Contrary to common belief, hepatitis-B, if acquired in adult stage, can be fully cured. Even a chronic one acquired in infancy can be easily mitigated. Hepatitis-B is an oft-forgotten and very much prevalent in the population.

1. H E P A T I T I S B
detailed research on one of the most fatal diseases
witnessed by the humankind
A B I O L O G Y P R O J E C T R E P O R T
E F F O R T S B Y : - S A U M Y A P A N W A R , S 6 B
S U B M I T T E D T O : - M S R I C H A B H A T I A

2. 2
T A B L E O F C O N T E N T S
S.no. Topic Pages
1. Acknowledgments 3
2. Introduction 5
3. Natural History of Hepatitis-B 8
4. Modes of Transmission 13
5. Signs & Symptoms 15
6. Diagnosis 16
7. Prognosis 23
8. Treatment 24
9. Prevention 26
10. Case Studies 29
11. Bibliography 33

3. 3
A C K N O W L E D G E M E N T S
I would like to express my heartfelt gratitude towards my Biology teacher Ms.
Richa Bhatia for giving me an opportunity to dig deeper into the science of
diseases by assigning us a task to create a project on one such disease. It indeed
turned out to be a rollercoaster of knowledge for me, debunking some of the
myths that even I believed in.
I would also take this opportunity to thank my loving parents who, since my
formative years, have tried inculcating my interest in science; these efforts have
presumably borne fruits. Mamma has played a vital role in the culmination of
this report by lending her vast knowledge about the subject, assisting me in
finding material and motivating me to put my best foot forward.
I am obliged beyond measure to all the well-known scientists and medical
professionals and unknown alike, for putting heart and soul into their
respective fields and working obstinately; it is only because of their painstaking
labors that we have achieved milestones in research and medicine and are now
aware of the various aspects of our being.
Lastly, I am grateful to Krishnji for always making me listen to my heart and
guiding me to do the right thing with the sweet sound of his flute!

4. 4
To Srish,
From the beautiful abode, that she is keeping an eye on me,
I am sure she will be proud. I love you…

5. 5
I N T R O D U C T I O N
iral hepatitis is a potentially life-threatening infection of the liver
caused by any of the half dozen viruses: hepatitis A virus (HAV),
hepatitis B virus (HBV), it was originally known as "serum hepatitis",
hepatitis C virus (HCV), hepatitis D virus (the delta agent) and
hepatitis E virus (HEV). Hepatitis G virus has been newly discovered and
resembles HCV, but more closely, the flaviviruses; the virus and its effects are
under study and though it is known to infect humans, but is not known to
cause human diseases. It is known that many other viruses may be implicated
to cause hepatitis such as cytomegalovirus, Epstein-Barr virus, yellow fever
virus, and rubella virus. Disease caused by non-hepatitis viruses is called
hepatitis A-E. Viruses of herpes simplex, varicella and adenoviruses can also
cause hepatitis in immunocompromised individuals, but these cases are rare.
However, this report shall be focusing primarily on hepatitis B.
The Problem Statement
Human beings are the only reservoir of this virus and it is highly fatal when not
diagnosed earlier and not treated on time. Chronic hepatitis B can cause liver
damage which can lead to many lethal outcomes like chronic hepatic
insufficiency, cirrhosis, hepatocellular carcinoma, and even death.
Hepatitis B is endemic throughout the world, especially in tropical and
developing countries and also in some regions of Europe. It has no seasonal
nature. Its prevalence varies from country to country depending on a complex
V
Figure 1: (Left) a healthy liver, (right) a cirrhotic liver

6. 6
mix of behavioral, environmental and host
factors. In general, it is lowest in countries
with high standards of living (e.g.: Australia,
North America, North Europe) and highest
in countries or area where socio-economic
levels are lower (e.g.: China, South-east
Asia, South America).
About a third of the world population has
been infected by hepatitis B at one point in
their lives, including 343 million who have
chronic infections. The Global Burden of
Disease study estimated that there were
686,000 deaths caused by hepatitis B in
2013 and a 5.9 per 100,000 age-
standardized death rates globally, 4 of
which 300,000 deaths were attributed to
liver cancer and 317,400 deaths to cirrhosis
of the liver secondary to hepatitis B. In
India, as per latest estimates, 40 million
people are chronically infected with
hepatitis B, making our country second in
the globe only to China. However, since
many episodes go unreported or
unrecognized, the actual number of
hepatitis B cases would be anybody’s guess.
Every year, nearly 10,000 patients die from HBV infection in India. HBV was
also implicated in a major epidemic outbreak in Ahmedabad (Gujarat) in 1984.
Deaths due to viral hepatitis are much more than due to AIDS and tuberculosis
according to a publication by WHO. This is because hepatitis B is 50-100 times
more infectious than HIV. Yet, while people are by and large aware of HIV,
there is little awareness about hepatitis. It has been a global health concern and
the WHO’s 2015 Agenda for Sustainable Development commits to combating
viral hepatitis to its elimination. A plethora of socio-economic factors have led

7. 7
to an increase in the burden of hepatitis, despite being preventable by
vaccination since 1982, which are as follows:
1. Poverty & illiteracy
2. Social stigma
3. Cultural, traditional practices
4. Ignorance about vaccination
5. Availability of authentic medication
6. Lack of awareness, myths, and inaccurate information, etc.
Due to poverty and illiteracy, people prefer quackery instead of medical advice
for prompt and cheap treatment. In many such cases, people with mild
problems, which can be addressed even without treatment end up with other
viral diseases by reusing injections. This transmission becomes problematic if
this viral disease is lethal and incurable or patients cannot afford the cost of
treatment. Apart from the increased chances of liver cancer, it is important to
remember that patients with hepatitis B may develop anemia as a result of
autoimmune hemolytic anemia and rarely aplastic anemia.
Figure 2: People belonging to lower income strata are neither able to get tested for hepatitis, nor afford patented
medicnes or the expensive treatment. Reuse of syringes is a more common practice in poorer regions.

8. 8
N A T U R A L H I S T O R Y O F
H E P A T I T I S B
Incubation period
The incubation period is from 45-180 days (2-6 months). Lower doses of the
virus often result in longer incubation periods. The median incubation period is
said to be lower than 100 days.
Agent factors
a) AGENT: Hepatitis B virus was discovered by Blumberg in 1963. It is a
complex, 42 nm, double-shelled DNA virus, originally known as the
“Dane particle”. It replicates in the
liver cells. It has 3 distinct antigens – a
surface antigen, also known as the
“Australian antigen” (HBsAg – envelope
glycoprotein), a core antigen (HBcAg – a
nucleocapsid “core” protein) and an “e”
antigen (HBeAg – a longer polypeptide
transcript with a pre-core and core region).
They stimulate the production of the
respective antibodies e.g., surface antibody
Figure 3: An artist's impression of the hepatitis virus

9. 9
(anti-HBs), core antibody (anti-HBc) and “e” antibody (anti HBe). The
antibodies and their antigens act as useful markers of HBV infection. It
has enzyme DNA polymerase that exhibits reverse transcriptase activity
and genomic replication occurs through an intermediate RNA template.
b) RESERVOIR OF INFECTION: Human is the only reservoir of the
infection which can be spread either through carriers or from cases. The
continued survival of
infection is due to a large
number of individuals who
are carriers of the virus,
estimated to be above 257
million. Cases may range
from symptomatic to
unapparent. The risk of an
adult becoming a carrier
following acute infection is 5-
15%; in infants, it may
exceed 50%.
c) INFECTIVE MATERIAL: Contaminated blood is the main source of
infection, although the virus has been found in body secretions like
mother’s milk, vaginal secretions, semen, and saliva (rare) of infected
persons.
d) RESISTANCE: The virus is quite stable and capable of surviving on
environmental surfaces for days. It can be readily destroyed by sodium
hypochlorite, as is by heat sterilization in an autoclave for 30-60 minutes.
e) PERIOD OF COMMUNICABILITY: The virus is present in the blood
during the incubation period (for a month before jaundice) and the acute
phase of the disease. Period of communicability is usually several
months (occasionally years in chronic carriers) or until the disappearance
of HBsAg and appearance of surface antibody.
Figure 4: Data suggests that the earlier a child acquires
hepatitis B infection, more is the probability of it becoming
severe in adulthood.

10. 10
Host factors
a) AGE: In countries in which infection with HBV is relatively uncommon,
the highest prevalence is found in the 20-40-year age group. In countries
where the
infection is
common, much
infection occurs
perinatally or
during early
childhood. The
younger an
individual is
when they
contract acute
HBV, the
higher the likelihood that they will develop the chronic form. This is
visualized in the graph alongside which reflects the percentage of
individuals who become chronic HBV carriers in relation to the age at
which they were acutely infected. Older age at diagnosis appears to be
an important determinant
of progression to cirrhosis
and increased mortality.
This may be because the
aging immune system
cannot contain the disease
process or simply because
of the longer duration of
infection.
b) GENDER: The
likelihood of Hepatitis B
persistence is 1.3 times
higher among males.
Fibrosis appears to
progress more slowly in

11. 11
females than in males with chronic hepatitis B, suggesting that estrogens
have a protective effect on fibrogenesis.
c) HIGH-RISK GROUPS: Certain groups carry higher risk. For example,
i) Tribal: The high endemicity of HBV infection in the tribal
populations has been attributed to inbreeding, poor hygienic living
conditions, close person-to-person contact and certain socio-culture
practices that may facilitate the transmission of HBV.
ii) Children: Chronic HBV infection in India is acquired in childhood,
presumably before 5 years of age, through horizontal transmission. In
South Asia, the age of acquisition of HBV is an important
determinant of outcome; the earlier the age, the higher the likelihood
of chronicity. The risk of chronicity in HBV infection acquired at
different ages ranges from >90% in newborns, 30% in children aged
2–5 years and
<5% in adults.
iii) Sexually
promiscuous:
There is a
significant excess
of serologic evidence of hepatitis type B infection in two high-
promiscuity populations: patients with venereal diseases and their
unrelated sexual contacts (15% to 18%) and male, but not
female, homosexuals (37% to 51%).
iv) Health Care Workers: The risk
of contracting HBV by Health
Care Workers (HCWs) is four-
times greater than that of the
general adult population. The
highest rates are seen among dentists,
physicians, laboratory workers, dialysis
workers, cleaning service employees, and
Figure 5: Pie chart representing the transmission risk
in HCWs

12. 12
nurses.
v) Drug abusers: India has an estimated 1.1 million injection drug users.
Outbreaks of viral hepatitis B in this group have been linked to the
usage of inadequately sterilized needles and syringes for the intake of
narcotics.
External factors
a) Chronic alcoholism plays a major role in increasing the rate of
progression to both cirrhosis and Hepatocellular Carcinoma (HCC).
Among patients with chronic hepatitis B, those with a history of heavy
drinking have a 6-fold higher risk of progression to cirrhosis.
b) Additional external factors that may increase the risk of liver cancer and
induce the development of carcinoma include tobacco smoking and
dietary carcinogens such as aflatoxins which contaminate food stored in
humid conditions.
c) Patients suffering from immunodeficiency syndromes are at a very high
risk of developing a fatal hepatitis infection. The prevalence of HBV
infection in HIV-infected persons has ranged between 2.25 and 29.7%.
Figure 6: Study shows that people who had been hospitalized for alcoholic hepatitis only had a 31.8% chance of living
for five or more years.

13. 13
M O D E S O F
T R A N S M I S S I O N
Transmission of HBV infection can happen mainly through 2 routes: (1)
Vertical, i.e. from the mother to the neonatal and (2) Horizontal, i.e. by other
routes like sexual contact, transmission through blood and other body fluids,
etc.
i. Perinatal/vertical route
Spread of HBV from carrier mothers to infants
appears to be an important factor for
the high prevalence of hepatitis B
infection in some regions, particularly
China and Southeast Asia. The risk of
infection varies from country to
country and may reach 40%. The
mechanism of perinatal infection is
uncertain. Although HBV can infect
the fetus in utero, this rarely happens and
infection usually occurs at the time of birth, as a result of
a leak of maternal blood into the baby’s circulation, or ingestion or accidental
inoculation of blood. Infection of the baby is usually anicteric and is recognized
by the appearance of surface antigen between 600-120 days of birth.
ii. Horizontal route
a. Parenteral route

14. 14
Hepatitis B is essentially a blood-
borne infection. It is transmitted by
infected blood and blood products
through transfusions, dialysis,
contaminated syringes, needles,
pricks if skin, handling of infected
blood, accidental inoculation of
minute quantities of blood such as during surgical and dental procedures,
immunization, traditional tattooing, body piercings, ritual circumcision,
acupuncture, etc. Accidental percutaneous inoculations by shared razors and
toothbrushes have been implicated as an occasional cause of hepatitis B. Close
living quarters/playground play as a toddler is also a source of HBV infection
(may contribute to high rate of horizontal transmission in Africa).
b. Sexual
transmission
There is ample evidence
for the spread of
infection by intimate
contact or by sexual
route. The sexually
promiscuous, particularly
male homosexuals, are at
a very high risk of
infection with hepatitis
B.
iii. Other routes
Transmission by blood-sucking arthropods (e.g.: mosquitoes, bed bugs) is
suspected but there is no convincing evidence to support this suggestion.
In short, transmission occurs in a wide variety of epidemiological settings. It
can spread either from carriers or from people with no apparent infection, or
during the incubation period, illness or early convalescence.

15. 15
S I G N S & S Y M P T O M S
Signs and symptoms of hepatitis B range from mild to severe. They usually
appear about one to four months after
you've been infected, although you
could see them as early as two weeks
post-infection. Some people, usually
young children, may not have any
symptoms.
Hepatitis B signs and symptoms
may include:
 Abdominal pain
 Dark urine
 Fever
 Joint pain
 Loss of appetite
 Nausea and vomiting
 Weakness and fatigue
 Jaundice (Yellowing of skin and
the whites of eyes)

16. 16
D I A G N O S I S
CLINICAL OBSERVATION:
Peculiar symptoms in one’s body may develop into a number of clinical
syndromes after exposure to hepatitis B virus, which are as follows:-
1. Carrier state: without clinically apparent disease or with chronic hepatitis
2. Asymptomatic infection: serologic evidence only
3. Acute hepatitis: anicteric or icteric
4. Chronic hepatitis: with or without progression to cirrhosis
5. Fulminant hepatitis: sub-massive or massive hepatic necrosis
Carrier State
A “carrier” is an individual
without manifest symptoms
who harbors and therefore can
transmit an organism. With
hepatotropic viruses, there are
(1) those who harbor one of the
viruses but are suffering little or
no adverse effects (a “healthy”
carrier) and (2) those who have
chronic liver disease but are
essentially free of symptoms or
disability. Both constitute
reservoirs of infection.
Infection in the early years, particularly through vertical transmission during
childbirth, produces a carrier state 90-95% of the times. In contrast, only 1-

17. 17
10% of adult infections yield a carrier state. Individuals with impaired immunity
are particularly likely to become carriers.
Asymptomatic Infection
Not surprisingly, patients in this group are identified incidentally on the basis of
minimally elevated serum transaminases or after the fact by the presence of
antiviral antibodies.
Acute Viral Hepatitis
This disease can be divided majorly into four phases: (1) an incubation period,
(2) asymptomatic preicteric period, (3) asymptomatic icteric phase, (4)
convalescence. Peak infectivity occurs during the last asymptomatic days of the
incubation period and the early days of acute symptoms.
The preicteric period is marked by non-specific, constitutional symptoms.
Malaise is followed in a few days by general fatigability, nausea, and anorexia.
Weight loss, low-grade fever, headaches, osteoporosis, shaking chills, pain, and
diarrhea are inconstant symptoms. Physical examination reveals a mildly
enlarged and tender liver.
Remarkably, as jaundice appears and the patient enters the icteric phase, other
symptoms begin to abate. The jaundice is caused predominantly by increased
bilirubin levels in the blood and hence is accompanied by dark-colored urine
and light-colored stools. Retention of bile salts results in distressing skin itching
(pruritus).
Figure 7: Symptoms of the preicteric phase of acute hepatitis B

18. 18
The icteric phase is absent in about half of hepatitis B patients. In a few weeks
to perhaps several months, jaundice and most of the other systemic symptoms
clear as convalescence begins.
Chronic Viral Hepatitis
The initial physical examination
should document the presence or
lack of signs of chronic liver
disease. For most patients with
chronic hepatitis B, the physical
examination is normal. The
clinical features of chronic
hepatitis are extremely variable and are not predictive of outcome. In some
patients, the only signs of chronic disease are persistent elevations of serum
transaminases, hence the misleading designation, “transaminitis”. The most
common symptoms are fatigue; less commonly, there are malaise, anorexia, and
occasional bouts of mild jaundice. Physical findings are few, most common
being spider angiomas, palmar erythema, mild hepatomegaly, hepatic
tenderness, mild splenomegaly. These symptoms are indicative of an advanced
disease.
Fulminant Hepatitis
When hepatic insufficiency progresses from the onset of symptoms to hepatic
encephalopathy within 2-3 weeks, it is termed as fulminant hepatic failure,
which is most often induced my hepatic viruses.
LABORATORY FINDINGS:
 Serological testing
There are six serological markers used in hepatitis B panel of blood tests that
are essentially three different tests (HBsAg, Anti-HBs, & Anti-HBc) to detect
Figure 8: Symptoms of chronic viral hepatitis

19. 19
the presence of different antigens and antibodies in our blood serum. These are
as follows:-
1. Hepatitis B surface antigen (HBsAg)
This is a protein on the surface of the HBV; it is detected in acute or
chronic hepatitis infection and is hence, used to detect if the patient has
hepatitis or not. This antigen is also used in making hepatitis B vaccines.
2. Hepatitis B e antigen (HBeAg)
A product of the nucleocapsid (envelope) gene of the hepatitis B virus, this
antigen is found in serum during acute and chronic hepatitis B infection. Its
presence indicates that the virus is replicating and the infected person has
high levels of HBV. However, patients that are HBeAg negative may also
have high levels of HBV.
3. Total hepatitis B core antibody (anti-HBc)
It appears at the onset of symptoms in acute hepatitis B infection and
persists for life. The presence of anti-HBc indicates previous or ongoing
infection with HBV.
4. IgM antibody to hepatitis B core antigen (IgM anti-HBc)
Its presence
indicates the
presence of
acute (>6
months) and
not chronic
hepatitis B
infection. It is
also found
during viral
reactivations
of chronic
hepatitis.

20. 20
5. Hepatitis B surface antibody (anti-HBs)
The presence of the antibody to the surface antigen indicates recovery and
immunity from HBV infection. Anti-HBs also develops in a person who has
been successfully vaccinated against hepatitis B.
6. Hepatitis B e antibody (HBeAb or anti-HBe)
Spontaneous conversion from e antigen to e antibody (a change known as
“e” seroconversion) is a predictor of long-term clearance of HBV in
patients undergoing antiviral therapy and indicates lower levels of HBV.
Seroconversion also occurs in natural infection.
The interpretation of the test results to create a diagnosis that can be done
in the following ways:

21. 21
 Liver-related tests
The hepatitis B virus specifically attacks the liver, so health care providers will
order blood tests to monitor the health of your liver. Some of the most
common liver-related blood tests are described below.
1. ALT (alanine aminotransferase) is found almost exclusively in the liver
and is monitored most closely in a chronic hepatitis B infection. This test
is useful in deciding whether a patient would benefit from treatment or
for evaluating how well a person is responding to therapy. The upper
limits of normal for ALT in healthy adults is 35 U/L for men and 25
U/L for women.
2. AST (aspartate aminotransferase) is found in the liver, heart, and muscle
so is less accurate than the ALT in measuring liver damage. However,
this enzyme is often ordered to help monitor potential liver damage
from the hepatitis B virus.
(ALT & AST are two enzymes the levels of which are checked in
liver function test or LFT)
3. AFP (Alpha-FetoProtein) - This is a normal protein produced in the
developing fetus, thus, pregnant women will have elevated AFP. Other
adults, however, should not have elevated AFP in their blood. This test
is used to screen for primary liver cancer patients with chronic hepatitis
B. Patients should have their AFP levels monitored at every visit since
hepatitis B is the leading cause of liver cancer. If the AFP level is high,
the health care provider will order more blood tests and imaging studies.
4. Ferritin - Iron is stored in the liver in the form of ferritin. Increased
levels of ferritin indicate that a high level of iron is being stored. This
could result from an increased iron intake in the diet (vitamin
supplements, food cooked in iron pots, etc.). For people living with
chronic hepatitis B, a high level can indicate liver damage since ferritin is
leaked into the bloodstream as liver cells are injured by the virus.

22. 22
 Liver imaging
Non-invasive imaging
procedures may be used
to monitor the health of
the patient’s liver. An
abdominal ultrasound is a
swift, painless procedure
that can be used to detect
abnormalities in the liver,
such as cancer. Some
people with chronic
hepatitis B require regular
(6 monthly) liver
ultrasounds because they have been assessed as having a high risk of
developing serious liver disease. Ultrasound is useful for detecting tumors
and can potentially detect cirrhosis. If the ultrasound test reveals a tumor,
the doctor may want the patient to have a CT scan or an MRI done. The
CT scan (computed tomography or CAT scan) is a specialized X-ray that
produces a picture of the liver. MRI (magnetic resonance imaging) also
takes a picture, but it uses a magnetic field and radio wave pulses.
 Liver Biopsy
A biopsy is a minor surgical procedure done in the hospital that allows experts
to examine tissue taken from the liver and determine how healthy the liver is.
Liver biopsy is more reliable than both ALT and HBV DNA levels in the
decision to treat patients with HBeAg-negative chronic HBV.
Figure 9: A sample liver ultrasound sonograph
Figure 10: Images of sample liver biopsy reports

23. 23
P R O G N O S I S
Prognosis can be variable for different types of hepatitis B. The hepatitis B
virus causing acute hepatitis usually only stays in the system for around one to
three months. The infection usually resolves without treatment and most adults
recover completely. However, in around 1 in 20 affected adults, the infection is
chronic and stays in the body for six months or more. This chronic form of
hepatitis B is very common in young infants and children. About 90% of
infants who are infected as newborns and 20% of young children affected go
on to develop chronic infection. Even if these children do not have symptoms,
they can still
pass the
infection onto
other people.
Children who
get the infection
from carrier
mothers have a
40% lifetime risk
of death from
cirrhosis or
hepatocellular carcinoma. Cirrhosis of the liver can take up to 20 years to
develop and may not cause any symptoms initially. Eventually, the liver damage
can lead to symptoms such as those mentioned above.
Fulminant hepatitis is a rare complication of acute hepatitis B where the
immune system attacks the liver and causes severe damage. The condition
affects around 1 in 100 adults who have chronic hepatitis B, but children are
affected much more rarely. Some of the symptoms of fulminant hepatitis B
include confusion, jaundice, and ascites. The most important factors for
predicting survival in FHF are the degree of encephalopathy and the patient's
age.
Figure 11: Possible courses of complications a chronic hepatitis infection can take, altering
the prognosis of the condition

24. 24
T R E A T M E N T
Once a patient is diagnosed with hepatitis
B, they are usually referred to a liver
specialist called a hepatologist. There are
decisions patients have to make to
protect their livers such as avoiding
alcohol and tobacco and eating healthy foods.
Current treatments for hepatitis B fall into two general
categories:
 Immune modulator Drugs – These are interferon-type drugs (drugs that
are proteins which are produced by host cells infected with viruses) that
boost the immune system to help get rid of the hepatitis B virus. They are
given as a shot (similar to how insulin is given to people with diabetes) over
6 months to 1 year.
 Antiviral Drugs – These are drugs that stop or slow down the hepatitis B
virus from reproducing, which reduces the inflammation and damage of
your liver. These are taken as a pill once a day for at least 1 year and usually
longer.
The majority of people with acute infection completely recover within a
couple of months and never go on to develop chronic hepatitis. There is no
specific treatment for short-term (acute) hepatitis B and unless symptoms are
severe, patients can generally manage these at home. Doctors usually advise
paracetamol for pain due to acute infection and strong painkillers like codeine
if severe pain is reported. Any nausea or vomiting symptoms can often be
relieved with medications such as metoclopramide (anti-emetic). Once
symptoms improve, patients need a further blood test to check they are free of
the virus and that chronic hepatitis B has not developed.
For chronic HBV infection, the World Health Organization (WHO)
recommend treating the individual with an antiviral medication. This is not a
cure, but it can stop the virus from replicating and prevent its progression into

25. 25
an advanced liver disease because a person with chronic HBV infection can
develop cirrhosis or liver cancer quickly and without warning. In low-income
settings, liver cancer can be fatal within months of diagnosis. Blood tests,
ultrasound scans and perhaps liver biopsy may also be required to check the
state of the liver and how much damage has been done.
The medications chosen to manage chronic hepatitis B depends on whether the
virus is causing persistent liver damage
because the immune system is sometimes able
to suppress the virus without any liver damage
being caused. For patients with a fairly healthy
liver function, the first treatment approach is
often a drug called peginterferon alfa 2-a
(immune modulator). If this therapy fails,
antiviral drugs such as entecavir and tenofovir
may be prescribed which are safe, highly effective and
recommended by the WHO.
In some cases, the medication is successful at
enabling the immune system to control the
virus and the treatment may no longer be
required.
There is no surgical treatment for hepatitis B. If
liver damage is severe enough that the liver starts
to fail, the only treatment that will help is a liver transplant. Liver transplant is a
major undertaking with an extended recovery period. It also depends on the
availability of a matching donor liver. If a liver transplant becomes a possibility
for the patient, the health care provider will discuss the risks and benefits with
him/her.

26. 26
P R E V E N T I O N
Since there is no specific treatment, prevention has been the major aim in
managing viral hepatitis B. The following measures are available –
a. Hepatitis B vaccine
i. Plasma-derived vaccine: This is based on the surface antigen
(HBsAg) which is harvested and purified from the plasma of human
carrier of HBV. The final vaccine is a formalin-inactivated sub-unit viral
vaccine for intramuscular
injection. Each 1 ml dose of
vaccine contains 20 µg of
hepatitis surface antigen
formulated in an alum
adjuvant. The vaccine is
given in 3 doses at 0, 1 and 6
months. An effective
antibody response is generally
attained after 3 doses in 95%
of vaccinees. Immunity
continues at protective levels
for approximately 3-5 years. Booster doses may be given after 3-5 years.
Both pre-exposure and post-exposure administration has been
recommended. Classical examples of post-exposure prophylaxis are the
protection of newborn infants born to HBV carrier mothers, and
individuals accidentally exposed to parenterally to HBV infection
through cuts, injuries, transfusions, and needlesticks. It is advisable but
not mandatory to give specific anti-HBs immunoglobin with or before
the vaccine dose in post-exposure cases.
Post-exposure prophylaxis is indicated in countries with a high
prevalence rate of HBV infection. In these countries, hepatitis B vaccine

27. 27
must be classified and
used in the same
category as DPT and
polio. Unfortunately,
the high cost of
vaccine preludes its
use in those parts of
the world where it is
most needed.
The vaccine has no effect on HBsAg carriers and is unnecessary in
persons with surface antibody from the previous infection.
ii. RDNA-yeast derived vaccine: An
alternate vaccine against hepatitis B was
licensed for the first time in the USA
in 1987. The recombinant DNA
vaccine was elaborated from the
cultures of yeast cloned with HBsAg
s-gene. Several field trials have shown that this vaccine is as
immunogenic, safe and effective as the plasma-derived vaccine and is
more cost-effective than the latter. The fact that this vaccine does
not depend on the scarce plasma resource is an added advantage.
b. Hepatitis immunoglobin (HBIG)
For immediate protection, HBIG is used for those acutely exposed to
HBsAg positive blood, for example, (a) surgeons, nurses or laboratory
workers, (b) newborn infants or carrier mothers, (c) sexual contacts of
acute hepatitis B patients. The HBIG should be given as soon as
possible after accidental inoculation (ideally before 6 hours and
preferably not later than 48 hours). At the same time, the victim’s blood
is drawn for HBsAg testing. If the test is negative, vaccination should be
started immediately and a full course be given. If the test is positive for
surface antibody, no further action is needed.

28. 28
c. Passive-active immunization
The simultaneous administration of HBIG and hepatitis B vaccine is
more efficacious than HBIG alone. HBIG does not interfere with
antibody response to the hepatitis B vaccine. This combined procedure
is ideal both for prophylaxis of person accidentally exposed to blood
known to contain HBV and for prevention of the carrier state in the
newborn babies of the carrier mothers. HBIG should be given as soon
as possible, preferably before 24 hours. Hepatitis B vaccine should be
given intramuscularly within 7 of exposure and second and third doses
given one and six months respectively, after the first dose.
d. Other measures
All blood donors should be screened for HBV infection, and those
positive for Australia antigen should be
rejected. Voluntary
blood donation should
be encouraged because
purchased blood has
shown a greater risk of
post-transfusion
hepatitis. Health
personnel should be
alerted about the importance of
adequate sterilization of all
instruments and to practice
simple hygienic procedures.
Carriers should be told not to
share razors or toothbrushes and use barrier
methods of contraception; they should not donate
blood.

29. 29
C A S E S T U D I E S
C A S E - 1
Name : Mr. Sunil Kumar, s/o Mr. Banwari Lal (Name changed)
Sex : Male
Age : 37 years
Civil status : Unmarried
Date admitted : 01/06/2018
Complaints : General weakness, headache, restlessness, loss of sleep
History of
present illness :
Mild headaches, restlessness, and loss of sleep started
occurring 6 months ago; general weakness began 3 weeks
ago; intensity of headaches increased since then; no
additional symptoms
Personal
history :
No previous hospitalizations; no records of substance abuse,
alcoholism, or tobacco; currently not under any medication
except the occasional use of ibuprofen for headaches (1-2
times a day); sexually active with several partners
Family history :
No history of cancer; no cases of hepatitis B, uterine fibroid,
heart diseases from the mother’s side
Examination
findings :
Appetite is mildly diminished; rounded
tender abdomen; patient sleeps for 2
hours a night; yellowish
eyes; dark urine
Blood test
reports :
ALT – 1520 IU/ml, AST – 1230 IU/ml; HBsAg +ve,
HBsAb –ve, HBeAg +ve, Anti-HBc IgM +ve

30. 30
Ultrasound
findings :
Hepatomegaly, no
splenomegaly, marginal
ascites, thickened GB wall,
normal bile ducts
Diagnosis : Acute hepatitis B (non-severe)
Treatment :
Rest recommended, proper nutrition, consumption of fluids,
replace ibuprofen with paracetamol
Follow-up after every six weeks with fresh serum test reports, additional
appointments necessary till HBV has been completely eliminated and reports
become normal
C A S E - 2
Name :
Late Mrs. Bimla Devi w/o Mr. Santosh Singh (Name
changed)
Sex : Female
Age : 44 years
Civil status : Married
Date admitted : 17/10/2018
Complaints : Diffuse abdominal pain, subjective fever, and jaundice
History of Brought to the hospital after four days of overpowering sore

31. 31
present illness : abdomen, continuous fever and yellowing of skin and eyes
Personal
history :
No history of alcoholism; no mention of ingestion of toxic
substances, homeopathic medicines or excessive use of
acetaminophen
Examination
findings :
Jaundice, painful epigastric palpation, painful right upper
quadrant palpation, no peritoneal irritation, no signs of
chronic liver disease, no signs of neurological distress and no
encephalopathy
Blood test
reports :
ALT – 6.315 mg/dl, AST – 8.947 mg/dl (worsened in the
next 3 days); HBsAg +ve,; HBsAb, HBeAg, Anti-HBc IgM
results requested
Ultrasound
findings :
Liver necrosis; starry night
appearance (acute edema,
necrosis); hyperechoic areas
Diagnosis : Prodromal period of hepatic failure
Treatment : Admitted for clinical observation; 0.5 mg doses of entecavir
started daily; patient was referred for liver transplantation
On the fourth day, the patient suffered overall
deterioration to grade II hepatic encephalopathy.
Applicable medicines to counter encephalopathy and
to manage liver disease were begun. The patient was
moved to the ICU for progression to hepatic
encephalopathy grade III and hemodynamic
deterioration requiring vasopressor support. She did
not respond favorably, and on the 5th day, she
developed grade IV hepatic encephalopathy. A CT
scan of her brain was taken that appeared to be

32. 32
normal. There was no clinical improvement. She had also developed upper
gastrointestinal bleeding for which infusion of omeprazole was initiated. She
was transfused with 15 cc/kg of plasma plus vitamin K. The patient progressed
to cardiac arrest. She was unresponsive to advanced maneuvers and died 5 days
after admission to the institution and nine days after onset of symptoms. The
cause of death was determined to be fulminant liver failure secondary to
hepatitis B.

33. 33
B I B L I O G R A P H Y
Park’s Textbook of Preventive and Social Medicine by K Park
Davidson’s Principles & Practice of Medicine by Sir Stanley Davidson
Robbins Pathologic Basis of Disease by Cortan, Kumar & Collins
www.mayoclinic.org
www.ncbi.nlm.nih.gov
www.hepb.org
www.news-medical.net
www.hepmag.com
www.wikipedia.org