Health Human Disease Blog

The term hepatitis is applied to a broad category of clinicopathological conditions that result from the damage produced by viral, toxic, pharmaco­logical, or immune-mediated attack upon the liver. The common pathological features of hep­atitis are hepatocellular necrosis, which may be focal or extensive, and inflammatory cell infiltra­tion of the liver, which may predominate in the portal areas or extend out into the parenchyma. Clinically, the liver is enlarged and tender with or without jaundice, and laboratory evidence of hepatocellular damage is invariably found in the form of elevated transaminase levels. Indepen­dent of its cause, the clinical course of hepatitis may range from mild or inapparent to a dramatic illness with evidence of severe hepatocellular dysfunction, marked jaundice, impairment of co­agulation, and disturbance of neurological func­tion. Hepatitis is further divided into acute and chronic types on the basis of clinical and patho­logical criteria.

Acute hepatitis implies a condition lasting less than six months, culminating either in complete resolution of the liver damage with return to nor­mal liver function and structure or in rapid pro­gression of the acute injury toward extensive ne­crosis and a fatal outcome.

Chronic hepatitis is defined as a sustained in­flammatory process in the liver lasting longer than six months.

Differentiation of acute from chronic hepatitis on histological criteria alone may be impossible. Extension of inflammatory cells beyond the limits of the portal tracts surrounding isolated nests of hepatocytes (piecemeal necrosis) and connection of portal and/or central areas of the hepatic lob­ules by swaths of inflammation, necrosis, and col­lapse of architecture (bridging necrosis) are seen in liver biopsies taken from patients with severe forms of chronic hepatitis. These features may also be seen, however, in uncomplicated acute hepatitis that will ultimately undergo complete resolution. A purely histological diagnosis of chronic hepatitis usually requires evidence of progression toward cirrhosis such as significant fibrous scarring and disruption of the hepatic lob­ular architecture.