Studies on subacute hepatitis with special reference to the quantitative evaluation on the areas of the hepatocellular necrosis

Abstract

The mesenchymal areas stained in blue and the parenchymal areas stained in purple in the staining sections of the liver specimens with azan were estimated in 17 patients of subacute hepatitis diagnosed according to the criteria of Tisdale. The ratios of two areas (M/P) or of the mesenchymal areas to the total areas (M/T) were calculated to evaluate the volume of hepatocellular destruction. The relation between the area ratios and the clinical features. was also studied.
Variations in the estimated values of the M/P or M/T ratios in any depth of the biopsy specimens or in any part of liver in the autopsy cases were very small in each case, indicating that the estimated values in any section may reflect the quantitative changes of hepatocellular damage throughout the entire liver. The values of the M/P (M/T) ratios in subacute hepatitis were all above 0.21 (17.3%), and were significantly higher than those in acute hepatitis. or chronic hepatitis including active form.
The M/P (M/T) ratios of the patients died of hepatic coma were all above 2.52 (71.6%) and were significantly higher than those of the survived cases. Severe clinical signs, such as prolonged jaundice, ascites, edema, neurological findings and gastrointestinal bleeding tended to be found more frequently in the cases showing the larger M/P (M/T) ratios among the survived cases. However, the development of hepatic cirrhosis was not correlated to the area. ratios in the initial biopsy specimens.
The results indicated that subacute hepatitis was clearly differentiated from acute or chronic hepatitis by the quantitative evaluation of the mesenchymal area. And the quantity of the initial destruction in the hepatocytes was closely related to the fatality or the developments of the severe clinical signs in the relatively early stage. However, the prognosis in the late stage, which means development of hepatic cirrhosis, may be influenced by the reaction in the host following the hepatocytic destruction rather than the quantity of the hepatocellular damage.