Biochemistry

Analysis of the Alpha-protein Level in Hepatitis Patient as an Aid in Assessing the Degree in Which It Generates to HCC

Analysis of the Alpha-protein Level in Hepatitis Patient as an Aid in Assessing the Degree in Which It Generates to HCC

CHAPTER ONE

1.0 INTRODUCTION

Hepatocellular carcinoma (HCC) is the most common primary liver cancer. It accounts for 60% of all cancer worldwide (Melissa 2004). The most significant cause is the presence of cirrhosis. HCC has unique geographic sex, age distribution that is likely determined by specific aetiology factors. Its distribution also varies among ethnic groups 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 southeastern Nigeria. However, a recent trend that reveals an increase in cases of liver cirrhosis and hepatitis in our environment suggests that there could be other contributory factors peculiar to our environment besides hepatitis B and C which could be a possible explanation for 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 the 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 hepatocellular carcinoma (HCC), common to the blood-borne types (HBV and HCV). Without a 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 hepatitis patients as an aid in assessing the degree to which it degenerates to HCC.

1.1 EPIDEMIOLOGY OF VIRAL HEPATITIS:

Hepatitis A virus spreads by the faecal-oral route, principally through faecal contamination of hands, food, or water. Many outbreaks 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 concentrate on 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 daycare centres and nursing homes and homosexual men. Infants and children with hepatitis A can eliminate the virus in their faeces for several months after symptoms begin, but the amount of virus in faeces 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 a 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 injected into the bloodstream or rubbed into minor wounds, the 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 viruses and risk of transmission is low.

Five per cent 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 toothbrushes, 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 and sexually transmitted diseases. The risk of contracting the disease from transfusion of a unit of blood is now only about 0.001%. (Gene Nester et al., 2004).

REFERENCES

Adachi, H., Kaneko, S, Matsushia, E. (1992) Clearance of HBsAg in seven patients with chronic hepatitis B Hepatology 16: 1334-1337.

Alter, M. J. (2003). Epidemiology & prevention of hepatitis B. Seminar in Liver Disease 23 (1): 39-46.

Barker, L.F., Shulman, N.R., and Murray, R, .(1996). Transmission of serum hepatitis. Journal American Medical Association 276 (10):841-844.

Beasley, R.P. (1988) Hepatitis B and C virus as the etiologic agent in hepatocellular carcinoma-Epidemiologic considerations. Hepatology 2 (suppl): 231-265.

Beck, J., and Nassal, F. (2007). Hepatitis B virus replication World Journal of Gastroenterology 13(1): 48-64.

Befeler, A.S, and Di Bisceglie, A.M. (2000). Hepatitis B infections diseases. Clinical North America 34: 1225-1241.



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