Cirrhosis is a nonneoplastic liver disease that is the end result of chronic liver disease from many causes. It is the diffuse process characterized by fibrosis and conversion of normal liver architecture into structurally abnormal nodules. In Ontario in 1997, the age-standardized mortality rate from chronic liver disease and cirrhosis was 7.4 per 100,000 population (9.7 for males, 4.5 for females).
Hepatic stellate cells transform into fibroblast-like cells in response to liver injury, and produce collagen. The stimulus for collagen production is probably inflammatory mediators, since cirrhosis is usually seen in chronic inflammatory processes. Other possible stimuli include factors produced by Kupffer cells or the disruption of the normal extracellular matrix due to inflammation. The deposition of type I and III collagen results in severe disruption of blood flow and the impaired diffusion of substances between blood and hepatocytes. Vascular architecture is reorganized by parenchymal damage and scarring with abnormal interconnections between vascular inflow and hepatic outflow (intrahepatic shunting).
In the Western world, the major causes of cirrhosis include excessive alcohol consumption (60-70%), viral hepatitis (10%), biliary diseases (5-10%) and hereditary hemochromatosis (5%), with an additional 5-10% with idiopathic origins.
Pathological findings depend on etiology. Grossly, the cirrhotic liver may be micronodular (<3mm), macronodular, or mixed – though the distinctions are only good for impressing staff. It may be enlarged, normal in size, or shrunken. The long-held view that cirrhosis is irreversible is now being challenged, with some evidence pointing to that early cirrhosis may be reversible.