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Lamivudine has been widely used in the treatment of CHB and is effective in suppressing HBV replication and in improving liver disease in both HBeAg-positive and HBeAg-negative patients (6, 7). After 1 year of therapy, HBeAg-positive patients showed a 4�C5?log10?copies/ml reduction in the serum HBV DNA level with 18�C20% HBeAg seroconversion http://www.selleckchem.com/products/sch772984.html (35). After 5 years of therapy, HBeAg seroconversion was reported in 35�C65%, with the highest response in those patients with high [>5 �� upper limit of normal (ULN)] ALT levels at baseline. In HBeAg-negative patients, 60�C70% showed HBV DNA suppression to below detectable limits after 1 year of therapy (6). However, around half of the HBeAg-positive patients and up to 90% of HBeAg-negative patients who respond to treatment relapsed if LAM was withdrawn. Loss of HBsAg, the ultimate serological goal of therapy, is very rare ( http://www.selleck.cn/products/z-vad-fmk.html with its long-term use is the high risk of LAM-resistant mutations, which arise in 60�C70% of patients after 5 years (6). Although long-term therapy can reduce the incidence of complications of HBV-related liver disease in patients with advanced liver disease, this is only true for as long as viral suppression is maintained and the development of resistance leads to virological rebound and biochemical breakthrough (38). The long-term safety profile of LAM is good in the absence of resistance development, but patients with LAM-resistant mutations are at risk of worsening liver disease (39). Despite the risk of resistance and its associated problems, LAM remains the mainstay of treatment in some regions due to its low cost. However, initial savings may be negated when salvage therapy http://www.selleckchem.com/products/dabrafenib-gsk2118436.html is required to manage resistance. It is possible that restricting first-line LAM to patients most likely to respond may be an option in such regions. A number of factors have been found to improve the likelihood of response to LAM, including high baseline ALT, female gender and younger age (35). A high pretreatment serum HBV DNA level and a high level of the residual virus after initiation of treatment are associated with an increased risk of the development of LAM-resistant mutations (6). Given this, it may be possible to select patients with favourable characteristics who may be more suitable for first-line LAM monotherapy. There is also evidence that on-treatment response to LAM can predict the treatment outcome. Serial HBeAg levels have been shown to be useful in predicting YMDD mutant emergence in HBeAg non-seroconverted patients, with a pattern of descending and then increasing HBeAg levels on-treatment during LAM treatment predicting the emergence of YMDD mutations with a sensitivity of 66% and a specificity of 100% (40).