CHRONIC HEPATITIS

6. CHRONIC HEPATITIS GENERAL CONSIDERATION
Chronic hepatitis is defined as a chronic inflammatory reaction of the liver with a duration of over 6 months as demonstrated by persistently abnormal liver tests. For proper treatment, it is crucial to determine whether the disease will resolve, remain static, or progress to cirrhosis. The causes of chronic hepatitis are only partially defined. It may be a sequela of infection resulting from hepatitis B virus. Chronic hepatitis has also been seen as a sequela of non-A, non-B hepatitis. Hepatitis A virus has not yet been shown to lead to chronic hepatitis. Additionally, identical clinical entitis may be associated with drug reactions, including oxyphenisatin, methyldopa and isoniazid.
    1. Chronic persistent hepatitis
    This form of chronic hepatitis represents an essentially benign condition with a good prognosis. The diagnosis is confirmed by liver biopsy. The biopsy may show portal tract infiltration with primarily mononuclear cells and occasional areas of focal inflammation in the parenchyma. The boundary between portal tracts and parenchyma remains sharp, and there is little or no "piecemeal necrosis." In essence, the architecture of the hepatic lobule remains intact. The symptomatology varies from the asymptomatic state to various vague manifestations including fatigability, anorexia, malaise and lassitude. Physical examination is usually normal.
    Liver biopsy helps establish the diagnosis of persistent hepatitis. Treatment is mostly reassurance of the patient. Corticosteroids and immunosuppressive drugs should not be given. Dietary restrictions, excessive vitamin supplementation and prolonged bed rest are not necessary. The prognosis is excellent. Rarely does the disease progress to chronic active hepatitis.
    2. Chronic active hepatitis
    This form of chronic hepatitis is usually characterized by progression to cirrhosis, although milder cases may resolve spontaneously. The histologic changes include chronic inflammatory infiltration involving portal zones and extending into the parenchyma, with piecemeal necrosis and the formation of intralobular septa. Piecemeal necrosis, a process of inflammatory cells and hepatocyte necrosis occurring at the interface of the portal area and the liver lobule, may extend well into the lobule and across zonal boundaries. In severe cases, piecemeal necrosis may be associated with considerable hepatic failure or fibrosis and ultimately with cirrhosis. In very mild cases, it may be difficult to distinguish this entity from chronic persistent hepatitis. Liver biopsies repeated at varying intervals may be necessary to make the distinction as well as to monitor therapy.
    The disease is thought to be caused by internal stasis of dampness and heat in
traditional Chinese medicine. The pathologic changes due to damp and heat pathogens stay deeply in the body. Thereby, various manifestations of gastrosplenic and cholehepatic dysfunctions may occur.
CLINICAL MANIFESTATIONS
     1. Symptoms and signs
     A. Chronic active hepatitis. This is generally a disease of young people, particularly young women. However, the disease can occur at any age. The onset is usually insidious, but about 25% of cases present as an acute attack of hepatitis. Although the serum  bilirubin is usually increased. 20% of these patients have anicteric disease. Examination often reveals a healthy-appearing young woman with multiple spider nevi, cutaneous striae, acne and hirsutism. Amenorrhea may be a feature of this disease. Multisystem involvement, including kidney, joints, lung and bowel and coombspositive  hemolytic anemia are associated with this clinical entity.
     B. Chronic active hepatitis (HBsAg-positive type). This type of hepatitis clinically resembles the lupoid type of disease. The histologic pictures of these two types of chronic active hepatitis are indistinguishable. The HBsAg form of chronic active hepatitis appears to affect males predominantly. It may be noted as a continuum of acute hepatitis or may be manifested only by biochemical abnormalities of liver function.
     2. Laboratory findings
     The serum bilirubin is usually normal or only modestly increased (4.5-7mg/dL);
SGOT (AST), IgG, IgM and gamma globulin levels are higher than normal. Late in
the disease, serum albumin levels are usually decreased and prothrombin time may
be significantly prolonged and will not respond to vitamin K therapy. Antinuclear
and smooth muscle antibodies are positive 15-50% of the time. Latex fixation tests
for rheumatoid arthritis and anticytoplasmic and immunofluorescent antimitochondrial antibodies are positive in 28-50% of patients. Hepatitis B antigen is not found in the blood of patients with classic "lupoid" hepatitis.
     Activity in chronic liver disease can be defined quantitatively quite readily by establishing arbitrary biochemical standards. For example, either a 10-fold increase in serum transaminase level or a 5-fold elevation of SGOT with a 2-fold increase in gamma globulin concentration constitutes "high-grade" activity.
DIAGNOSIS
     Patients with chronic hepatitis may be entirely asymptomatic and exhibit only
minimal abnormalities in routine laboratory tests, or maybe incapacitated by progressive liver failure and the complications of portal hypertension. At any given
time, the clinical and laboratory features may not correlate well with histopathology or long-term prognosis. For this reason and because concepts of the natural history and response to treatment are changing for some of these disorders, decisions regarding diagnosis, management and prognosis are often difficult and uncertain.
     The concept of traditional Chinese medicine is that the stagnation of pathogenic damp and heat factors in the liver and the gallbladder influences and causes the spleen and stomach to become deficient. If this condition lasts for a long time, the stagnation of