Definition

 • Infection of the liver by hepatitis B, C, or D lasting longer than 6 months.

Epidemiology

 • Chronic HCV is common worldwide, with ~3% of the world’s population infected.

• Chronic HBV shows more geographical variation, being rarer in western countries, but very common in areas of Africa and Asia where infection rates are as high as 15%.

 Immunopathogenesis

 • Chronic viral hepatitis is the result of an immune response that fails to clear the virus following infection.

• 10% of people fail to clear HBV infection.

 • 90% of people fail to clear HCV infection.

 • HDV is an incomplete DNA virus which can only cause infection in patients who already have HBV. If the two infections occur together, this is co- infection; if the HDV follows HBV, this is superinfection. the latter produces more serious diseases.

Presentation

 • Often asymptomatic and diagnosed incidentally on abnormal liver function tests (LFts).

• Many patients do not present until advanced cirrhosis with ascites.

Serology

 • Chronic HBV: presence of serum HBsAg (hepatitis B surface antigen) and anti- HBcAg (hepatitis B core antigen) antibodies.

 • Chronic HCV: presence of serum anti- HCV antibodies and HCV rNA by PCr.

 • HDV: presence of serum IgM anti- HDV antibodies or the detection of the virus in liver biopsies.

 Macroscopy

• the liver may feel slightly firm due to fibrosis.

 Histopathology

 • Portal inflammation is dominant and composed mostly of lymphocytes.

• Interface hepatitis (‘piecemeal necrosis’) refers to the extension of the portal inflammatory infiltrate into the hepatocytes at the limiting plate, associated with hepatocyte degeneration.

 • Lobular inflammation is usually focal and mild in chronic viral hepatitis (compare with acute viral hepatitis where it is the dominant site). In cases of HBV with superinfection with HDV, lobular changes may be prominent.

 • Fibrosis is a marker of how advanced the disease is. extensive bridging fibrosis through the liver terminates in cirrhosis.

• A liver biopsy report should include a description of the degree of inflammation (stage) and how advanced the fibrosis is (grade). these can be summarized using a semi- quantitative scoring system (e.g. Ishak or MetAVIr).

* Note that all of these changes may be seen in chronic liver injury from a number of causes. Clues to a viral aetiology may be present, however, ‘ground glass’ hepatocytes in hepatitis B and portal lymphoid aggregates, inflammatory bile duct damage, and fatty change in hepatitis C. As described earlier, HDV is characterized by lobular damage. It should be noted that because of the availability of markedly improved treatment, patients with HCV are, now, infrequently biopsied.

 Prognosis

 • Prognosis largely depends on the extent of fibrosis present on liver biopsy.

 • Viral genotype is also important in hepatitis C.

 • High risk of hepatocellular carcinoma (HCC), especially in patients with cirrhosis. this may occur, especially in endemic areas, in patients without cirrhosis.