ANALYSIS THE ALPHA-PROTEIN LEVEL IN HEPATITIS PATIENT AS AN AID IN ACCESSING THE DEGREE IN WHICH IT GENERATES TO HCC


ANALYSIS THE ALPHA-PROTEIN LEVEL IN HEPATITIS PATIENT AS AN AID IN ACCESSING THE DEGREE IN WHICH IT GENERATES TO HCC

CHAPTER ONE

1. 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.

1.0 LITERATURE REVIEW:

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.

Figure 1.1: viral particles (Warren levinson et al., 2000)

The envelope contains a protein called the surface antigen (HBsAg), which is important for laboratory diagnosis and immunization. Within the core is a DNA- dependent DNA polymerase. The genome contains four genes (four open reading frames) that encode the following proteins. Surface (envelope) protein, core (nucleocapsid) protein, DNA polymerase, and X protein, an activator of viral RNA dependent (reverse transcriptase) and DNA dependent activity.

Hepatitis C virus (HCV) is a member of the flavivirus family. It is an enveloped virion containing a genome of single-stranded, positive-polarity RNA. (Earnest Jawetz et al., 2000).

It has no virion polymerase. HCV has six serotypes and multiple subtype based on differences in its envelope glycoprotein. This antigenic variability is due to the high mutation in the gene encoding one of the two envelop glycoprotein’s. (Warren Levinson et al., 2000).

1.4 TRANSMISSION OF HAV, HAV AND HCV

⦁ Hepatitis A virus:

There is an important distinction between this virus and hepatitis B and hepatitis C viruses. Hepatitis A virus is spread through the fecal-oral route (and is sometimes known as infectious hepatitis) (Mayorie et al., 2001)

In general, the disease is associated with deficient personal hygiene and lack of public health measures. In countries with inadequate sewage control, most out breaks are associated with fecally contaminated water and food. The united states has a yearly reported incidence of 15,000 to 20,000 cases. (Kathleen et al., 2004). Most of these result from close institutional contact, unhygienic food handling, eating shellfish, sexual transmission, or travel to other countries. In 2003, the largest single hepatitis A outbreak to date in United States was traced to contaminated green onions used in salsa dips at a Mexican restaurant. At least 600 people who had eaten at the restaurant fell ill with hepatitis A. (UNICEF).

In developing countries children are the most common victims because exposure to the virus tends to occur early in life, whereas in North America and Europe, more cases appear in adults. Becauses the virus is not carried chronically, the principal reserviours are asymptomatic, short-term carriers (often children) or people with clinical disease (Arora et al., 2008).

⦁ Hepatitis B virus (HBV):

Hepatitis B virus infection can be transmitted to individuals in so many ways which includes, transmission by percutaneous or mucosal exposure to infected blood or other body fluids. HBV transmission has  been observed with numerous forms of human contacts. Perinatal household (non sexual), sexual, needle sharing and occupational (Health care related). The highest concentration of infected HBV are found in blood and serum. However, other serum deprival body fluids such as semen and saliva are also infection (Bond et al., 1977). Person with chronic HBsAg is potentially infectious to both household and sexual contacts. Transmission through sexual contacts of chronically infected persons has shown to have higher prevalence of HBV infection than control populations including household, contact of infected person (Heath cote et al., 1974). Men who are homosexual have long been known to have high rate of the diseases (Dietzman et al., 1977). Injection drug users are at high risk for HBV infection because of behaviours such as sharing of needles, syringes and other drug paraphemalia. On the basis of data collection more than 19 years ago, the majority of injection drug users in the south East  and elsewhere have serologic evidence of past or current HBV infection (Levine et al., 1994). Outbreaks linked to other percutaneous exposure besides injection drug use, such as tattoing and acupuncture have been reported (Limentani et al., 1979). Health care related transmission long been recognized as an important source of new HBV infections world wide provide-to patient, patient –to-provider and patient-to-patient transmission have all been observed although the frequencies with which these type of transmission occur are widely divergent. Patient-to-provider transmission was common before wide spread hepatitis B vaccination of health care workers. It is estimated that 12,000 health care workers per year were infected in the united state in the prevaccine era (Hadler et al., 2000). Patient-to-patient HBV transmission is a major source of new HBV infection in the developing world. Patient-to-patient HBV transmission can result from percutaneous exposure to contaminated equipment used for injection or other procedure or from blood or mucosal exposure to contaminated medication. In developing countries, exposure to contaminated therapeutic injection equipment are common in many setting because of lack of awareness of infection control practices, lack of resources for sterilization and the purchase of new disposable equipment, and economic incentives and preference favouring over use of injections. Contaminated injections caused as estimated 21 million HBV infections world wide in 2000, accounting for 32% of all new infections (Hauri et al., 2004).

Transmission of HBV via blood transfusion products has been largely eliminated in most part of the world by screening blood donors and implementing techniques that ensure viral inactivation  of products made from blood such as factor concentrates (Busch et al., 2003).

⦁ Hepatitis C virus (HCV)

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. (Bush et al., 2003). Approximately 60% of transmissions in the united states are due to sharing of syrings by illegal drug abusers. Transmissions by sexual intercourse is probably rare, although it apparently can occur among those with multiple patners. The risk of contracting the disease from transfusion of a unit of blood is now only about 0.001% (WHO).

1.4.1 MECHANISMS OF INFECTION OF HOST CELLS BY HEPATITIS A, B AND C.

Hepatitis A (infectious hepatitis) usually is transmitted by fecaloral contamination of food, drink or shellfish that live in contaminated water and contain the virus in their digestive system (Prescott et al., 2005).

The hepatitis A virus is an icosahedral, linear, positive-strand RNA virus that lacks an envelope. Once in the digestive system, the viruses multiply within the intestinal epithelium. Usually only mild intestinal symptoms result. Occasionally viremia (the presence of viruses in the blood occurs and the viruses may spread to the liver (Prescott et al., 2005).

The virus reproduce in the liver, enter the bile, and are release into the small intestine. This explains why feces are so infections..

Hepatitis B virus enters the liver via the blood stream and replicates only in liver tissue. The intact, infections virus is 42-47nm in diameter and circulates in the blood in concentration as high as 108 virions per ml. The inner core of the virus contains hepatitis B core antigen, hepatitis B surface antigen (HBsAg),  a partially double-stranded 3, 200 nclueotide DNA molecule, and DNA polymerase with reverse transcriptase activity. Infection with hepatitis B virus is associated with a board spectrum of liver injuring ranging from acute self injured infection to fulminant hepatitis. Approximately 5-10% of adults who are infected with hepatitis B virus will go on carry the virus for the rest of their lives. These people will pass the virus into others (Horizontal transmission). The route of transmission can occur in homosexual or heterosexual activity, blood-borne exposure, needles (transfusion), mother-infant (Vertical transmission), close personal contact and even by consuming contaminated food or drinks (Mcmabon et al., 1985).

Hepatitis C virus is transmitted by contact with virus-contaminated blood, by the fecal-oral route, by utero transmission from mother to foetus, sexually or through organ transplantation. (Prescott et al., 2005).

1.5 HEPATITIS INFECTIONS AS A PREDISPOSING FACTOR TO HCC.

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. Patients  who are HBsAg positive develop chronic persistent hepatitis (CPH) and chronic active hepatitis (CAH). Patients with chronic active hepatitis have progressive liver damage with the outcome being portal fibrosis, cirrhosis or hepatocellular carcinoma (HCC) while patient with chronic persistent hepatitis usually remain in good health (Basil et al., 2003).

People with either chronic hepatitis B (HBV) or hepatitis C (HCV) have an increased risk of developing HCC. However the mechanism of causing HCC differs for HBV and HCV.

⦁ HEPATITIS B:

There is a strong correlation between chronic hepatitis B and the development of HCC. Furthermore, HCC can occur in people with chronic HBV even in the absence of cirrhosis. This is partly because HBV is a DNA virus and may actually in-corporate it’s DNA to hepatocytes DNA of the infected person promoting gene mutation which may lead to HCC even without underlying cirrhosis. People doubly infected with both HBV and HCV do carry an increased risk of- HCC (Melissa 2004).

⦁ HEPATITIS C

A strong correlation exists between chronic hepatitis C and the development of HCC. In contrast to hepatitis B, cirrhosis is present in all hepatitis C-associated HCC, possibly because HCV is an RNA virus and cannot incorporate itself into host DNA. Certain undefined HCV protein may also contribute to the formation of HCC (Melissa 2004).

1.5 SIGNS AND SYMPTOMS OF HEPATITIS A, B, AND C INFECTION.

⦁ HEPATITIS A INFECTION

Most infections by this virus are either subclinical or accompanied by vague, flu-like symptoms. In more overt cases, the presenting symptoms may include jaundice and swollen liver (Goldstein et al., 1998). Darkened urine is often seen in this and other hepatitis. Jaundice is present in only about 10% of the cases. Hepatitis A occasionally occurs as a fulminating disease and causes liver damage, but this manifestation is quite rear. The virus is not oncogenic (Cancer causing), and complete uncomplicated recovery results.

⦁ HEPATITIS B INFECTION:

The clinical signs of hepatitis B vary widely. Most cases are asymptomatic. In most cases, you will have a fever and other symptoms of a viral syndrome that will clear up by itself. However, in about 10% of cases, your body may not be able to clear all the virus, and you will then be a “Carrier” of hepatitis B. if you are a carrier, the virus may lurk in your blood for years and gradually wreak havoc on your liver. 

Symptoms of disease include; patigue, loss of appetite, Abdominal discomfort, nausea, Brown or dark urine, weakness and other symptoms gradually appear following an incubation period of 6weeks-6months. The virus infects liver hepatic cells and causes liver tissue degeneration and release of liver associated enzyme (Transaminase) into the blood stream. This is followed by jaundice, the accumulation of bilirubin (a break down product of haemoglobin) in the skin and other tissue with a resulting yellow appearance (Joanne et al., 2008). Acute infection with HBV in a patient causes more severe liver disease fulminant hepatic failure while chronic HBV infection also cause the development of primary liver caner known as hepatocellnlar carcinoma.

⦁ HEPATITIS C INFECTION:

The symptoms of hepatitis C are the same as hepatitis A and B except generally milder. About 65% of infected individuals have no symptoms relating to the acute infection, while only about 25% have Jaundice.

1.7 DIAGNOSIS OF HEPATITIS A, B AND C:

⦁ HEPATITIS A INFECTION:

Diagnosis of the disease is aided by detection of anti-HAV IgM antibodies produced early in the infection and by tests to identify HA antigen or virus directly in stool sample.

A patients history, liver and blood tests; serological test, and viral identification all play a role in diagnosing hepatitis A and differentiating it from the other forms of hepatitis. Certain liver enzymes are elevated, and leukopenia is common. There is no specific treatment for hepatitis A once the symptoms begins. Patients who receive immune serum globulin early in the disease usually experience milder symptoms than patients who do not receive it.

⦁ HEPATITIS B INFECTION:

A blood test is the only way to tell whether you are infected. Hepatitis B viral antigens and antibodies detectable in the blood following acute infection. Hepatitis B viral antigens and antibodies are detectable in the blood of a chronically infected person. The test called assays for detection of hepatitis B virus infection involve serum or blood test that detect either viral antigens (Proteins produced by the virus) or antibodies (Produced by the host). Interpretation of these assay is complex (Bonino et al., 1987).

The hepatitis B surface antigen (HBsAg) is most frequently used to screen for the presence of this infection. It is the first detectable viral antigen to appear during infection. However, early in an infection this antigen may not be present and it may be undetectable later in the infection as it is being cleared by the host. The infection virion  contain an inner “core particles” enclosing viral genome. The icosahedral core particles is made up of 180 or 240 copies of core protein, alternatively known as hepatitis B core antigen (HBcAg). During this “window” in which the host remains infected but is successfully clearing the virus, immunoglobin M antibodies to HBcAg (anti-HBclgM) may be the only serological evidence of disease.

Shortly after the appearance of the HBsAg, another antigen named as the hepatitis B e antigen (HBeAg) will appear. Traditionally, the presence of HBcAg in a host’s serum is associated with much higher rates of viral replication and enhanced in effective, however variants of the hepatitis B virus do not produce the “e” antigen, so this rule does not always hold true. During the natural course of an antibodies to the “e” antigen will arise immediately afterwards. This conversion is usually associated with a dramatic decline in viral replication. If the host is able to clear the infection, eventually the HBsAg will become undetectable and will be followed by IgG antibodies to the HBsAg and core antigen (anti-HBs and anti-HBclgG) (Zuckerman et al., 1996).

Individual negative for HBsAg but positive for anti-HBs has either cleared an infection or has been vaccinated previously. Individual who remain HBsAg positive for at least six months are considered to be hepatitis B which would be reflected by elevated serum alanine aminotransferase levels and inflammation of the liver revealed by biopsy.

More recently, polymerase chain reaction (PCR) test have been developed to detect and measure the amount of viral nucleic acid in clinical specimens. These test are called viral loads and are used to asses a person’s infection status and to monitor treatment (Zoulin; 2006).

⦁ HEPATITIS C INFECTION

This virus is transmitted by contacts with virus-contaminated blood, by the fecal-oral route, by utero transmission from mother to foetus, sexually or through organ transplantation.

Diagnosis is made by a first-generation enzyme-linked immunosorbent assay (ELISA), which detects serum antibody to a recombinant antigen of hepatitis C virus.

1.8 TREATMENT OF HEPATITIS A, B, AND C INFECTION.

1.8.1 HEPATITIS A INFECTION

No specific medicine is available for hepatitis A once the symptoms begins. Drinking lots of fluids and avoiding liver irritants, such as aspirin or alcohol, will speed recovery. Patients who receive immunoglobulin early in the disease usually experience milder symptoms than patients who do not receive it.

1.8.2 HEPATITIS B INFECTION

Although none of the available drugs can clear the infection, they can inhibit the virus from replication and immunize liver damage such as cirrhosis and cancer. Currently, there are seven medications licensed for treatment of hepatitis B infection, these includes: Antiviral drugs such as:- Lamivadine (Epivir), Adefovir (Hepsera), Tenofovir (Viread), Telbivaudine (Tyzeka), Entecavir (Baraclude), two immune system modulators interferon alpha 2a and peglated interferon alpha-2a (pagasys).

The use of interferon which requires infections daily or thrice weekly has been supplanted long-acting pegylated interferon which injected only once weekly (Dienstag; 2008) some individuals are much more likely to respond  than other and thus might because of the genotype of the infecting virus or the patients heredity. The treatment works by reducing the viral load  (the amount of virus particles as measured in the blood) which in turn reduces viral replication in the liver.

1.8.3 HEPATITIS C INFECTION

This is no satisfactory treatment for the chronic disease, although 30% to 50% of individuals are helped by interferon injections combined with ribavirin, antiviral nucleoside derivative prolonged interferon treatment of the acute illness may prevent the chronic disease.

1.9 HEPATITIS A, B, AND C VACCINES

1.9.1 HEPATITIS A

Hepatitis A vaccine consisting of formalin inactivated preparation of virions grown in human fibroblast or monkey kidney cell lines, adsorbed to alum as an adjutant can be used for active immunization. Two doses infected one month apart with or without a booster after 6months elicit a good immune response in 99% of vaccines lasting for some years. Because of the low yield of virus from cultured cells the vaccine is costly. It may be given to high risk individuals like long-term visitors to countries in which HAV is endemic, sewage worker, sexually active homosexual men and intravenous drug users. (Arora et al., 2008).

1.9.2 HEPATITIS B

Several vaccines have been developed for the prevention of HBV infection. These rely on the use of one of the viral envelop protein (Hepatitis B surface antigen HBsAg). The vaccines was originally prepared from plasma obtained from patients who had long standing hepatitis B virus infection. However, currently, these are more often made using recombinant  DNA technology, through plasma-derived vaccines continues to be used, the two types of vaccines are equally effective and safe (Zuckerman, 2006).

Following vaccination, hepatitis B surface antigen may be detected in serum for several days; this is known as vaccine antigenamia (Martin-Ancd et al., 2004). Vaccine is generally administered in either a two, three or four doses schedules (2, 3 or 4 doses) and can be received by infants to adults. It provides for 85-90% of individuals (Joint Committee on vaccination and immunization, 2006) and last for 23years (Mayoclinic staff; 2008).

More so, active prophylactic with recombinant vaccines energix-B, recombinant HB pediatrix and twinix (Joanne et al., 2008). These vaccines are widely used and are commended for routine prevention of HBV in infants to 18years old, and risk groups of all ages (for example, household contacts of HBV carriers, health care and public safety professionals, men who have sex with other men (MSM), international travelers hemodialysis patients.

1.9.3 HEPATITIS C

There is no vaccine for hepatitis C infection. Control measures focus on prevention activities that reduce risks for contracting HCV. These include: screening and testing blood, plasma, organ, tissue, and semen donors; virus inactivation of plasma derived products, counseling of persons with high-risk drug or sexual practices, implementation of infection control practices in health care and other settings and professional and public education (Geo et al., 2004).

1.10 PREVENTION AND CONTROL OF HEPATITIS A, B AND C INFECTION

1.10.1HEPATITIS A INFECTION

The appearance of hepatitis in camps or institutions is often an indication of poor sanitation and poor personal hygiene. Prevention of hepatitis A is based primarily on immunization. An inactivated viral vaccine (Havrix) is currently approved, and an oral vaccine based on an attenuated strain of virus is in development.

Control measures are directed towards the prevention of fecal contamination of food, water, or other sources by the individual. Reasonable hygiene such as hand washing, the use of disposable plates and eating utensils, and the use of 0.5% sodium hypochlorite (eg, 1:10 dilution of chlorine bleach) as a disinfectant-is essential in preventing the spread of HAV during the acute phase of the illness.(Geo et al., 2004).

1.10.2 HEPATITIS B INFECTION

General measures for prevention and control of HBV infection include:-

⦁ Excluding contact with HBV-infected blood and secretion

⦁ Minimizing accidental needle-sticks

⦁ Passive prophylaxis with intramuscular injection of hepatitis B immunoglobulin with 7 days of exposure

⦁ Avoiding unprotected sexual contact

⦁ Avoiding blood transfusion

⦁ Screening of blood donors

⦁ Preparations of plasma-derived products in a way that inactivates HBV.

⦁ Implementation of infection control measures.

⦁ Avoiding reuse of contaminated needles and syringes. (Mayoclmistaff 2008)

1.10.3 HEPATITIS C INFECTION

Hepatitis C infection can be prevented by screening of blood donors, avoidance of use of unsterile needles for intravenous drug abuse, tattooing and for medical and dental procedures. Many of the public health measures adapted to prevent transmission of human immune deficiency virus and HBV by parenteral routes will assist efforts at controlling HCV.

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ANALYSIS THE ALPHA-PROTEIN LEVEL IN HEPATITIS PATIENT AS AN AID IN ACCESSING THE DEGREE IN WHICH IT GENERATES TO HCC



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