JPTS

Institute Of Management,
Science and Technology
TERM PAPER ON:

THE PRESENCE OF HEPATITIS B ENVELOPE ANTIBODY

IN PATIENTS WHO HAVE BEEN PREVIOUSLY SCREENED
FOR THE SURFACE ANTIGEN
BY:

UMEH NGOZICHUKWU LOVELYN

REG/31839 / 300L

SUBMITTED TO:
HEALTH CARE MANAGEMENT AND NURSING
DEPARTMENT
JPTS

INSTITTUTE OF MANAGEMENT, SCIENCE AND

TECHNOLOGY

FULL-TIME CENTRE KABBA.

JULY, 2021.
 Dedication

This work is dedicated to God Almighty.

 Acknowledgements

My sincere gratitude goes to God Almighty, my family and everyone that

contribute to the success of this work.
TABLE OF CONTENTS

Title page

Dedication

Acknowledgements

Abstract

CHAPTER ONE: INTRODUCTION

1.1 Background of the study

1.2 Objectives of the study

1.3 Purpose of study

CHAPTER TWO: LITERATURE REVIEW

2.1 Epidemiology

2.2 Hepatitis B Symptoms

2.3 How is Hepatitis B spread?

2.4 Diagnosis Hepatitis B

2.5 Hepatitis B risk factors

CHAPTER THREE: RESEARCH METHOD

3.1 Research Location

3.2 Sample Collection

3.3 Sample Population

3.4 Research Method

CHAPTER FOUR:

4.1 Data presentation an analysis

4.2 Discussion of findings

CHAPTERFIVE: SUMMARY, CONCLUSION AND

RECOMMENDATIONS

5.1 Summary

5.2 Conclusion

5.3 Recommendations

References
 ABSTRACT

There were 55 (48.2%) discrepant cases, and the range of HBsAg titers determined
by high-sensitivity HBsAg assays was 0.005–0.056 IU/mL. Multivariate analysis
showed that the presence of nucleos(t)ide analog therapy, liver cirrhosis, and
negative anti-HBs contributed to the discrepancies between the two assays.
Cumulative anti-HBs positivity rates among discrepant cases were 12.7%, 17.2%,
38.8%, and 43.9% at base-line, 1 year, 3 years, and 5 years, respectively, whereas
the cor-responding rates among consistent cases were 50.8%, 56.0%, 61.7%, and
68.0%, respectively. Hepatitis B virus DNA negativity rates were 56.4% and
81.4% at baseline, 51.3% and 83.3% at 1 year, and 36.8% and 95.7% at 3 years,
among discrepant and consistent cases, respectively. Hepatitis B surface antigen
rever-sion was observed only in discrepant cases.
 CHAPTER ONE

INTRODUCTION

1.1 BACKGROUND OF THE STUDY

A virus is a small infectious agent having a simple acellular organization with a

nucleic acid and aprotein coat. It lacks independent metabolism and replicate only
within living hosts. A virus invades living cells and uses its chemical machinery to
keep itself alive and replicate in the host. It may reproduce with fidelity or with
errors (mutations); this ability to mutate is responsible for the ability of some
viruses to change slightly in each infected person, making treatment difficult.
Viruses cause many human infections and are also responsible for a number of rare
diseases. The human diseases they cause may affect different organs or parts of the
body. An inflammation of the liver is often referred to by a general term called
Hepatitis, which is often caused by a variety of viruses which include hepatitis A,
B, C, D and E. Of the viral causes of hepatitis, there are few of greater global
importance than hepatitis B (Ganem et al, 2001).

The hepatitis B virus (HBV) belongs to the family Hepadnaviridae, which consists
of hepatotropic DNA viruses. The family of Hepadna viruses comprises members
recovered from animal species including the woodluck hepatitis virus (WHV), the
ground squirrel hepatitis virus (GSHV), and the duck HBV. Common features of
all of these viruses are enveloped virions containing 3 to 3.3 kb of relaxed circular
partially duplex DNA and have reverse transcriptase activities. Hepadnaviruses
show narrow host ranges, growing only in species close to the natural host, like
gibbons, African green monkeys, rhesus monkeys and woolly monkeys
(Gitlin,1997).The Hepatitis virus belongs to the genus Hepadnavirus. It is a 42nm
partially double stranded DNA virus, composed of a 27nm nucleic acid core
(HBcAg), a DNA polymerase reverse transcriptase, surrounded by an outer
lipoprotein coat (called envelope) containing the surface antigen (HBsAg)that play
a major role in the diagnosis of HBV infection (Ganem et al; 2001; Gitlin,1997).
The genome consists of a partially double-stranded circular DNA molecule of
about 3200 base pairs in length with known sequence as well as genetic
organization. Virion particles are identical to the virion ‘tails’- they vary in length
and have a mean diameter of about 22nm. They sometimes display regular, non-
helical transverse striations.

The viral DNA polymerase-reverse transcriptase is encoded by the polymerase

gene [P] and is of central importance for viral replication. Different from all known
mammalian DNA viruses, hepadna viruses replicate via reverse transcription of a
RNA intermediate (Summerset al.,1982), the pregenomic RNA, which is a strategy
central to the life cycle of RNA retroviruses. Similarities and differences between
retroviral and hepadnaviral replication have been defined (Nassal, 1999). Based on
the unique replication cycle of HBV, antiviral therapeutic strategies aimed at the
reverse transcription of HBV RNA or at HBV reverse transcriptase have been
successfully used as antivirals to treat HBV infection (Feld, 2002).

The prevalence of HBV infection varies in different countries or regions in the

world as well as in different ethnic groups. HBV endemicity has been classified
into three categories, high (>8%), intermediate (2–8%), and low (<2%), depending
on the prevalence of hepatitis B surface antigen (HBsAg) seropositivity. The
highly endemic areas in the world include East and Southeast Asia, the Pacific,
sub-Saharan Africa (Nigeria inclusive), and parts of southern Europe. In North
America, and western and northern Europe, HBV infection is relatively rare, with a
prevalence rate of around 0.1%.Hepatitis B virus (HBV) infection is a serious
global health problem, with 2 billion people infected world-wide, and 350 million
suffering from chronic HBV infection. HBV is the 10th leading cause of death
worldwide, HBV infections result in 600 000 deaths annually (Ott et al 2012). 1.2
million deaths per year are caused by chronic hepatitis, cirrhosis, and
hepatocellular carcinoma; the last accounts for 320 000 deaths per year (WHO,
2000). In Western countries, the disease is relatively rare and acquired primarily in
adulthood, whereas in Asia and most of Africa, chronic HBV infection is common
and usually acquired perinatally or in childhood.

The whole of Africa is regarded as highly endemic, coming only behind Asia.
Although overall Africa is considered a high endemic area with 7–26% prevalence
of HBsAg, Tunisia, Morocco, and Zambia have intermediate endemicity (Andre,
2000). In West Africa, countries like Senegal and Gambia have over 90% of their
populations exposed to and becoming infected with HBV during their lives
(Edmund WJ. et al., 1996). In Nigeria, not less than 23 million people are
estimated to be infected with HBV (Bukola, 2015), making Nigeria one of the
countries with the highest incidence of HBV infection in the world.

Hepatitis B is caused by hepatitis B virus. The virus interferes with the functions of
the liver while replicating in hepatocytes. The immune system is then activated to
produce a specific reaction to combat and possibly eradicate the infectious agent.
As a consequence of pathological damage, the liver becomes inflamed. HBV may
cause up to 80 per cent of all cases of hepatocellular carcinoma (HCC) worldwide,
second only to tobacco among known human carcinogens (WHO, 2001). Most
people do not experience any symptoms during the acute infection phase.
However, some people have acute illness with symptoms that last several weeks,
including yellowing of the skin and eyes (jaundice), dark urine, extreme fatigue,
nausea, vomiting and abdominal pain. In some people, the hepatitis B virus can
also cause a chronic liver infection that can later develop into cirrhosis of the liver
or liver cancer (WHO, 2014).

Susceptibility to HBV infection is general. Only people who have been vaccinated
successfully or have developed anti-HBs antibodies after HBV infection are
immune to HBV infection. Persons with congenital or acquired immunodeficiency
including HIV infection, those with immunosuppression including those with
lymphoproliferative disease, patients treated with immunosuppressive drugs
including steroids and by maintenance haemodyalisis are more likely to develop
persistent infection with HBV.

Hepatitis B can be spread by

• unprotected sex

• sharing IV drug needles

• living in a household with an infected person

• An infected mother to her newborn child at birth

• sharing earrings, razors, or toothbrushes with an infected person

• unsterilized needles, including tattoo or piercing needles

• Human bites (www.hepb.org).

People are most at risk for hepatitis B if they

• are born to mothers who are infected with HBV

• live in close household contact with a chronically infected individual

• adopt a child from a country where HBV is prevalent

• have unprotected sex or have more than one sexual partner in a six month period

• have ever been diagnosed with a sexually transmitted disease (STD)

• are men who have sex with men

• share needles and syringes

• are health care provider or emergency responder with possible contact with
bodily fluids

• are a patient on kidney dialysis

• live or work in an institutional setting, such as a prison or group home

(www.hepb.org).

Diagnosis of hepatitis is made by biochemical assessment of liver function. Initial

laboratory evaluation should include: total and direct bilirubin, ALT (alanine
transaminase,) AST (aspartate aminotransferase), alkaline phosphatase,
prothrombin time, total protein albumin, globulin, complete blood count, and
coagulation studies(Hollingeret al.,2001). Diagnosis is confirmed by demonstration
of specific antigens and/or antibodies.

There is yet no treatment for acute HBV infection, but it is a vaccine-preventable

infection. Several vaccines have been used in the prevention of this infection, the
prominent ones including Lamivudine, Adefovir, Dipivoxil, Famvir, FTC,
Ritonavir, Theradigm-HBV, Ganciclovir (Hadziyannis et al.,1999).
1.1 OBJECTIVES OF THE STUDY

Hepatitis B virus infection is of global concern. More importantly, it is of national

concern as over 23 million Nigerians are infected with HBV. The incidence of the
infection in South-Western Nigeria is of no less importance as the region is still
ravaged with high cases of immunization difficulties. Most texts have been on
HBsAg, whereas other markers are equally important.

1.2 PURPOSE OF THE STUDY

The purpose of this study, therefore, is:

 To determine the presence of Hepatitis B envelope antibody in patients who

have been previously screened for the surface antigen.
 To determine the class of individuals mostly affected.
 CHAPTER TWO

RELATED LITERATURE REVIEW

2.1 Epidemiology

Hepatitis B is an infection of your liver. It’s caused by a virus. There is

a vaccine that protects against it. For some people, hepatitis B is mild and lasts a
short time. These “acute” cases don’t always need treatment. But it can become
chronic. If that happens, it can cause scarring of the organ, liver failure, and cancer,
and it even can be life-threatening.

It’s spread when people come in contact with the blood, open sores, or body fluids
of someone who has the hepatitis B virus.

It's serious, but if you get the disease as an adult, it shouldn’t last a long time. Your
body fights it off within a few months, and you’re immune for the rest of your life.
That means you can't get it again. But if you get it at birth, it’ unlikely to go away.

“Hepatitis” means inflammation of the liver. There are other types of hepatitis.
Those caused by viruses also include hepatitis A and hepatitis C.

2.2 Hepatitis B Symptoms

Short-term (acute) hepatitis B infection doesn’t always cause symptoms. For

instance, it’s uncommon for children younger than 5 to have symptoms if they’re
infected.

If you do have symptoms, they may include:

  Jaundice (Your skin or the whites of the eyes turn yellow, and your pee turns
brown or orange.)

 Light-colored poop

 Fever

 Fatigue that persists for weeks or months

 Stomach trouble like loss of appetite, nausea, and vomiting

 Belly pain

 Joint pain

Symptoms may not show up until 1 to 6 months after you catch the virus. You
might not feel anything. About a third of the people who have this disease don’t.
They find out only through a blood test.

Symptoms of long-term (chronic) hepatitis B infection don’t always show up,

either. If they do, they may be like those of short-term (acute) infection.

2.3 How is Hepatitis B spread?

You can become infected with hepatitis B through exposure to blood, semen and
other bodily fluids of an infected person. You can get the infection by:

 Having unprotected sex.

 Sharing or using dirty needles for drug use, tattoos or piercing.

 Sharing everyday items that may contain body fluids, including razors,
toothbrushes, jewelry for piercings and nail clippers.
  Being treated medically by someone who does not use sterile instruments.

 Being bitten by someone with the infection.

 Being born to a pregnant woman with the infection.

Hepatitis B is not spread by:

 Kissing on the cheek or lips.

 Coughing or sneezing.

 Hugging, shaking hands or holding hands.

 Eating food that someone with the infection has prepared.

 Breastfeeding.

2.4 Diagnosis Hepatitis B

There are three main ways to diagnose HBV infection. They include:

 Blood tests: Tests of the blood serum (or plasma) shows how your body’s
immune system is responding to the virus. A blood test can also tell you if
you are immune to HBV.

 Abdominal ultrasound: An ultrasound uses sound waves to show the size

and shape of your liver and how well the blood flows through it.

 Liver biopsy: A small sample of your liver tissue is removed though a tiny
incision and sent to a lab for analysis.
The blood test that is used to diagnose hepatitis B is not a test that you get
routinely during a medical visit. Often, people who’ve become infected first learn
they have hepatitis B when they go to donate blood. Blood donations are routinely
scanned for the infection.

The virus can be detected within 30 to 60 days of infection. About 70% of adults
with hepatitis B develop symptoms, which tend to appear an average of 90 days
after initial exposure to the virus.

2.5 Hepatitis B risk factors

Due to the way that hepatitis B spreads, people most at risk for getting infected
include:

 Children whose mothers have been infected with hepatitis B.

 Children who have been adopted from countries with high rates of
hepatitis B infection.
 People who have unprotected sex and/or have been diagnosed with a
sexually transmitted infection.
 People who live with or work in an institutional setting, such as prisons
or group homes.
 Healthcare providers and first responders.
 People who share needles or syringes.
 People who live in close quarters with a person with chronic hepatitis B
infection.
 People who are on dialysis.
 CHAPTER THREE

RESEARCH METHODOLOGY

3.1 Research Location

The study was conducted in Kano state of the federal republic of Nigeria, which is
located at north-west zone of Nigeria. The study was carried out at Aminu Kano
Teaching Hospital (AKTH), Kano, Nigeria from April – November 2012.

3.2 Sample Collection

The samples were collected from the subjects using 2ml syringes, which were
labeled with the subjects’ name/number in the general out-going patient of the
laboratory. A tourniquet was tied on the arm of the subject at about three- quarter
inch above the venipuncture site. The subject was asked to fist so that the veins
appear more prominent, and the most prominent vein was cleaned with alcohol.
The syringe’s needle was then inserted into the vein with its graduation facing
upward and the syringe’s piston was drowning until the required amount of blood
reached. The tourniquet was released and the subject’s hand was then opened,
cotton wool was placed over the vein puncture site and the needle was slowly
removed, and the blood was properly dispensed into EDTA bottle immediately.
The samples were centrifuged at 2000rpm (rpm= revolution per minute) for 5
minutes to separate the serum from the blood cells (Cheesbrough, 2005).
3.3 Sample Population

Two hundred blood samples were used for the study, of which one hundred and
forty eight (148) were obtained from male subjects, while fifty-two (52) were from
female subjects.

3.4 Research Method

Rapid Detection of Hepatitis B Surface Antigen (HBsAg)

The rapid strip for HBsAg was removed from sealed package and then immersed
vertically into the serum for 15 seconds, then the strip was removed from the
serum and placed on flat tile surface, and the timer was started. The results were
read and interpreted after 15 minutes. Positive samples were presented with two
distinct red colour bands, one at the control region and the other at the test region.
Negative results were presented with appearance of a single band at control region
and invalid results were presented with no band appearance or with single band
appearance at the test region.

Detection of Hepatitis B Envelope Antigen (HBeAg) using HBV Combo Kit

Using special kit known as HBV combo (Cortez diagnostics), which has wells
where the serum are dropped and reading area. The kit has the ability to test for
five different HBV antigens namely: HBsAg, anti-HBsAb, HBeAg, anti-HBeAb
and anti- HBc. The kit was removed from the pouch and placed horizontally on the
workbench, 3-4 drops of the serum were made in to the well of HBsAg and that of
HBeAg and the results were read between 25-30 minutes.
Determination of Alanine Aminotransferase (ALT) Level

The reagent used was ALT reagent (Ramdox, laboratories, UK). It contains two
reagents tagged as R1 and R2 which contain AL100 buffer and 2, 4- dinitrophenyl
hydrazine respectively. Zero point five (0.5) ml of the sample was pipetted using
micro-pipette into a sterile empty test tube, then 0.5ml of reagent I (R 1) was added
to the sample, mixed and then incubated for 30 minutes at 270C together with
reagent blank which is the mixture of 0.5ml of R 1 and 0.1ml of distilled water.
Zero point five (0.5) ml of R2 was then dispensed into each of the reagent blank
and the sample mixtures, these were then mixed and allowed to stand for 20
minutes at temperature range of between 20-250C. zero point four (0.4) mol/L
sodium hydroxide solution (0.4mol/L NaOHaq) was prepared by dissolving 16g of
NaOHs in 1L of distilled water. Then 0.5ml of 0.4mol/L NaOHaq was added to
each of the reagent blank and the sample mixture and then mixed. The absorbance
of the sample (Asample) against reagent blank was read digitally using
Spectrophotometer.

Determination of Aspartate Aminotransferase (AST) Level

The reagent used was AST reagent (Ramdox laboratories, UK). It also has two
reagents R1 and R2, which consist of AS101 buffer and 2, 4- dinitrophenyl
hydrazine respectively. The procedures are the same as that of ALT.

Determination of Alkaline Phosphatase (ALP) Level

The material used was alkaline phosphatase (ALP) reagent (Teco, diagnostics,
USA). This consists of ALP substrate, ALP colour developer and standard. Sterile
test tubes labeled with the specimens’ number were used. Zero point five (0.5) ml
ALP substrate was dispensed into each of the test tubes. In addition, 0.5ml of ALP
substrate was dispensed into each of two different test tubes labeled reagent blank
and standard. The temperatures of all the test tubes were equilibrated to 37 0C for
30 minutes. At regular intervals, 0.05ml (50µl) of the sample was added to each of
the tube except that of the reagent blank and standard, instead 0.05ml of deionized
water and 2-3 drops of ALP standard were added to them respectively. Following
the same time intervals as above, 2.5ml of ALP colour developer was then added
to all the test tubes including that of the reagent blank and the standard and then
mixed gently well. The absorbance of the sample (Asample) against reagent blank
was read as that of the standard digitally using spectrophotometer.
 CHAPTER FOUR

RESEARCH ANALYSIS

Two hundred blood samples were used for the study, of which one hundred and
forty eight (74%) were obtained from male subjects, while fifty-two (26%) were
from female subjects (Table 1). Out of the 148 male samples, 31 (15.5%) were
HBeAg- seropositive and 117 (58.50%) were HBeAg-seronegative while only 3
(1.5%) out of the 52 female samples were HBeAg- seropositive and 49 (24.5%)
were HBeAg-seronegative (Table 1). When 166 (83%) which were HBsAg-
seropositive but HBeAg-seronegative were subjected to liver enzymes test, 82,
120, and 50 were said to have high level of AL, TAST and ALP respectively
(Table 3), while out of 34 (17%) that were seropositive for both HBsAg and
HBeAg, 28, 30 and 18 have high level of ALT, AST and ALP respectively.

Table1: Sex related % prevalence of HBeAg

Sex HBsAg- HBeAg %HBe HBeA %HBeAg Total %

Ag g (-

carriers (+) (+) (-) )

Males 148 31 15.50 117 58.50 148 74.00

Females 52 3 1.50 49 24.50 52 26.60

Total 200 34 17.00 166 83.00 200 100.00

Key: HBeAg= Hepatitis B Envelope Antigen, HBsAg= Hepatitis B Surface

Antigen
Figure 1: Sex related % prevalence of HBeAg.

Table 2: Age related % prevalence of HBeAg.

Age range HBsAg-Carries % HBeAg (+) %

≤ 20 34 17.00 12 6.00

21-30 61 30.50 6 3.00

31-40 54 27.00 3 5.00

41-50 37 18.50 4 2.00

51-60 9 4.50 6 3.00

60 5 2.50 3 1.50

Total 200 100.00 34 17.00

Key: ≤ = lessthan or equal

Table 3: Analysis of the liver enzyme test of HBeAg

Level ALT% AST% ALP%

Normal 82 (49.40) 46 (27.71) 116 (69.88)

High 84 (50.60) 120 (72.29) 50 (30.12)

Total 166 (100.00) 166 (100.00) 166 (100.00)

Key: ALT= Alanine Aminotransferase, AST= Aspartate Aminotransferase, ALP=

Alkaline Phosphatase

Table 4: ALT, AST and ALP levels of HBeAg seropositive samples.

LEVEL ALT (%) AST (%) ALP (%)

NORMAL 6 (17.65) 4 (11.76) 16 (47.06)

HIGH 28 (82.35) 30 (88.24) 18 (52.94)

TOTAL 34 (100.00) 34 (100.00) 34 (100.00)

DISCUSSION

It has been reported that in most patients with hepatocellular carcinoma, the
disease develops after the development of antibodies against HBeAg (Heyward et
al. 1982). In this study, with all blood samples collected and assayed before the
diagnosis of hepatocellular diseases the results showed that, the seroprevalence of
hepatitis B envelope antigen (HBeAg) was higher among male sex with about
20.95% prevalence than that among female sex with about 5.77%. Though the
reason is not yet known but it might probably be due to rapid exposure of male
which render the virus become used to their physiology and anatomy (Liaw et al.,
1983).

Age related seroprevalence of HBeAg analysis, showed that age group ≤ 20 years
with 6.00% prevalence has the highest prevalence rate. This could be due to weak
or immature immune response of children. This also supports the findings of
Chang (2007) who stated that in the endemic areas, Chronic infection occurs
during childhood and mother to infant transmission which collectively accounts for
approximately 50% of chronic infection cases.

Statistical analysis revealed that there was significant difference with regard to the
development of hepatocellular diseases (HCD) among those who are seropositive
for HBeAg and those that are seronegative for HBeAg, with higher prevalence
among sero-positive subjects. This might be because of active replication of the
virus in HBeAg-seropositive subject that increase the titer volume of the virus in
blood and consequently make the virus available in sufficient amount to cause
carcinoma of the liver or other liver related complications. Both indirect and direct
carcinogenic mechanisms are involved in the pathogenesis of hepatocellular
carcinoma induced by chronic HBV infection (Kew, 1998). HBV may induce
hepatocellular carcinoma indirectly by causing chronic Necro-inflammatory
hepatic disease (Chisari et al., 1989). When HBV replication is sustained, as
indicated by positivity for HBeAg, malignant transformation may occur as a result
of continuous or recurrent cycles of Hepatocyte necrosis and regeneration. The
accelerated rate of cell turnover may act as a tumor promoter through the
accumulation of spontaneous mutations or DNA damage caused by exogenous
factors, resulting in an increased selective growth advantage for transformed cells.
The accelerated turnover rate may also result in cleavage of viral DNA at specific
motifs; resulting in linear DNA that is inserted into chromosomal DNA through
increased intracellular topoisomerase I activity (Wang, 1985). Active replication of
HBV may also initiate malignant transformation through a direct carcinogenic
mechanism by increasing the probability of insertion of viral DNA in or near
proto-Oncogenic, tumor-suppressor genes, or their regulatory elements of cellular
DNA23, 24. The integration of viral DNA may increase the production of
transactivate protein hepatitis B X antigen, which may induce the malignant
transformation of Hepatocyte, as well as bind to the p53 tumor-suppressor gene
and disrupt its functions (Popper et al., 1987 and Kin et al., 1991). High levels of
ALP, AST and ALP were found in most patients who are positive for HBeAg, and
in a substantial proportion of those with only HBsAg. Therefore, HBeAg is the
most important predictor of the development of hepatocellular diseases.
 CHAPTER FIVE

SUMMARY, CONCLUSION AND RECOMMENDATION

5.1 SUMMARY

There were 55 (48.2%) discrepant cases, and the range of HBsAg titers determined
by high-sensitivity HBsAg assays was 0.005–0.056 IU/mL. Multivariate analysis
showed that the presence of nucleos(t)ide analog therapy, liver cirrhosis, and
negative anti-HBs contributed to the discrepancies between the two assays.
Cumulative anti-HBs positivity rates among discrepant cases were 12.7%, 17.2%,
38.8%, and 43.9% at base-line, 1 year, 3 years, and 5 years, respectively, whereas
the cor-responding rates among consistent cases were 50.8%, 56.0%, 61.7%, and
68.0%, respectively. Hepatitis B virus DNA negativity rates were 56.4% and
81.4% at baseline, 51.3% and 83.3% at 1 year, and 36.8% and 95.7% at 3 years,
among discrepant and consistent cases, respectively. Hepatitis B surface antigen
rever-sion was observed only in discrepant cases.

5.2 CONCLUSION

From this study, HBeAg was more prevalent in males than females and age group
of <20 years has the highest prevalence. This study also revealed that, there is
association between the positivity of HBeAg and the development of
hepatocellular diseases.
5.3 RECOMMENDATIONS

Based on the results obtained in this study, it is recommended that further studies
should be carried out using larger number of specimens to determine whether the
results obtained in this preliminary investigation are truly representative of the
situation with regard to the potentiality of hepatitis B Viral infection as a major
cause of mortality as well as morbidity world-wide. The public should be
enlightened about viral hepatitis, its rate of increase and possible modes of
transmission.
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