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HEPATITIS B DISEASE
Hepatitis B virus is the cause of what was formerly known as “serum hepatitis.” This name was used to distinguish it from “infectious hepatitis” and reflected the association of this form of hepatitis with needle use or blood transfusion. Hepatitis B is usually an asymptomatic or limited illness with fever and jaundice for days to weeks. It becomes chronic in up to 10% of patients and may lead to cirrhosis or hepatocellular carcinoma.
Hepatitis B infection is found worldwide, with prevalence rates varying markedly between countries. Chronic carriers constitute the main reservoir of infection: in some countries particularly in the far East, as many as 5 to 15% of all persons carry the virus and most are asymptomatic. About 10% of patients with human immunodeficiency virus (HIV) infection are chronic carriers of hepatitis B.
In the United States, it is estimated that 1.5 million people are infected with he-patitis B and that 300,000 new cases occur annually. About 300 of these patients die of acute fulminant hepatitis, and 5–10% of infected patients become chronic hepatitis B virus carriers. As many as 4000 people die yearly of hepatitis B–related cirrhosis, and 1000 die of hepatocellular carcinoma. Approximately 50% of infections in the United States are sexually transmitted, and the prevalence of HBsAg in serum is higher in certain populations, such as male homosexuals, patients on hemodialysis or immuno-suppressive therapy, patients with Down’s syndrome, and injection drug users. Routine screening of blood donors for HBsAg has markedly decreased the incidence of post-transfusion hepatitis B. Multiple-pool blood products still cause occasional cases. Exposure to hepatitis viruses from direct contact with blood or other body fluids, probably through needlestick injuries, has resulted in a higher risk of hepatitis B in medical personnel. Attack rates are also high in spouses and sexual partners of in-fected patients.
Hepatitis B infection of infants does not appear to be transplacentally transmitted to the fetus in utero but is acquired during the birth process by the swallowing of infected blood or fluids or through abrasions. The rate of virus acquisition is high (up to 90%) in infants born to mothers with acute hepatitis B infection or carrying HBsAg and HBeAg. Most infants do not develop clinical disease; however, infection in the neonatal period is associated with failure to produce antibody to HbsAg, allowing chronic carriage to occur in nearly 100% with perpetuation of transmission in the family setting.
Hepatocellular carcinoma has been strongly associated with persistent carriage of hepatitis B virus by serologic tests and by detection of viral nucleic acid sequences in-tegrated in tumor cell genomes. In many parts of Africa and Asia, primary liver cancer accounts for 20 to 30% of all types of malignancies, but in North and South America and Europe, only 1 to 2%. The estimated risk of developing the malignancy for persons with chronic hepatitis B is increased between 10- to more than 300-fold in different populations.
In the past, hepatitis B was known as posttransfusion hepatitis or as hepatitis associated with the use of illicit parenteral drugs (serum hepatitis). However, over the past few years it has become clear that the major mode of acquisition is through close personal contact with body fluids of infected individuals. HBsAg has been found in most body fluids, in-cluding saliva, semen, and cervical secretions. Under experimental conditions, as little as 0.0001 mL of infectious blood has produced infection. Transmission is therefore possible by vehicles such as inadequately sterilized hypodermic needles or instruments used in tat-tooing and ear piercing.
The factors determining the different clinical manifestations of acute hepatitis B are largely unknown; however, some appear to involve immunologic responses of the host. The serum sickness–like rash and arthritis that may precede the development of symp-toms and jaundice appear to be related to circulating immune complexes that activate the complement system. Antibody to HBsAg is protective and associated with resolution of the disease. Cellular immunity also may be important in the host response, because pa-tients with depressed T-lymphocyte function have a high frequency of chronic infection with the hepatitis B virus. Antibody to the HBcAg, which appears during infection, is present in chronic carriers with persistent hepatitis B virion production and does not ap-pear to be protective.
The morphologic lesions of acute hepatitis B resemble those of other hepatitis viruses. In chronic active hepatitis B, the continued presence of inflammatory foci of in-fection results in necrosis of hepatocytes, collapse of the reticular framework of the liver, and progressive fibrosis. The increasing fibrosis can result in the syndrome of post-necrotic hepatic cirrhosis.
Integrated hepatitis B viral DNA can be found in nearly all hepatocellular carcinomas. The virus has not been shown to possess a transforming gene but may well activate a cel-lular oncogene. It is also possible that the virus does not play such a direct molecular role in oncogenicity, because the natural history of chronic hepatitis B infection involves cycles of damage or death of liver cells interspersed with periods of intense regenerative hyperplasia. This significantly increases the opportunity for spontaneous mutational changes that may activate cellular oncogenes. Whatever the mechanism, the association between chronic viral infection and hepatocellular carcinoma is clear, and liver cancer is a major cause of disease and death in countries in which chronic hepatitis B infection is common. The proven success of combined active and passive immunization in aborting hepatitis B infection in infancy or childhood makes hepatocellular carcinoma of the liver a potentially preventable disease.
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