European Gastroenterology & Hepatology Review, 2009;5:38-42
Abstract
Hepatitis B is a global health problem that affects millions of people and causes over 1 million deaths every year. The goals of hepatitis B therapy are to prevent disease progression and improve patient survival and quality of life. Currently, many experts agree that patients with a high hepatitis B viral load should be treated, because the risks of hepatitis B disease progression and complications are associated with HBV viral load. The treatment options include interferon injection and oral nucleotide and nucleoside analogues. In this article, we discuss recent developments in who should be treated for hepatitis B, treatment strategies and special conditions associated with hepatitis B treatment.
Keywords
HBV, hepatitis B, therapy, viral load, peginterferon alpha-2a, lamivudine, adefovir dipivoxil, entecavir, telbivudine, tenofovir
Disclosure
The authors have no conflicts of interest to declare.
Received:
June 11, 2009 Accepted
June 30, 2009
Correspondence:
Zhiping Li, Johns Hopkins University, 912 Ross Bldg, 720 Rutland Ave, Baltimore, MD 21205, US. E: zhipingli@jhmi.edu
Infection with hepatitis B virus (HBV) is a significant global public health problem. It is estimated that 350 million people worldwide are chronically infected with HBV and that one-third of the world’s population has evidence of exposure to the virus.1 Sequelae of chronic infection with hepatitis B (CHB) include end-stage liver disease and hepatocellular carcinoma (HCC), and have been associated with over 1 million deaths per year.2–4
The natural history of HBV infection is a dynamic process involving interactions between host, viral and external factors. HBV infection therefore results in a range of clinical manifestations with varying risk of progression. This natural history can be divided into four distinct phases, which are not necessarily sequential or experienced by all patients. First, the ‘immune-tolerant’ phase is characterised by high levels of viraemia with minimal elevation or normal level of aminotransferase and minimal inflammation on histology. This phase is more frequent and more sustained during infection early in life.5,6 Second, during the ‘immune-reactive’ phase, HBV DNA levels and replication are low. Unlike the immune-tolerant stage of infection, this phase is associated with histological evidence of liver disease and more rapid disease progression. It may also be referred to as the ‘immune-clearance’ phase.1,2,7 Third, transition into the ‘inactive carrier’ stage often occurs with hepatitis B e antigen (HBeAg) seroconversion. The inactive carrier stage is characterised by very low or undetectable HBV DNA. Hepatitis B surface antigen (HBsAg) may be lost in 1–3% of patients; however, even these individuals can experience disease reactivation.8 Finally, approximately one-third of inactive carriers will enter the ‘reactivation’ phase of the disease, which is characterised by fluctuating high levels of HBV DNA and aminotransferases.9,10 Other patients directly transition into this phase from the immune reactive stage upon HBeAg seroconversion.
Some chronic HBV patients are infected with mutations in the pre-core and/or basal core promoter regions, leading to a decrease or loss of HBeAg expression.11 These patients have low rates of spontaneous remission and a high risk of liver disease progression.11 It is therefore important to distinguish them from inactive carriers; hence, serial monitoring of HBV DNA and alanine aminotransferase (ALT) for all HBsAg-positive, HBeAg-negative individuals is recommended.
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