Brief Article
Copyright ©2012 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Oct 21, 2012; 18(39): 5570-5575
Published online Oct 21, 2012. doi: 10.3748/wjg.v18.i39.5570
Quantitation of HBsAg predicts response to entecavir therapy in HBV genotype C patients
Etsuro Orito, Kei Fujiwara, Hiroshi Kanie, Tesshin Ban, Tomonori Yamada, Katsumi Hayashi
Etsuro Orito, Kei Fujiwara, Hiroshi Kanie, Tesshin Ban, Tomonori Yamada, Katsumi Hayashi, Department of Gastroenterology, Nagoya Daini Red Cross Hospital, Nagoya 466-8650, Japan
Author contributions: Orito E, Fujiwara K, Kanie H, Ban T, Yamada T and Hayashi K designed the study, enrolled the patients, analyzed the data, and drafted the manuscript; and Ban T contributed to the statistical analysis.
Supported by A grant from the Japanese Ministry of Health and Welfare
Correspondence to: Etsuro Orito, MD, PhD, Department of Gastroenterology, Nagoya Daini Red Cross Hospital, Myoken-cho 2-9, Showa, Nagoya 466-8650, Japan. orito@nagoya2.jrc.or.jp
Telephone: +81-52-8321121 Fax: +81-52-8325369
Received: February 10, 2012
Revised: March 28, 2012
Accepted: April 9, 2012
Published online: October 21, 2012
Abstract

AIM: To analysis the factors that predict the response to entecavir therapy in chronic hepatitis patients with hepatitis B virus (HBV) genotype C.

METHODS: Fifty patients [hepatitis B e antigen (HBeAg)-negative:HBeAg-positive = 26:24] with HBV genotype C, who received naïve entecavir therapy for > 2 years, were analyzed. Patients who showed HBV DNA levels ≥ 3.0 log viral copies/mL after 2 years of entecavir therapy were designated as slow-responders, while those that showed < 3.0 log copies/mL were termed rapid-responders. Quantitative hepatitis B surface antigen (HBsAg) levels (qHBsAg) were determined by the Architect HBsAg QT immunoassay. Hepatitis B core-related antigen was detected by enzyme immunoassay. Pre-C and Core promoter mutations were determined using by polymerase chain reaction (PCR). Drug-resistance mutations were detected by the PCR-Invader method.

RESULTS: At year 2, HBV DNA levels in all patients in the HBeAg-negative group were < 3.0 log copies/mL. In contrast, in the HBeAg-positive group, 41.7% were slow-responders, while 58.3% were rapid-responders. No entecavir-resistant mutants were detected in the slow-responders. When the pretreatment factors were compared between the slow- and rapid-responders; the median qHBsAg in the slow-responders was 4.57 log IU/mL, compared with 3.63 log IU/mL in the rapid-responders (P < 0.01). When the pretreatment factors predictive of HBV DNA-negative status at year 2 in all 50 patients were analyzed, HBeAg-negative status, low HBV DNA levels, and low qHBsAg levels were significant (P < 0.01). Multivariate analysis revealed that the low qHBsAg level was the most significant predictive factor (P = 0.03).

CONCLUSION: Quantitation of HBsAg could be a useful indicator to predict response to entecavir therapy.

Keywords: Chronic hepatitis B; Quantitation of hepatitis B surface antigen; Entecavir; Hepatitis B virus genotype C; Slow-responders; Hepatitis B core-related antigen; Core promoter mutation; Pre-C mutation