Chronic hepatitis is defined as inflammation of the liver persisting for more than 6 months.

Chronic hepatitis it is not a single disease but a syndrome with many causes.
It is clinically defined as persistent abnormal liver function tests of hepatitic type of 6 months' duration.

There are three main types of chronic hepatitis, each of which carries a different risk of developing into cirrhosis.

In chronic active hepatitis (CAH), which is also known as 'chronic aggressive hepatitis', inflammatory changes are associated with continued necrosis of liver cells.
 
The main complication of this pattern of chronic hepatitis is the development of cirrhosis.

In some cases, necrosis extends from one portal area to another (bridging necrosis) early in the course of disease and is an index of likely rapid progression to cirrhosis.

In chronic persistent hepatitis (CPH), inflammation is confined to the portal tracts, and necrosis of liver cells is not seen.
Generally this type of chronic hepatitis is not associated with development of progressive fibrosis or cirrhosis. However, some patients who exhibit this pattern of inflammation and are HBeAg-positive (indicating active viral replication) progress to
chronic active hepatitis, with seroconversion to anti-HBeAg positivity and development of cirrhosis.

Patients with CPH due to HCV infection may also develop progressive disease with cirrhosis. 

In chronic lobular hepatitis (CLH) there is inflammation of portal tracts, with spotty parenchymal inflammation but no piece-meal necrosis.
This pattern of chronic hepatitis is usually associated with a viral aetiology.
Cases that are associated with hepatitis B infection and are positive for HBeAg may later develop chronic active hepatitis.
Other cases generally do not progress to cirrhosis.

Histologically there is lymphocytic inflammatory infiltration in portal tracts, which spills over into the adjacent parenchyma.
Piecemeal necrosis of liver cells is seen at the interface with the connective tissue of the portal tract. With time, this necrosis extends, star-like, from portal areas and, in late stages, progresses to bridging fibrosis between adjacent portal tracts.

In chronic persistent hepatitis, lymphoid infiltration is seen in portal tracts. However, in contrast to chronic active hepatitis, there is no necrosis of liver cells in the limiting plate.

Chronic hepatitis following viral infection may progress to cirrhosis

Following infection by hepatitis B or hepatitis C viruses, a proportion of patients develop persistent viral infection and chronic hepatitis.

In hepatitis B infection liver cells have a characteristic 'ground glass' appearance.
In these cases, evaluation of HBeAg and anti-HBeAg can be used to predict likely progress to cirrhosis.
Patients who have chronic active hepatitis are at risk of developing cirrhosis.

An important complication of chronic infection by hepatitis B and C is the development of hepatocellular carcinoma.

Some patients present with advanced chronic liver disease and no clinical history of acute hepatitis, yet can be shown to have viral infection by serology and liver biopsy. In these cases it is assumed that there has been sub-clinical acute infection.

In chronic hepatitis due to hepatitis B infection, liver cells accumulate HBsAg in the cytoplasm, which appears homogeneous, pale and glassy. These so-called 'ground glass' hepatocytes may be immunostained by antibodies to HBsAg, where they are stained brown.