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Acute Viral Hepatitis

  • Acute Viral Hepatitis refers to a clinico-pathological pattern of disease caused by infection with Hepatitis Viruses that results in short-term inflammation of the liver.
  • Infection with any of the Hepatitis Viruses (HAV, HBV, HCV, HDV) can initiate acute viral hepatitis. However, it should be noted that these viruses each have different propensities to induce such a syndrome as discussed in their individual pages. Generally speaking, HAV only produces acute viral hepatitis, HBV produces acute syndromes in adults but rarely when infection occurs in infants, and HCV produces acute syndromes in a minority of cases.
  • It is important to note that the hepatocellular damage caused in acute viral hepatitis is not due to direct viral injury but rather due to the immune response. Consequently, patients with weak immune systems such as children and immunocompromised patients may not develop any symptomology. In these groups infection may only be detectable due to serological and laboratory markers of infection and the immune response.
Classic Clinical Syndrome
  • Incubation Period
    • All of the Hepatitis Viruses possess an incubation period where there is no clinical or serological evidence of infection. The incubation periods vary for each virus but generally last between one to two months.
  • Prodrome
    • The prodromal period is characterized by nonspecific symptoms associated with systemic infection. The prodrome characterizes rapid viral proliferation prior to the development of an immune response. During this period serological markers of viral proteins as well as serum aminotransferase (ALT and AST) levels will skyrocket. Clinically, constitutional symptoms along with malaise, fatigue, and anorexia may be present.
  • Icteric Phase
    • During this phase clinical signs of jaundice and scleral icterus will appear and some right upper quadrant tenderness may develop due to enlargement of the liver. However, this phase coincides with a building immune response which begins to bring the virus under control
    • During this period IgM antibodies to certain viral antigens begin to develop and viral protein levels will decline. Constitutional symptoms also decrease in intensity and serum aminotransferases begin to fall.
  • Recovery Phase
    • During this phase clinical signs of jaundice subside as do most constitutional symptoms. The immune response also matures and many of the anti-viral IgM antibodies begin to class switch to the IgG subtype. Levels of serum aminotransferases also return to normal.
  • Overview
    • The complications of acute viral hepatitis largely depend on the identity of the infectious agent along with the immune response of the host. Below we list possible complications along with the probability of these outcomes occurring for different hepatitis virus subtypes.
  • Chronic Viral Hepatitis
    • Depending on the virus certain subsets of individuals may go on to develop chronic infections.
    • Hepatitis A Virus: Never occurs
    • Hepatitis B Virus: Occurs infrequently in adults but frequently in children and immunocompromised patients
    • Hepatitis C Virus: Occurs in majority of the cases.
  • Fulminant Hepatitis
    • Fulminant Hepatitis is a rare but catastrophic complication of acute viral infection and occurs when the immune response becomes over-exuberant.
    • Hepatitis A Virus: Rare but possible
    • Hepatitis B Virus: Occurs in a small minority of cases but increased risk during concomitant Hepatitis D Virus
    • Hepatitis C Virus: Almost never occurs.
  • Type III Hypersensitivity
    • This is especially prominent during HBV infection where infected hepatocytes can shed enormous amounts of HBsAg (Viral Surface Antigen). Shed HBsAg can form immune complexes that can then deposit in multiple tissues causing certain glomerular pathologies, skin rash, and arthralgia.
  • Gross Appearance
    • The liver may be enlarged and slightly reddened.
  • Histological Appearance
    • Hepatocytes respond to injury in a number of ways including cytoplasmic vacuolation (Termed "Ballooning Degeneration"), cellular rupture, or simply apoptosis. In severe cases, areas of hepatic tissue may undergo necrosis. The hepatic tissue displays striking inflammation in acute viral hepatitis which manifests with proliferation of kupffer cells as well as parenchymal infiltration with mononuclear cells, especially lymphocytes. Within this inflammatory war zone, areas of hepatocyte regeneration can be observed. Finally, in the case of HBV infection, the cytoplasm of hepatocytes may appear full of granules, giving them a characteristic "Ground-Glass Appearance", representing dense granules of HBV Surface Antigen (HBsAg).