For patients with MELD

scores above 30, MELD score was the only independent predictor. click here Patients with MELD scores over 30 were at the late stage of ACLF, and factors other than viral replication had a great impact on the prognosis. The livers of these patients had already undergone massive or sub-massive hepatic necrosis. Suppressing viral replication with lamivudine at this late stage was unlikely to be effective, as the main determinants for recovery were liver regeneration and the rapid cessation of ongoing necroinflammation. This could be the reason why some patients’ conditions deteriorated even though the replication of HBV had been suppressed by lamivudine. Our study has suggested that the prognosis of patients with ACLF may be related to the pretreatment HBV DNA load and the Palbociclib cell line decline of HBV DNA load during therapy. We found that the mortality of the patients with high HBV DNA load was higher than that

of patients with low HBV DNA load, which may be due to high HBV DNA load patients failing to eradicate HBV at an early stage of liver failure, and a continuously stimulated immune system clearing HBV causes progressive liver damage. Liver failure in patients with low HBV DNA level may be due to the excess of immune reaction. Our study also suggested that for patients with a MELD of score 20–30 (at the early and middle stage of liver failure), by week 4, the mortality with a HBV DNA load decline of more than 2 log10 MCE was lower than that of a less than 2 log10 decline. The decreased mortality may be related to the marked reduction of HBV DNA level by lamivudine relieving inflammatory reaction and improving liver function. Therefore, for the patients with a MELD score of 20–30, an early and effective antiviral therapy based on the combination therapy (including artificial liver support system and liver transplantation) could achieve a better therapeutic outcome. More potent antiviral drugs such as entecavir and tenofovir are now available. It is conceivable that these drugs might be even better, especially in reaching a rapid decrease in viral load and a faster

recovery, for the patients with a MELD score of 20–30 who can not achieve a 2 log10 HBV DNA decline. This study has proved that there is no significant difference in mortality between HBeAg-positive and -negative patients treated with lamivudine. HBeAg status before treatment has little effect on mortality in the lamivudine treatment group. HBV DNA load is more valuable than HBeAg status in predicting the prognosis of patients. In this study, we have confirmed that pretreatment HBV DNA load and the decline of HBV DNA load during therapy are not associated with the mortality of HBeAg-negative patients. It may be related to the late stage of chronic hepatitis, severe necrosis and fibrosis of liver, mutation of pre-core and basic core promoter, low HBV DNA load and cases limitation.