[Morphological possibilities of detecting HBc-antigen in liver tissue in chronic hepatitis and cirrhosis].

It has been shown that detection of HBc-antigen in the organ tissue requires the use of a complex of the morphologic methods: histologic, immunohistochemical and electron microscopic. Ultrastructurally, the eosinophilic material in hepatocytic nuclei appears as flocks of electron dense granules 27 nm in size and produces intensive fluorescence with antiserum to HBc-antigen, all this pointing to the presence of deep antigen in the organ tissue. The patients with chronic active hepatitis and active liver cirrhosis associated with the presence of HBc-antigen in the blood serum demonstrates accumulation of both the surface and deep antigen by hepatocytes.

[Morphological characteristics of ground glass hepatocytes in chronic hepatitis and liver cirrhosis].

Histochemical and electron microscopic examinations of liver punctates from 57 patients with chronic hepatitis and cirrhosis of the liver were carried out. "Ground Glass" hepatocytes were found to occur with similar frequency both in patients with HB-antigen in the blood serum and in patients with alcoholic involvement of the liver and no antigen in the blood serum. The presence of HB-antigen in the cytoplasm of such hepatocytes can be detected by staining of the sections with orsein, aldehydethionine and aldehydefucsin.

[Morphological characteristics of acute alcoholic hepatitis].

Liver biopsies from 60 patients with acute alcoholic hepatitis (AAH) developing against the background of steatosis, chronic hepatitis and cirrhosis were studied histologically, histochemically and electron microscopically. AAH is characterized by necrosis of hepatocytes with deposition of alcoholic hyalin, obesity of the organ, and polymorphonuclear leukocyte infiltration. Hyperplasia of the smooth endoplasmic reticulum, the appearance of megamitochondria, and an increased amount of peroxisomes reflect the participation of MEOS and the catalase system in alcohol metabolism with a progressive decrease in the activity of alcoholdehydrogenase.