Abstract
HBsAg and HBcAg in liver tissue were studied in formalin fixed paraffin sections of 806 liver biopsy materials. HBsAg in liver tissue was negative in 429 specimens without HBsAg in serum and in 39 cases (45 specimens) with acute hepatitis type B (AH-B). The positive rate of HBsAg in liver tissue with AH-B is supposed to be influenced mainly by the interval from the onset of AH-B to the time liver biopsy was done. HBsAg in liver tissue was detected in 249 (89.9%) out of 277 specimens with HBsAg carriers, in that HBsAg in serum was persistently positive more than three months. Detection of HBsAg in liver tissue is very useful to differentiate acute exacerbation in HBsAg carriers from AH-B.
Inclusion (I), cytoplasmic (C) and membranous (M) types were recognized with regard to the shape of HBsAg in hepatocytes. M type was distributed focally in pericentral area of the lobule. In cases with M type, a lot of C type were also found in the same section and HBsAg-titer in serum was high significantly. It is thought that both I and C types exist in the liver of HBsAg carriers with variation of quantity and distribution of those and the variation influences the positive rate of HBsAg in paraffin sections. According as the disease progressed to liver cirrhosis, I type was distributed focally or diffusely in the lobule and irregularly among the lobules. The positive rate of HBsAg in liver tissue was lower and it of HBcAg higher in "active" group of chronic liver diseases (CLD) as compared with in "inactive" group of CLD.
It was suggested that HBs & cAg were produced almost simultaneously in Rappaport's Zone 1, therefore hepatitis B virus multiplied in this area. That seems to be one of the most important factors which cause acute exacerbation in CLD. Changes of HBs & cAg in liver tissue in the course of acute exacerbation resembled those in the course of AH-B, except that HBs & cAg continued to exist after recovery from acute exacerbation in CLD. Distribution patterns of HBs & cAg in liver tissue did not suggest prognosis of the disease, nor progression from chronic hepatitis to liver cirrhosis.
