In this study, they indicated that ETV given at 1 mg/day for 48 weeks resulted in lesser hepatitis B virus (HBV) DNA and alanine aminotransferase (ALT) reduction in the LAM/ADV-resistant group than compared with the LAM-resistant group. They also noted that HBV

DNA loss was significantly higher in the LAM-resistant group compared with the LAM/ADV-resistant group (34% versus 10%). However, they showed that virological breakthrough was similar in both groups. They also underlined that virological response at 12 weeks determined the degree of HBV DNA reduction over 48 weeks of therapy, regardless of previous antiviral MK-2206 ic50 treatment. In their study, Shim et al. underlined the importance of multidrug resistance in cases with inappropriate use of antivirals in HBV infection. The same authors suggested, in the introduction section, that “in terms of salvage therapy for LAM-resistant or ADV-resistant chronic hepatitis B infection, the American Association for the Study of Liver Diseases (AASLD) practice guideline recommended switching to ETV” monotherapy as an optimal Inhibitor Library order strategy. However, according to the current guidelines,

including AASLD 2009,2 European Association for the Study of the Liver 2009,3 and Asian Pacific Association for the Study of the Liver 2008,4 what the authors did seemed to be inappropriate to suggest to the readers. The guidelines mentioned above unanimously indicated that

ETV can be recommended as a rescue therapy only for ADV-resistant chronic HBV infection having Asp236-to-Thr236 (N236T) and/or Ala181-to-Thr181/Val181 (A181T/V) substitutions. Contrary to what the authors MCE公司 wrote in the introduction section of their article, AASLD guidelines in 20092 on HBV infection clearly indicate that ETV is not an optimal treatment for LAM-refractory HBV. It is clearly known that Leu180-to-Met180 (L180M) + Met204-to-Val204 (M204V) and L180M + M204V + Asn236-to-Thr236 (N236T) mutants behaved 6.25-fold resistant to ETV compared with wild-type HBV.5 We also know that genotypic resistance to ETV will develop at a rate of 43% at the end of 4 years.6 Expectedly, two patients in the series of Shim et al.1 developed virological breakthrough with Ser202-to-Gly202 (S202G) ETV resistance substitutions at 36 weeks of treatment, and one patient developed biochemical breakthrough in the LAM-resistant group of patients. Unfortunately, the readers were not informed in this article how the authors treated these two cases in their series. Another relevant article in this field showed that although HBV DNA suppression was achieved in a higher percentage of patients, there was an emergence of nearly 8% resistance to ETV monotherapy in cases with previous LAM resistance in year 2.7 Thus, this strategy led to selection of multidrug-resistant HBV strains with maximal viral resistance in the near future.