The clinical features of liver cirrhosis are manifestation of altered hepatic hemodynamics and of reduced hepatic cell mass, represented by portal hypertension and sometimes hepatic failure. Histologically, cirrhosis is defined in general as a diffusely altered reconstruction of the lobular parenchyma with widespread connective tissue septa, which circumscribe regenerative nodules of the hepatocytes and contain anastomoses between efferent as well as afferent vascular systems linking central and portal canals. Thus, a large portion of portal blood flow bypasses the hepatocytes and reticuloendothelial cells, depleting them of their metabolic and detoxifying function. It is often impossible to make a morphologic classification of liver cirrhosis based on tiny biopsy specimens, and the histologic criteria are neither specific nor mutually exclusive. Furthermore, a frequent lack of correlation between the etiologic and morphologic types of cirrhosis has led the clinicians to classify the cirrhosis based on the main etiologic factor. According to the statistics (1991) of 40 representative medical institutes in Japan, covering approximately 8,600 liver cirrhosis cases, 16.9% of the cirrhosis is supposedly due to type B hepatitis virus infection, 54.9% to type C, 10.7% to alcoholic abuse and the remainder are of unknown etiology. It would be reasonable to apply the etiologic classification to liver biopsy specimens and morphologic classification to autopsy materials for thorough examination.

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