|LETTER TO EDITOR
|Year : 2012 | Volume
| Issue : 9 | Page : 427-428
Seroconversion of hepatitis B virus surface antigen in chronic hepatitis B child treated with entecavir
Dong Li, Junping Wang, Junqing Zhou, Yan Wang
Department of Liver Disease, Bethune International Peace Hospital, Shijiazhuang, Hebei, China
|Date of Web Publication||14-Sep-2012|
Department of Liver Disease, Bethune International Peace Hospital, Shijiazhuang, Hebei
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Li D, Wang J, Zhou J, Wang Y. Seroconversion of hepatitis B virus surface antigen in chronic hepatitis B child treated with entecavir. North Am J Med Sci 2012;4:427-8
|How to cite this URL:|
Li D, Wang J, Zhou J, Wang Y. Seroconversion of hepatitis B virus surface antigen in chronic hepatitis B child treated with entecavir. North Am J Med Sci [serial online] 2012 [cited 2017 Mar 30];4:427-8. Available from: http://www.najms.org/text.asp?2012/4/9/427/100996
Hepatitis B virus (HBV) infection in children possesses a higher rate of progression to chronic hepatitis, however, a consensus guideline for treatment has not been established so far. , Entecavir as carbocyclic analog with inhibition of HBV replication  is shown encouraging effects in control of chronic HBV infection.  In the present article, we present seroconversion of hepatitis B virus surface antigen (HBsAg) by entecavir administrated in a young child with chronic hepatitis B.
A 4-year-old girl was presented in a history of chronic HBV infection for 2 years. The perinatal history indicated that her mother was a HBV carrier, and grandmother died of cirrhosis due to chronic hepatitis B. The patient was vaginally born, and was immunized with hepatitis B vaccine and high-titter immunoglobulin against HBV at birth.
During past 2 years, the patient had been administrated with Chinese herbal medicines. Because of unsatisfying theroputic effect, the patient was then transferred to our department. On admission, abdominal computed tomography (CT) scan demonstrated a normal size of the liver, but the spleen was enlarged in size. The laboratory tests showed that alanine aminotransferase (ALT) 92 U/L, aspartate transaminase (AST) 96 U/L, γ-glutamyl transpeptadase (GGT) 8 U/L, HBsAg positive, HBeAg positive, anti-HBV core antibody positive, and HBV DNA level 2.703 × 10 7 copies/mL. The autoimmune antibodies were absent, and serum markers for hepatitis A virus, hepatitis C virus, hepatitis E virus, cytomegalovirus, and Epstein Bar virus were negative. The patient was diagnosed with chronic hepatitis B with positive HBsAg.
After informed consent was obtained from her parents, the patient was started with oral administration of entecavir at dose of 0.16 mg once a day. During administration of entecavir, the patient was regularly monitored by tests of liver function, HBsAg and HBV DNA level, and hematologic system. Tests showed that ALT was declined 2 weeks after entecavir administrator, and was normalized 4 weeks after treatment. The level of HBV DNA decreased in 2 weeks, and negative 24 weeks after entecavir administration. Interestingly, we noticed that HBeAg seroconversion was started 12 weeks after the treatment, and HBsAg became negative 48 weeks after treatment, followed by HBsAg seroconversion 72 weeks after treatment. Entecavir was terminated at 192 nd week when liver function and HBV DNA were back to normal.
Entecavir was tolerated well in this little patient, and nephrotoxicity or myopathy were not noticed during the treatment. The patient has so far been followed-up for a period of 96 weeks since the termination of entecavir. The patient has positive anti-HBs, anti-HBe, anti-HBc, and normal liver function [Table 1]. The girl is well and in healthy condition now.
|Table 1: Variations of laboratory tests before and aft ertreatment of entecavir|
Click here to view
The ultimate goal of antiviral treatment in chronic HBV infection is to eradicate replicating HBV. HBV requires HBsAg to propagate infection and cause disease. Entecavir is a nucleoside analog with therapeutic effect on chronic HBV, ,,, and has been shown to decrease HBsAg in animal research.  Although potential effects of entecavir on chronic HBV infection were reported in some other studies, ,,, those studies had no involved lowering of HBsAg or HBsAg seroconversion. The satisfied outcome observed in our little girl patient using entecavir might be the first case, specifically lowering HBsAg or HBsAg seroconversion, in the reported literatures. Large sample are, however, needed to evaluate entecavir in term of clinical efficacy in children with chronic HBV.
| References|| |
|1.||Alberti A, Brunetto MR, Colombo M, Craxi A. Recent progress and new trends in the treatment of hepatitis. J Med Virol 2002;67:458-62. |
|2.||Lok AS, McMohan BJ. Chronic hepatitis B. Hepatology 2007;45:507-39. |
|3.||Sherman M, Yurdaydin C, Sollano J, Silva M, Liaw YF, Cianciara J, et al. Entecavir for treatment of lamivudine-refractory HbeAg-positive chronic hepatitis B. Gastroenterology 2006;130:2039-49. |
|4.||Shim JH, Suh DJ, Kim KM, Lim YS, Lee HC, Chung YH, et al. Efficacy of entecavir in patients with chronic hepatitis B resistant to both lamivudine and adefovir or to lamivudine alone. Hepatology 2009;50:1064-71. |
|5.||Liaw YF, Raptopoulou-Gigi M, Cheinquer H, Sarin SK, Tanwandee T, Leung N, et al. Efficacy and safety of entecavir versus adefovir in chronic hepatitis B patients with hepatic decompensation: A randomized, open-label study. Hepatology 2011;54:91-100. |
|6.||Fung J, Lai CL, Young J, Wong DK, Yuen J, Seto WK, et al. Quantitative hepatitis B surface antigen levels in patients with chronic hepatitis B after 2 years of entecavir treatment. Am J Gastroenterol 2011;106:1766-73. |
|7.||Keating GM. Entecavir: A review of its use in the treatment of chronic hepatitis B in patients with decompensated liver disease. Drugs 2011;71:2511-29. |
|8.||Colonno RJ, Genovesi EV, Medina I, Lamb L, Durham SK, Huang ML, et al. Long-term entecavir treatment results in sustained antiviral efficacy and prolonged life span in the woodchuck model of chronic hepatitis infection. J Infect Dis 2001;184:1236-45. |