[A study on the hepatic histological changes and clinical manifestations in chronic HBV carriers].

OBJECTIVE

To investigate the relationship between hepatic histopathological changes and clinical characteristics in chronic HBV carriers.

METHOD

A retrospective analysis was performed based on the hepatic biopsy findings, clinical laboratory results, and ultrasound examinations in 142 chronic HBV carriers. The patients were divided into two groups according to their serum HBV DNA replication and the pathological alterations in their livers.

RESULTS

The average age of the 142 patients was (24.8+/-8.7) years old. Among them, 129 were diagnosed as chronic HBV carriers based on their positive HBV DNA results. Thirteen were diagnosed as non-active HBsAg carriers. Hepatitis B family history was found in 31.0% of the cases. Normal liver tissues (G0S0) were found in the specimens of 33 cases (G > or = 1 and/or S > or = 1) chronic hepatitis B was diagnosed based on the biopsies in 106 cases, including an early stage of hepatic cirrhosis in 1 case (G4S4). There were no obvious differences between HBV DNA positive and negative group cases. The levels of HBV DNA in all the 129 cases of chronic HBV carriers were more than 1.0 x 10(4) copy/ml and the average value was (7.58+/-0.99) log10 copy/ml. Of the 129 cases, 123 were HBeAg positive (95.3%). Increased levels of gamma-globulin were detected in 45.8% of the cases and fibrosis index increased in 37.1%; 40.1% of the cases showed abnormalities in their ultrasound examinations. The average PCIII value of the chronic HBV carrier group (G > or = 1 and/or S > or = 1) was higher than that of the non-active HBsAg carrier group (P = 0.016). Spearman's analysis indicated that the inflammation grade (G) was correlated with the hepatic fibrosis index PCIII, and the correlation coefficient was 0.391 (P = 0.003).

CONCLUSION

The patients in our study have a higher HBV DNA replication in their sera and have mild inflammation in their livers. Inflammation grade (G) and fibrosis stage (S) have no correlation with the level of HBV DNA or the state of HBeAg positivity. The increased level of PCIII might be related to their hepatic inflammation.