Chronic HBV infection can be entirely bening with normal liver blood tests (chronic carrier state) or my be an aggressive inflammatory process (chronic active hepatitis) which can lead  to severe scarring(cirrhosis). The risk of liver cancer(     hepatoma)is high in cirrhosis caused by HBV

RISK OF HEPATOCELLULAR CARCINOMA IN CIRRHOTIC
HEPATITIS B PATIENTS

Hepatitis B :
          – There is a chance the condition will clear up on it’s own. (2-5% per year)
          – There is an increased risk of liver cancer (5%)
          – There is risk of liver cirrhosis (25%) or other severe liver problems. This is most likely if you have chronic active HB. This can be fatal and a liver transplant may be required.
– You may be highly infectious and can infect other people.

(Around 10% of cases do not clear up completely and a chronic infection remains)

Hepatocellular carcinoma (HCC) is a well known complication of chronic hepatitis B (HBV) infection. The risk appears to be related to the duration of infection.  Asian patients who acquire the disease in childhood, by virtue of the long duration of the disease, are at a significantly higher risk of developing HCC. The cumulative probability of developing HCC in patients who are HBsAg-positive has been estimated to be 6% at 5 years and 15% at 10 years. Once HCC develops, the prognosis is very poor. Survival of patients with symptomatic untreated tumours beyond 3 years is rare.

Apart from cirrhosis, other factors that increase the patient’s risk for developing HCC include long duration of infection, male gender, greater than 55 years, continued alcohol consumption and co-infection with HBV. Having cirrhosis increases the risk of developing hepatocellular carcinoma (50% of persons with hepatoma have cirrhosis).

The relationship between persistent HBV infection and HCC, which usually develops decades after onset of infection, has been well documented. A large prospective study, conducted in Taiwan, reported a relative risk of 98 after 8.9 years of follow-up. Chronic infections resulting from maternal- neonatal transmission present a greater risk of HCC than those acquired as adults, probably reflecting differences in the incubation time. Whereas it is probably the etiologic agent for the vast majority of HCC in Asia and Africa, HBV can be implicated in only 20% of HCC cases in low
endemic regions (North America and Europe) and Japan. Cirrhosis, found in 60% to 90% of patients, is the best known precursor, but HCC may occur independently from this lesion. Other risk factors for HCC among HBsAg carriers are
male gender and age over 40 years.

Large studies where people acquired infection at birth or in early childhood reported an annual probability of developing HCC in chronic HBV carriers of 0.49% per year in Taiwan (among men) and of 0.4% per year and 0.06% per year in male and female Alaskan natives. In Toronto, Sherman, et al reported hepatoma to be as frequent as in endemic regions for HBV, with an annual incidence of 0.47% per year (0.66% per year in men). Studies in Western Caucasian populations have reported no occurrence of HCC in asymptomatic young carriers followed for 11 years and 16 years. The prevalence of cirrhosis, a major risk factor for HCC might have been low in those patients. On the other hand, the risk of developing HCC in Caucasian carriers from low endemic areas where transmission of HBV infection occurs mainly in later life, is likely to be very low. However, HCC in non-cirrhotic livers has been reported to occur in chronic hepatitis B.