18 - World Journal of Gastroenterology

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Özen H. . Glycogen storage diseases 2553 human acid alpha-glucosidase enzyme therapy for infantile glycogen storage disease type II: results of a phase I/II clinical trial. Genet Med 2001; 3: 132-138 162 Lebo RV, Anderson LA, DiMauro S, Lynch E, Hwang P, Fletterick R. Rare McArdle disease locus polymorphic site on 11q13 contains CpG sequence. Hum Genet 1990; 86: 17-24 163 Grunfeld JP, Ganeval D, Chanard J, Fardeau M, Dreyfus JC. Acute renal failure in McArdle's disease. Report of two cases. N Engl J Med 1972; 286: 1237-1241 164 Howard TD, Akots G, Bowden DW. Physical and genetic mapping of the muscle phosphofructokinase gene (PFKM): reassignment to human chromosome 12q. Genomics 1996; 34: 122-127 165 Tarui S, Okuno G, Ikura Y, Tanaka T, Suda M, Nishikawa M. Phosphofructokinase deficiency in skeletal muscle. A new type of glycogenosis. Biochem Biophys Res Commun 1965; 19: 517-523 S- Editor Zhu LH L- Editor Zhu LH E- Editor Chen GJ www.wjgnet.com
PO Box 2345, Beijing 100023, China World J Gastroenterol 2007 May 14; 13(18): 2554-2567 www.wjgnet.com World Journal of Gastroenterology ISSN 1007-9327 wjg@wjgnet.com © 2007 The WJG Press. All rights reserved. TOPIC HIGHLIGHT Giuseppe Montalto, Series Editor Future prospectives for the management of chronic hepatitis B WF Leemans, HLA Janssen, RA de Man WF Leemans, HLA Janssen, RA de Man, Department of Gastroenterology & Hepatology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands Correspondence to: RA de Man, MD, PhD, Department of Gastroenterology and Hepatology, Room H 437, Erasmus MC, University Medical Center Rotterdam’s-Gravendijkwal 230, 3015 CE Rotterdam, The Netherlands. r.deman@erasmusmc.nl Telephone: +31-104-635942 Fax: +31-104-365916 Received: 2006-12-15 Accepted: 2007-03-08 Abstract Chronic hepatitis B virus infection affects about 400 million people around the globe and causes approximately a million deaths a year. Since the discovery of interferon-α as a therapeutic option the treatment of hepatitis B has evolved fast and management has become increasingly complicated. The amount of viral replication reflected in the viral load (HBV-DNA) plays an important role in the development of cirrhosis and hepatocellular carcinoma. The current treatment modalities for chronic hepatitis B are immunomodulatory (interferons) and antiviral suppressants (nucleoside and nucleotide analogues) all with their own advantages and limitations. An overview of the treatment efficacy for both immunomodulatory as antiviral compounds is provided in order to provide the clinician insight into the factors influencing treatment outcome. With nucleoside or nucleotide analogues suppression of viral replication by 5-7 log10 is feasible, but not all patients respond to therapy. Known factors influencing treatment outcome are viral load, ALT levels and compliance. Many other factors which might influence treatment are scarcely investigated. Identifying the factors associated with response might result in stopping rules, so treatment could be adapted in an early stage to provide adequate treatment and avoid the development of resistance. The efficacy of compounds for the treatment of mutant virus and the cross-resistance is largely unknown. However, genotypic and phenotypic testing as well as small clinical trials provided some data on efficacy in this population. Discontinuation of nucleoside or nucleotide analogues frequently results in viral relapse; however, some patients have a sustained response. Data on the risk factors for relapse are necessary in order to determine when treatment can be discontinued safely. In conclusion: chronic hepatitis B has become a treatable disease; however, much research is needed to tailor therapy to an individual patient, to predict the sustainability of response and determine the best treatment for those www.wjgnet.com failing treatment. © 2007 The WJG Press. All rights reserved. Key words: Hepatitis B virus; Cirrhosis; Treatment; Interferon; Nucleoside analogues; Nucleotide analogues; Lamivudine; Adefovir; Entecavir; Telbivudine; Tenofovir; Resistance; Genotype Leemans WF, Janssen HLA, de Man RA. Future prospectives for the management of chronic hepatitis B. World J Gastroenterol 2007; 13(18): 2554-2567 http://www.wjgnet.com/1007-9327/13/2554.asp INTRODUCTION Treatment of chronic hepatitis B remains an important clinical objective. Estimates are that 2 billion people have been infected worldwide and chronic hepatitis B currently affects about 400 million people, particularly in developing countries [1] . Chronic hepatitis B is responsible 500 000 to 1.2 million deaths annually from liver cirrhosis and hepatocellular carcinoma (HCC) [2] . It is one of the most common infectious diseases and among the world’s leading causes of death. There are two strategies to decrease these numbers, prevention of new infections and treatment of those already chronically infected. Treatment options consist of immunomodulatory and viral suppressant drugs. In this review the current standard of care and the future developments in the field of chronic hepatitis B are discussed. WHAT IS THE OPTIONAL TREATMENT Naïve patients The ideal treatment for hepatitis B is an effective cheap treatment, resulting in HBsAg loss and formation of anti-HBs, with finite treatment duration and little side effects. Currently none of the HBV treatments fulfill these conditions. With interferon based therapy HBsAg loss occurs in 3%-10% of the patients within one year of start of therapy and increases in sustained responders to 11%-32% [3-9] . HBsAg loss is rare (< 2% after one year of treatment) in patients treated with nucleos(t)ide analogues, which is about the rate observed in the natural history of the disease [10-16] . However, in a small cohort treated with tenofovir, HBsAg loss was observed in 14% of 35
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18 - World Journal of Gastroenterology

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