as part of regular childhood immunizations
programmes and also with other vaccines for travellers.
Immunization efforts
Vaccination against hepatitis A should be part of a comprehensive plan for the
prevention and control of viral hepatitis. Planning for large-scale immunization
programmes should involve careful economic evaluations and consider alternative
or additional prevention methods, such as improved sanitation, and health
education for improved hygiene practices.

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Whether or not to include the vaccine in routine childhood immunizations


depends on the local context. The proportion of susceptible people in the
population and the level of exposure to the virus should be considered. Several
countries, including Argentina, China, Israel, Turkey, and the United States of
America have introduced the vaccine in routine childhood immunizations.
While the 2 dose regimen of inactivated hepatitis A vaccine is used in many
countries, other countries may consider inclusion of a single-dose inactivated
hepatitis A vaccine in their immunization schedules. Some countries also
recommend the vaccine for people at increased risk of hepatitis A, including:

travellers to countries where the virus is endemic;

men who have sex with men; and

people with chronic liver disease (because of their increased risk of serious
complications if they acquire hepatitis A infection).

Regarding immunization for outbreak response, recommendations for hepatitis A


vaccination should also be site-specific. The feasibility of rapidly implementing a
widespread immunization campaign needs to be included.
Vaccination to control community-wide outbreaks is most successful in small
communities, when the campaign is started early and when high coverage of
multiple age groups is achieved. Vaccination efforts should be supplemented by
health education to improve sanitation, hygiene practices and food safety.

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REFERENCES
1.World Health Organization. Hepatitis A. Fact sheet. Available at
http://www.who.int/mediacentre/factsheets/fs328/en/
2. http://www.mayoclinic.org/diseases-conditions/hepatitisa/basics/definition/con-20022163
3. Centers for Disease Control and Prevention (CDC), Atlanta, USA:10
http://www.cdc.gov/ncidod/diseases/hepatitis/slideset
4. Burke DS, Graham RR, and Heisey GB. Hepatitis A virus in primates outside
captivity. Lancet, 1981, 2:928.
5. Centers for Disease Control and Prevention. Prevention of hepatitis A through
active or passive immunization: recommendations of the Advisory Committee on
Immunization Practices. Morbidity and Mortality Weekly Report, 1996,
45(RR15):1-30.
6. Hollinger FB. An overview of the clinical development of hepatitis A vaccine.
Introduction. Journal of Infectious Diseases, 1995, 171(Suppl 1):S1.

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