Pattern of histologic progression from acute and chronic hepatitis B to cirrhosis.
- Author:
Whan Kook CHUNG
;
Joon Yeol HAN
- Publication Type:Original Article
- MeSH:
Biopsy;
Biopsy, Needle;
Classification;
Fibrosis*;
Follow-Up Studies;
Hepatitis B;
Hepatitis B, Chronic*;
Hepatitis, Chronic*;
Humans;
Korea;
Necrosis;
Sample Size
- From:The Korean Journal of Hepatology
1996;2(2):134-144
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The chronic active or aggressive hepatitis B, in which periportal inflammation(piecemeal necrosis) is conventionally accepted as the pattern of progression to cirrhosis', implies little concern with intralobular necroinflammation as a process responsible for aggravation and progression. Some published observations, however, refer to episodes of acute necrotizing bouts(subacute hepatic necrosis) have been reported". For technical reasons, relatively few sequential biopsy studies of chronic hepatitis B are available and particularly, initial acute hepatitis B is barely documented since biopsies are now rarely perfomed in acute stages of hepatitis4. Moreover, most published sequential studies are complicated by therapeutic intervention. The availability of Korean sequential biopsy specimens and the increasing interest in parenchymal changes in the evolution of hepatitis B encouraged the description of the progression of acute and chronic hepatitis B to cirrhosis. During the long-term follow-up study, acute bouts of intralobular parenchymal necroinflammation are observed whenever the stage of aggravation is caught and the biopsy is possible. Whatever the result of these studies, the observation presented suggests a major role of parenchymal changes in the evolution of chronic hepatitis B and this experience focuses on the important lesions of the lobular parenchyma in classification and evaluation of chronic hepatitis'. Seven patients are selected on the basis of elevated S-ALT level, and submit to repated needle biopsies during a 6-month period". Of these, 2 cases show chronic active hepatitis with early cirhosis constantly, and in 5 cases CAH appear 1 or 2 times in each case during the follow-up period. In clinical follow-up after the sequential biopsies, these 7 patients were all healthy at least for an average of 18.6 years ranging from 14 to 27 years, except for one who developed into HCC without complication of cirrhosis. Thus, while the sample size of this study is small, continuous piecemeal necrosis seems not to be a pattern of progression to cirrhosis. In conclusion, acute and chronic hepatitis B experienced in Korea appear to progress to cirrhosis by means of repeated acute episodic bouts of intralobular necroinflammation, and the conventional concept that continuous progress by piecemeal necrosis seems not to hold true.
