Hepatitis Central

95% of adult patients who develop acute Hepatitis B will recover so that only less than 5% become persistently infected.

Fulminant hepatitis which has a high mortality rate unless liver transplantation occurs actually happens in only 1% or less of patients with acute Hepatitis B.

Of those patients who are persistently infected, the majority will be asymptomatic carriers although some patients will develop chronic hepatitis.

It is the group of patients who develop ongoing chronic hepatitis who are at risk of developing cirrhosis and ultimately dying from liver failure due to this.

All patients with chronic Hepatitis B, whether they have chronic hepatitis or are asymptomatic carriers, are at risk of developing hepatocellular carcinoma.

However in Western societies the majority of patients who do develop liver cell cancer have pre-existing cirrhosis.

Serology

Serologically in chronic Hepatitis B what one sees is a high titer of Hepatitis B surface antigen over weeks to years. This is unlike the case in acute Hepatitis B where surface antigen levels drop off within a period of weeks and become undetectable with the appearance of surface antibody.

Chronic carriers do not develop protective levels of Hepatitis B surface antibody. Core antibody is detectable in chronic carriers, usually this is of the IgG fraction. Core IgM antibody can be found in either acute Hepatitis B or in the reactivation of Hepatitis B in a chronic carrier.

Also characteristically in chronic Hepatitis B carriers, Hepatitis Be antigen and Hepatitis B viral DNA remain detectable in serum over months to years. In liver cells Hepatitis B DNA exists in a non-integrated or episomal form. After a period of many years, for reasons that are not totally understood, Hepatitis B DNA integrates into the host genome and at that point viral replication drops off.

Hepatitis B DNA is no longer detectable in serum and e antigen converts to e antibody.

However patients do remain Hepatitis B surface antigen positive. The spontaneous clearance of Hepatitis B surface antigen occurs in Eastern populations at 0.5 to 0.8% per annum.

In Western societies this is slightly higher at 1-2% per annum, but overall spontaneous clearance of Hepatitis B surface antigen is uncommon.