Published online Mar 7, 2015. doi: 10.3748/wjg.v21.i9.2739
Peer-review started: June 17, 2014
First decision: August 6, 2014
Revised: August 29, 2014
Accepted: December 5, 2014
Article in press: December 8, 2014
Published online: March 7, 2015
Processing time: 265 Days and 17.1 Hours
AIM: To investigate the dynamic changes of serum hepatitis B surface antigen (HBsAg) levels apportioned by the same hepatic parenchyma cell volume (HPCV), namely, hepatic cell quantities.
METHODS: Serum HBsAg levels were detected by electrochemiluminescence and serum HBsAg levels apportioned by the same HPCV were figured out according to the theory of sphere geometry. HBsAg levels were compared among different liver inflammation grades, as well as different hepatic fibrosis stages.
RESULTS: In hepatitis B e antigen-negative chronic hepatitis B, serum HBsAg levels in liver histological inflammation grades 1-4 were 3.66 ± 0.40, 3.74 ± 0.35, 3.74 ± 0.26 and 3.71 ± 0.34 log10 COI (cut off index), respectively, and there were no differences before apportion (P = 0.640). Serum HBsAg levels apportioned by the same HPCV were 5.57 ± 0.62, 5.98 ± 0.65, 6.59 ± 0.50 and 6.81 ± 0.84 log10 COI, respectively, and there were significant differences after apportion (P < 0.001). Serum HBsAg levels in hepatic fibrosis stages I-IV were 3.66 ± 0.43, 3.75 ± 0.33, 3.71 ± 0.28 and 3.75 ± 0.26 log10 COI, respectively, and there were no differences before apportion (P = 0.513). Serum HBsAg levels apportioned by the same HPCV were 5.53 ± 0.66, 5.98 ± 0.53, 6.29 ± 0.46 and 7.06 ± 0.48 log10 COI, respectively, and there were significant differences after apportion (P < 0.001).
CONCLUSION: Serum HBsAg levels apportioned by the same HPCV (hepatic cell quantities), rather than serum HBsAg levels, increase with liver inflammation grades and hepatic fibrosis stages.
Core tip: Hepatitis B surface antigen (HBsAg)-negative chronic hepatitis B patients always feature increasing liver fibrosis and decreasing hepatic parenchyma cells. Does it influence the circulating HBsAg released into the serum? It requires research on the condition that the impact of fibrous volume on hepatic cell quantities should be deducted. It turns out that there were significant differences in serum HBsAg levels apportioned by the same hepatic cell quantities among different liver histological inflammation grades, as well as different hepatic fibrosis stages. In conclusion, although hepatitis B virus replication place - hepatic cell quantities - were shrinking while fibrosis progresses, its replication and expression became more active rather than declined or silenced.