Wu ZQ, Tan L, Liu T, Gao ZL, Ke WM. Evaluation of changes of serum hepatitis B surface antigen from a different perspective. World J Gastroenterol 2015; 21(9): 2739-2745 [PMID: 25759544 DOI: 10.3748/wjg.v21.i9.2739]
Corresponding Author of This Article
Wei-Min Ke, MD, Professor, Department of Infectious Diseases, Third Affiliated Hospital of Sun Yat-sen University, Key Laboratory of Topical Disease Control, Sun Yat-sen University, Ministry of Education, Shipai Road, Guangzhou 510630, Guangdong Province, China. tcl3626@gmail.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Retrospective Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Mar 7, 2015; 21(9): 2739-2745 Published online Mar 7, 2015. doi: 10.3748/wjg.v21.i9.2739
Evaluation of changes of serum hepatitis B surface antigen from a different perspective
Ze-Qian Wu, Lei Tan, Ting Liu, Zhi-Liang Gao, Wei-Min Ke
Ze-Qian Wu, Zhi-Liang Gao, Wei-Min Ke, Department of Infectious Diseases, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, Guangdong Province, China
Ze-Qian Wu, Zhi-Liang Gao, Wei-Min Ke, Key Laboratory of Topical Disease Control, Sun Yat-sen University, Ministry of Education, Guangzhou 510630, Guangdong Province, China
Lei Tan, Department of Medical Ultrasonic, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, Guangdong Province, China
Ting Liu, Department of Infectious Diseases, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou 510630, Guangdong Province, China
Author contributions: Wu ZQ, Gao ZL and Ke WM contributed to the analysis and interpretation of data, drafting of the manuscript and approval of the final version of the manuscript; Tan L and Liu T contributed to the acquisition of data and critical revision of the manuscript.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Wei-Min Ke, MD, Professor, Department of Infectious Diseases, Third Affiliated Hospital of Sun Yat-sen University, Key Laboratory of Topical Disease Control, Sun Yat-sen University, Ministry of Education, Shipai Road, Guangzhou 510630, Guangdong Province, China. tcl3626@gmail.com
Telephone: +86-20-85253171 Fax: +86-20-85252250
Received: June 16, 2014 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
Core Tip
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.
