Chronic Active Hepatitis or Postnecrotic Cirrhosis

The term chronic hepatitis implies a continuing inflammatory process without improvement for at least 6 months, that may become irreversible. If the inflammation leads to the progressive accumulation of intrahepatic fibrous tissue $, this may cause impairment of liver cell function, distortion of the hepatic architecture, and, ultimately, cirrhosis and all its consequences. 
A common clinical, biochemical and hepatic histological picture can be associated with more than one etiological agent. Three main types have been identified. One is associated with continuing hepatitis B virus infection $, another is related to chronic hepatitis C virus infection and the third is termed “lupoid” or “autoimmune” because of association with positive serum autoantibodies. Viral causes (hepatitis B and C) may be suggested by contact with blood of person carrying hepatitis, by history of receiving a blood transfusion or blood products, homosexuality or drug abuse. In the neonate, and occasionally in the immunosuppressed  patient, other viral infections, such as cytomegalovirus, may lead to chronic hepatitis. Identical clinical, functional and morphological features may be found associated with some drug  reactions. a1-antitripsin deficiency may lead to a chronic hepatitis, but more often presents as cholestasis in the neonates. In some patients the cause is unknown. 
Three types of autoimmune hepatitis have been described in pediatric patients: the first type is associated with high circulating titres of anti-smooth muscle (SMA); the second type is associated with autoantibodies against liver-kidney microsome (LKM) &; the third type is characterized by severe giant cell hepatitis with autoimmune hemolytic anemia &. Immunosuppressive drugs (corticosteroids alone or associated to azathioprine) is the therapy of choice &.
The most important clinical symptom is fatigue. Other clinical signs include jaundice, rarely vascular spiders, a large or small liver splenomegaly. Symptoms of portal hypertension (ascites, bleeding oesophageal varices) appear well after the onset of the disease. Biochemical tests show a variably elevated serum bilirubin level. Serum transaminase values are usually increased and gamma-globulin concentration is also elevated. Serum bilirubin, albumin and phosphatase  are normal except in severe disease.
The liver shows varying degrees of hepatocellular necrosis and inflammation &. The portal zones are expanded by an inflammatory infiltrate primarily of lymphocytes and plasma cells. There is some fibrosis with increasing severity, the inflammation extends into the liver lobule causing erosion of the limiting plate and piecemeal necrosis. The histological picture may resemble acute viral hepatitis but the duration is longer and the picture is predominantly that of intralobular inflammation and necrosis.
The old classification into chronic persistent, chronic active and chronic lobular hepatitis has been replaced by a new nomenclature & based on aetiology, clinical grade, histological severity (necro-inflammatory activity) and the stage (extend of fibrosis).
The treatment of chronic hepatitis HBV and HCV-correlated is aimed at controlling infectivity, eradicating the virus and preventing the development of cirrhosis and, possibly, hepatocellular carcinoma. Successful antiviral therapy can reduce or stop inflammatory necrosis of hepatocytes. Interferon-alpha &, nucleoside analogues (fialuridine, lamivudine , famcyclovir)&, corticosteroids  & in HBV-chronic hepatitis and interferon-alpha &, ribavirin & and ursodeoxycholic acid & in HCV-chronic hepatitis have been used successfully.