Serum HBV DNA and ALT Kinetics in The Trials of Antiviral Agents
in Patients with Chronic Hepatitis B (Appropriate sampling time for
Response Assessment of Antiviral Therapy in Chronic Hepatitis B
Patients)

Juseop Kang; Minho Lee

doi:10.4172/2161-0479.1000e103

ISSN: 2161-0479

Journal of Autacoids and Hormones

Make the best use of Scientific Research and information from our 700+ peer reviewed, Open Access Journals that operates with the help of 50,000+ Editorial Board Members and esteemed reviewers and 1000+ Scientific associations in Medical, Clinical, Pharmaceutical, Engineering, Technology and Management Fields.

Meet Inspiring Speakers and Experts at our 3000+ Global Conferenceseries Events with over 600+ Conferences, 1200+ Symposiums and 1200+ Workshops on Medical, Pharma, Engineering, Science, Technology and Business

Serum HBV DNA and ALT Kinetics in The Trials of Antiviral Agents in Patients with Chronic Hepatitis B (Appropriate sampling time for Response Assessment of Antiviral Therapy in Chronic Hepatitis B Patients)

*Juseop Kang^1,2, Minho Lee²**
¹Department of Pharmacology & Division of Molecular Therapeutics Development
²Internal Medicine, College of Medicine, Hanyang University
Corresponding Author :	Juseop Kang Professor and Director Department of Pharmacology and Clinical Pharmacology Laboratory Hanyang University, College of Medicine Seoul 133-791, South Korea Tel: 82 2 2292 0523 Fax: 82 2 2292 6686 E-mail: jskang@hanyang.ac.kr
Received December 17, 2010; Accepted December 20, 2011; Published December 24, 2011
Citation: Kang J, Lee M (2011) Serum HBV DNA and ALT Kinetics in The Trials of Antiviral Agents in Patients with Chronic Hepatitis B (Appropriate sampling time for Response Assessment of Antiviral Therapy in Chronic Hepatitis B Patients). Autacoids 1:e103. doi: 10.4172/2161-0479.1000e103
Copyright: © 2011 Kang J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Related article at Pubmed Scholar Google

Visit for more related articles at Journal of Autacoids and Hormones

View PDF Download PDF

Hepatitis B virus (HBV) infection is a widespread disease that affects about 350 million people worldwide, contributing to global public health problems and 25-40% of these will die from liver cirrhosis or primary hepatocellular carcinoma [1-3]. Therapeutic tools for patients with chronic HB include the nucleoside analogue lamivudine and cytokine interferon α (IFN-α) based on several credible clinical trials [3-5]. In the study by Disenstag et al. [3] and Jonas et al. [4] provide the reliable results about antiviral agent, lamivudine that was well tolerated and suppressed serum levels of HBV DNA, viral replication marker, profoundly in patients with chronic HB in children and adult population. They conducted same sampling time for assessment of efficacy of antiviral agents about virological markers HBV DNA and hepatitis B antigen (HBeAg) and biochemical markers, serum alanine aminotransferase (ALT) in patients with HBV infection.
Consistently, because clinical observations and animal studies clearly show that abolish of HBV DNA by HBV-specific cytotoxic T lymphocytes always precedes changes of ALT level as a marker of hepatocellular inflammation and necrosis in chronic hepatitis B [4-7], we suggest to consider different profiles of serum ALT and viral HBV DNA kinetics after administration of antiviral agents in chronic HB patients to monitor responses about antiviral therapy against HBV infection. Therefore, we need to get samples with different time for assessment of viral and biochemical response after treatment with antiviral agents in patients with chronic HB.
Generally speaking, responses to antiviral agents in treatment of patients with chronic HB are usually no detection of viral concentrations such as HBV DNA using non-amplified assays, sustained loss of HBeAg with or without detection of anti-HBe. HBeAg is a viral protein produced by infected cell. It is not that its production is not directly inhibited by lamivudine, but that it is inhibited by INF-α and this response thought to represent the lysis of infected hepatic cell by the host’s immune response and changes in the serum HBeAg concentration can be reflects changes in infected hepatic cell mass [6-8]. ALT is the hepatic cytoplasmic enzyme that is released from damaged cells and a reliable indicator of the level of cell damage and death [6].
Therefore, the strategies of antiviral regimen that primary endpoint is HBeAg seroconversion (undetectable HBeAg, detectable anti-HBe, and undetectable HBV DNA) has danger of viral mutation dependent on duration of treatment and demerits of high cost. Therefore, based on difference of serum HBV clearance and ALT kinetics in patients with chronic HB, we may consider that switching regimen with potent antiviral agents as a primary drugs to reduce the viral DNA concentrations to undetectable level and agents with anti-inflammatory effect to reduce serum ALT level below upper limit of normal range of ALT rather than combined regimen with antiviral agents and INF-α or adefovir to escape the viral mutation and high cost to control patients with chronic HB.


References
Weissberg JI, Andres LL, Smith CI, Weick S, Nichols JE, et al. (1984) Survival in chronic hepatitis B. An analysis of 379 patients. Ann Intern Med 101: 613-616. Beasley RP, Hwang LY, Lin CC, Chien CS (1981) Hepatocellular carcinoma and hepatitis B virus. A prospective study of 22 707 men in Taiwan. Lancet 2:1129-1133. Dienstag JL, Schiff ER, Wright TL, Perrillo RP, Hann HW, et al. (1999) Lamivudine as initial treatment for chronic hepatitis B in the United States. N Engl J Med 341: 1256-1263. Jonas MM, Mizerski J, Badia IB, Areias JA, Schwarz KB, et al. (2002) Clinical trial of lamivudine in children with chronic hepatitis B. N Engl J Med 346: 1706-1713. Hagmann S, Chung M, Rochford G, Jani M, Trinh-Shevrin C, et al. (2003) Response to lamivudine treatment in children with chronic hepatitis B virus infection. Clin Infect Dis 37: 1434-1440 Nowak MA, Bonhoeffer S, Hill AM, Boehme R, Thomas HC, et al. (1996) Viral dynamics in hepatitis B virus infection. Proc Natl Acad Sci U S A 93: 4398-402. Guidotti LG, Rochford R, Chung J, Shapiro M, Purcell R, et al. (1999) Viral clearance without destruction of infected cells during acute HBV infection. Science 284: 825-829. Chang CN, Skalski V, Zhou JH, Cheng YC (1992) Biochemical pharmacology of (+)- and (-)-2',3'-dideoxy-3'-thiacytidine as anti-hepatitis B virus agents. J Biol Chem 267: 22414-22420. Liu CJ, Chen PJ, Lai MY, Kao JH, Chang CF, et al. (2003) A prospective study characterizing full-length hepatitis B virus genomes during acute exacerbation. Gastroenterology 124: 80-90.