Chronic persistent hepatitis

CPH is a mild non-progressive inflammation limited to the portal triad (Triaditis) but without hepatic necrosis or fibrosis. It can occur following hepatitis B or hepatitis non-A non-B.

The patient is usually asymptomatic or may have mild discomfort over right quadrant, malaise, fatigue, anorexia and weight loss. Serum bilirubin, SGOT, SGPT and alkaline phosphatase may be elevated but serum albumin and prothrombin time are normal.

Liver biopsy gives the diagnosis. There is no specific treatment.

Chronic active hepatitis

CAH is an aggressive and progressive inflammation of the liver cells with piecemeal necrosis and fibrosis which can lead to cirrhosis.

It occurs following hepatitis B and hepatitis non-A non-B viruses.

Some patients are asymptomatic and detected by abnormal blood tests done on routine check-up. In most of the patients there is severe illness with fever, malaise, pain in the right hypochondriac region, edema or ascites.

Autoimmune features like arthralgia and arthritis, skin eruption and pleurisy may be present. Secondary amenorrhea and infertility may be present in females. Serum bilirubin, SGOT, SGPT prothrombin time and gamma globulins are markedly elevated.

Serum albumin is low. Antinuclear, antithyroid and anti-smooth muscle antibodies are present and LE cell preparations may be positive. Liver biopsy shows severe hepatic necrosis involving the hepatic lobule in an irregular and patchy manner (piecemeal necrosis).

In severe cases, bands of necrosis may join the adjacent portal tracts and central vein (bridging hepatic necrosis). In untreated cases, this may progress to cirrhosis with fibrosis and regenerating nodule.

The course in an untreated case is gradually downhill, with development of cirrhosis and all its complications like encephalopathy, ascites and bleeding esophageal varices.

Prednisolone alone and in combination with azathioprine significantly improve survival even when cirrhosis has developed.