TABLE OF CONTENT
CHAPTER ONE
1.0
INTRODUCTION
1.1 EPIDEMIOLOGY OF VIRAL HEPATITIS:
1.2 FORMS OF HEPATITIS – A,B AND C VIRUS
INFECTIONS
1.2.1 ACUTE HEPATITIS A VIRUS INFECTION
1.2.2 ACUTE AND CHRONIC AS
A FORMS OF HEPATITIS B VIRUS INFECTION
1.2.3 ACUTE AND CHRONIC FORMS OF HEPATITIS C VIRUS
INFECTION
1.3 STRUCTURE OF THE
VIRUSES:
1.4 TRANSMISSION OF HAV,
HAV AND HCV
1.4.1 MECHANISMS OF INFECTION OF HOST CELLS BY HEPATITIS A,
B
AND C.
1.5 HEPATITIS INFECTIONS AS A PREDISPOSING FACTOR TO HCC.
1.5 SIGNS AND SYMPTOMS OF HEPATITIS A, B, AND C INFECTION.
1.7 DIAGNOSIS OF HEPATITIS A, B AND C:
1.8 TREATMENT OF HEPATITIS A, B, AND C
INFECTION.
1.8.1 HEPATITIS A INFECTION
1.8.2 HEPATITIS B INFECTION
1.8.3 HEPATITIS C INFECTION
1.9 HEPATITIS A, B, AND C VACCINES
1.9.1 HEPATITIS A
1.9.2 HEPATITIS B
1.9.3 HEPATITIS C
1.10 PREVENTION AND CONTROL OF HEPATITIS A, B AND C INFECTION
1.10.1HEPATITIS
A INFECTION
1.10.2 HEPATITIS B INFECTION
1.10.3 HEPATITIS
C INFECTION
CHAPTER
TWO
2.0
MATERIALS AND METHOD
2.1 MATERIALS
2.2 METHODS
2.2.1 SPECIMEN COLLECTION
2.3 PRINCIPLES OF THE TEST STRIP.
2.3 TEST PROCEDURE USING TEST STRIP
2.5 INTERPRETATION OF
RESULTS.
2.6 ALPHA FETOPROTEIN TESTS
2.6.1 PRINCIPLE OF THE TEST
2.7 REAGENTS
2.7.1 REAGENT PREPARATION
2.8 EXPECTED VALUES AND SENSITIVITY
2.9 QUALITY CONTROL
CHAPTER THREE
RESULT
CHAPTER FOUR
4.0 DISCUSSION
REFERENCES
CHAPTER ONE
1.0
INTRODUCTION
Hepatocellular carcinoma (HCC) is the most common primary liver
cancer. It accounts for 60% of all cancer world wide (Melissa 2004). The most
significance cause is the presence of cirrhosis. HCC has unique geographic sex,
age distribution that are likely determined by specific actiology factor. It’s
distribution also varies among ethnic group
within the same country (Munoz 1989). A high incidence of hepatitis B and C may
have been an important factor contributing to the development of liver disease
(HCC and Cirrhosis) in south eastern Nigeria. However, a recent trend which
reveals an increase in cases of liver cirrhosis and hepatitis in our
environment suggest that there could be other contributory factors perculiar to
our environment besides hepatitis B and C which could be possible explanation
to the recent trend. In so doing, it would be necessary to look into the
various predisposing/causative factors of chronic hepatitis which could lead to
increased cases of liver cirrhosis and HCC in our environment. The risk of
developing HCC differs depending on the cause of cirrhosis. For example,
cirrhosis due to hepatitis B has a high risk of leading to HCC while the risk
of HCC in people with primary biliary cirrhosis, although present is very low. All
these human hepatitis viruses are RNA viruses except for hepatitis B virus,
which is a DNA virus. Although these viruses can be distinguished by their
molecular and antigenic properties, all types of viral hepatitis produce
clinically similar illnesses. These range from asymptomatic and unapparent to
fulminant and fatal acute infections common to all types, on one hand, and from
subclinical persistent infections to rapidly progressive liver disease with
cirrhosis and even hepatocullular carcinoma (HCC), common to the blood-borne
types (HBV and HCV). Without specific virological test, it is not possible to
determine which hepatitis virus is responsible for a case of hepatitis.
(Kathleen park et al., 2004).
AIMS
-
To analyze the αfetoprotein level
in hepatits patient as an aid in assessing the degree in which it degenerate to
HCC.
1.1 EPIDEMIOLOGY OF VIRAL HEPATITIS:
Hepatitis A virus spreads by the fecal-oral route, principally
through fecal contamination of hands,
food, or water. Many out breaks of the disease have originated from restaurants
because food handlers who carried the virus failed to wash their hands. Eating raw shellfish is
a frequent source of infection since these animals concentrates the hepatitis A
virus from fecally polluted seawater. (Gene Nester et al., 2004). A high percentage of hepatitis A occurs in low
socioeconomic groups of people because of crowding and inadequate sanitation.
Other groups at high risk of hepatitis A include attendees of day care centers
and nursing homes, and homosexual men. Infants and children with hepatitis A
can eliminate the virus in their feces for several months after symptoms begin,
but the amount of virus in feces usually drops markedly with the appearance of
jaundice. (Barker et al.,1996).
Hepatitis B, from 1965 to 1985, a progressive rise in reported
hepatitis B cases occurred (William; 2006). Since then, the incidence of the
disease has appeared to plateau and decline. HBV is spread mainly by blood, blood
products, and semen. Persisting viremia, meaning virus circulating in the
bloodstream, can follow both symptomatic and asymptomatic cases, and the virus
may continue to circulate in the blood for many years. (Chang; 2007). Carriers are
of major importance in the spread of hepatitis B because they are often unaware of
their infection. If only a minute amount of blood from an infected person is
infected into the bloodstream or rubbed into minor wounds, infection can
results. Blood and other body fluids can be infectious by mouth, the virus
probably infecting the recipient through small scratches or abrasion.
Many hepatitis B virus infections result from sharing of needles
by drug abusers. Unsterile tattooing and ear-piercing instruments and shared
toothbrushes, razors, or towels can also transmit HBV infections. (Majorie et al., 2001)
Sexual intercourse is responsible for transmission in nearly
half of hepatitis B cases in the united states. (William; 2006). HBV antigen is often present in saliva
and breast milk, but the quantity of infectious virus and risk of transmission
is low.
Five percent or more of pregnant women who are HBV carriers transmit the disease to their babies at
delivery, and more than two-thirds of
women who develop hepatitis late in pregnancy or soon after delivery do so.
Most of these babies have asymptomatic infections and become long-term
carriers, but some die of liver failure (Gene Nester et al., 2004).
Hepatitis C although transmitted by blood from an infected
person, the mechanism of exposure is not always obvious. Sharing tooth brushes,
razors, and towels can be responsible. Tattoos and body piercing with unclean
instruments have transmitted the disease. Approximately 60% of transmission in the united states are due to sharing of syringes by illegal drug
abusers (Mayorie et al., 2001).
Transmission by sexual intercourse is probably rare, although it apparently can
occur among those with multiple partners an sexually transmitted diseases. The
risk of contracting the disease from transfussion of a unit of blood is now
only about 0.001%. (Gene Nester et al.,
2004). The table that shows the transmission and causative agent of viral
hepatitis is shown below:
Table 1.1 viral hepatitis (Gene Nester et al., 2004
)
Disease Hepatitis
A Hepatitis B Hepatitis C
Causative agent Non-enveloped, single Enveloped, double Enveloped, single
Stranded
RNA Picornavirus, stranded DNA RNA flavivims, HCV
HAV hepadnavirus,
HBV
Mode of spread Fecal-oral
Blood, semen Blood ,possibly
semen
Incubation period 3 to
5 weeks 10 to 15 weeks 6 to 7 weeks
(range, 2 to 7 weeks) (rage, 6 to 23 weeks) ranges
2 to 24 weeks)
Prevention Gamma
globulin; Recombinant vaccine; No vaccines
Inactivated
vaccine. Immunoglobulin
Comments usually
mild symptoms, more severs than the progressive liver
but roloften ponged, full recovnery; hepatitis
A leads damage or cancer
no
long term carriers to liver damage and
also to cirrhosi
and cancer.
The able above showed the causative agent of each viral
hepatitis and their mode of transmission. From the table also it was shown that
hepatitis C has no vaccines, therefore, it can be prevented by screening of
blood donors.
1.2 FORMS OF HEPATITIS – A,B AND C VIRUS INFECTIONS
1.2.1 ACUTE HEPATITIS A VIRUS INFECTION
Hepatitis A has only one form which is acute hepatitis A
infection. Acute hepatitis A infection is a self-limiting disease with an
incubation period of 2- 6weeks. The onset is abrupt with fever, malaise,
anorexia, nausea and lethargy which comprise the podromal (Preicteric) stage.
(Arora et al., 2008). Hepatomegaly,
due to cell necrosis, causes blockage of the biliary excretion resulting in
jaundice (Goldstein et al., 1998). It
may also produce pain in the right upper abdominal quadrant. The fulminant form
of hepatitis A and liver failure can occur in less then 0.5% cases. Complete
recovery occurs in 8-12 weeks. Hepatitis A has no apparent adverse effect on
the outcome of pregnancy. (Prescott et al.,
2008).
Transmission during birth by exposure to maternal faeces or by
breast-feeding has been reported.
1.2.2 ACUTE AND CHRONIC AS
A FORMS OF HEPATITIS B VIRUS INFECTION
ACUTE HBV
INFECTION:
This is subclinical in 70% of adults. For
newly infected persons who develop acute hepatitis, the average incubation
period after infection last one to four months. Symptoms of acute HBV infection
include;
Nausea, anorexia, fatigue, low-grade fever, and right upper quadrant or epigastric pain.
Also, changes in stool colour, hepatomegaly or splenomegaly may ensure (Goldstein et al., 1998). Symptoms of acute disease resolve by one to three
months, although some persons have prolonged fatigue treatment of acute
infection is generally supportive, although some patients require
hospitalization for intravenous fluid administration (seff et al., 1987).
Acute HBV
infection leads to fulminant hepatic failure from massive hepato cellular
necrosis in about 1 percent (1%) infection. Rarely, patient with an “exuberant”
immune response present with clinical symptoms but progress hepatic
decomposition, including encephalopathy
and coagulopathy. Mortality is high, and live transplantation often is
necessary (Befeler et al., 2000). In
person who recover from HBV infection, HBsAg is eliminated from the blood and
antibody to HBsAg (anti-HBs) develops during convalescence. The presence
of immunity to HBV infection, most
person who recover from natural infection (resolved infection) will be positive
for both anti-HBs and anti-HBc. Acute hepatitis B infection can be managed by
eating high caloric diet, having a good best rest and taking vitamins.
· CHRONIC HBV INFECTION
This is defined as hepatitis B
surface antigen (HBsAg) positivity for at least six months (Lok et al., 2001). Also, according to (Liaw
et al.,1991). Chronic HBV infection is described as either the presence of
HBsAg in the serum for at least 6- months or the presence of HBsAg in a person
who test negative for immunoglobulin M (IgM) antibodies to HBcAg. Unlike
individuals who recover from acute HBV infection, persons with chronic HBV
infection do not develop anti-HBs, and
HBsAg typically persists of decades. Approximately 0.5% of adult with
chronic HBV infection will clear HBsAg and develop anti-HBs annually (Adachi et
al., 1992). In most affected individuals, chronic viral hepatitis is a
symptomatic either indefinitely or until there is sufficient liver damage for
the patient to develop manifestation of end stage liver disease leading to
cirrhosis over a period of several years. This type of infections dramatically
increases the incidence of hepato- cellular carcinoma (Liver cancer). Chronic
carrier are encouraged to avoid consuming alcohol as it increases risk for
cirrhosis and liver cancer. HBV has been linked to the development of
membranous glomerulonephritis (MGN) (Lai et
al., 1991).
Person with chronic HBV infection
should receive periodic medical evaluation and some authorities recommended
regular screening for hepato cellular using alpha-fetoprotein or ultrasonography
(Lok et al., 2001).
Recently approved therapeutic
agents for treatment of chronic hepatitis B are numbering used to achieve
sustained suppression of HBV replication and remission in liver disease for
some patients.
However, adverse events
associated in the treatment, expense, development of antiviral resistance and
low rates of HBsAg clearance remain barriers for treatments in many patients in
with chronic infection.
1.2.3 ACUTE AND CHRONIC
FORMS OF HEPATITIS C VIRUS
INFECTION
· ACUTE HCV INFECTION:
Exposure to HCV infection can cause acute hepatitis in majority
(about 80%) of the patients of whom 10-20% progress to liver cirrhosis with an
increased risk of hepato cellular carcinoma (HCC). (Bond et al., 1997). The virus causes liver cell damage either by immune
mediated mechanism against the virus infected hepatocytes or by direct
cytopathetic effect. T4 and cytotoxic T cell play a dominant role in the immune
mediated injury. This results in necroinflammatory changes in the liver, which
may resolve after acute infection. (Arora et
al; 2008).
However, in some of the patients, low-grade necroinflammation continues
leading to chronic HCV infection.
·
CHRONIC HCV INFECTION:
Autoimmune thyroiditis is the
most common disorder in patients with chronic HCV infection. (Martin-Ancel et
al., 2004). It also causes lymphocytic sialadenitis with Xerostomia,
thrombocytopenic purpura, non-Hodgkin lymphoma, diabetes mellitus and
polyarteritis nodosa in 8-36%, 88%, 20-40%, 14% and 5-50% of patients with
chronic HCV infection respectively. (Arora et
al., 2008)
The most serious late outcome of
chronic HCV infection is HCC. HCV is frequently detected in patients with
hepatocellular carcinoma (HCC) with high rates being found in southern Europe,
and Japan, intermediate in Australia, Taiwan and Saudi Arabia and low in United
States and South Africa (WHO).
1.3 STRUCTURE OF THE
VIRUSES:
Hepatitis A virus (HAV) is a
non-enveloped, single stranded RNA enterovirus (Marjorie et al., 2001). The disease is caused by the hepatitis A virus (HAV)
of the genus Hepatovirus in the family picornaviridae (Locarnini, 2004). In general,
HAV disease is far milder and shorter term than the other forms. (Pungpapony et
al., 2007).
Hepatitis B virus (HBV) is a
member of the hepadnavirus family it is a 42-nm enveloped virion, with an
icosahedral nucleocapsid core containing a partially double-stranded circular
DNA genome.
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