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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).
· 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
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
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
· 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
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