E common participating factors include viral hepatitis reactivation, alcohol, hepatotoxic drugs/herbs. In acute on chronic hepatitis B liver failure (ACHBLF), HBV reactivation is the major acute insults and precipitation liver failure [3]. It may occur after withdrawal of HBV antiviral treatment but more often, due to non- HBV treatment related events, which include disease reactivation either spontaneous or secondary to intensive chemotherapy/immunosuppressive therapy. Liver transplantation is the only curative therapeutic option for ACHBLF with a 5-year survival rate of 85 [4,5]. However, infectious complications often preclude transplant in patients with ACHBLF and many die on the waiting list due to the shortage of organs [6]. In 2008, the localDynamic Changes of LPS in ACLF with HBVstandard of care for ACHBLF other than transplantation for ACHBLF was supportive care. Prior to the time we concluded this study, there was no prospective randomized control trial to support the effectiveness and safety use of antiviral therapy in patients with ACHBLF [7]. In addition, Lange et al reported that a significant portion of patients with high MELD scores and treated with entecavir developed lactic acidosis resulting in high mortality [8]. Thus, the local standard of care at that time required a detailed discussion with patients and obtaining the consent prior to the antiviral use in patients with ACHBLF. Due to the lacking of evidence on the use of antiviral for ACHBLF during our study period, two patterns of clinical practice were observed in our center: patients who believed the potential benefit of antiviral treatment were treated with nucleoside (tenofovir was not available in China), whereas, patients who believed that the antiviral had no role on hepatic regeneration during acute setting or unwilling to take the risk of lactic acidosis could defer the antiviral treatment until they recovered from the acute event, and then received antiviral treatment for CHB when their disease 298690-60-5 site severity was improved (low MELD scores had less frequency of lactic acidosis). Our study was designed to capture those patients who deferred antiviral treatment but were able to recover spontaneously from ACHBLF without intervention. The mechanism of ACHBLF remains unclear. It was speculated that pro-inflammatory BIBS39 supplier cytokines mediated hepatic inflammation along with oxidative stress and the production of nitric oxide initiated 
the acute hepatic injury, followed by neutrophil dysfunction from circulating endotoxins (the cause of secondary liver damage), resulting in sepsis, multi-organ failure and impairment of liver regeneration [9,10,11,12,13]. LPS is an endotoxin derived from Gram-negative bacteria in the intestinal micro-flora. Evidently, trace amounts of LPS were measurable in serum samples from portal vein in normal healthy subjects since LPS may penetrate the intestinal 1326631 mucosa. However, the majority of LPSs were cleared by liver filtration [10,14]. West et al demonstrated that about 40 ?0 of an intravenous dose of LPS was cleared up by the liver filtration in animal models [13]. In addition to the filtration, hepatic and Kupffer cell (KC) uptake in the liver with detoxification played a key role in preventing high circulating levels of LPS [9]. In CHB patients, Sozinov et al observed that high incidence of Gram-negative bacteria overgrowth leads to the over production of LPS and results in higher serum levels of LPS [14]. On the other hand, several studies in.E common participating factors include viral hepatitis reactivation, alcohol, hepatotoxic drugs/herbs. In acute on chronic hepatitis B liver failure (ACHBLF), HBV reactivation is the major acute insults and precipitation liver failure [3]. It may occur after withdrawal of HBV antiviral treatment but more often, due to non- HBV treatment related events, which include disease reactivation either spontaneous or secondary to intensive chemotherapy/immunosuppressive therapy. Liver transplantation is the only curative therapeutic option for ACHBLF with a 5-year survival rate of 85 [4,5]. However, infectious complications often preclude transplant in patients with ACHBLF and many die on the waiting list due to the shortage of organs [6]. In 2008, the localDynamic Changes of LPS in ACLF with HBVstandard of care for ACHBLF other than transplantation for ACHBLF was supportive care. Prior to the time we concluded this study, there was no prospective randomized control trial to support the effectiveness and safety use of antiviral therapy in patients with ACHBLF [7]. In addition, Lange et al reported that a significant portion of patients with high MELD scores and treated with entecavir developed lactic acidosis resulting in high mortality [8]. Thus, the local standard of care at that time required a detailed discussion with patients and obtaining the consent prior to the antiviral use in patients with ACHBLF. Due to the lacking of evidence on the use of antiviral for ACHBLF during our study period, two patterns of clinical practice were observed in our center: patients who believed the potential benefit of antiviral treatment were treated with nucleoside (tenofovir was not available in China), whereas, patients who believed that the antiviral had no role on hepatic regeneration during acute setting or unwilling to take the risk of lactic acidosis could defer the antiviral treatment until they recovered from the acute event, and then received antiviral treatment for CHB when their disease severity was improved (low MELD scores had less frequency of lactic acidosis). Our study was designed to capture those patients who deferred antiviral treatment but were able to recover spontaneously from ACHBLF without intervention. The mechanism of ACHBLF remains unclear. It was speculated that pro-inflammatory cytokines mediated hepatic inflammation along with oxidative stress and the production of nitric oxide initiated the acute hepatic injury, followed by neutrophil dysfunction from circulating endotoxins (the cause of secondary liver damage), resulting in sepsis, multi-organ failure and impairment of liver regeneration [9,10,11,12,13]. LPS is an endotoxin derived from Gram-negative bacteria in the intestinal micro-flora. Evidently, trace amounts of LPS were measurable in serum samples from portal vein in normal healthy subjects since LPS may penetrate the intestinal 1326631 mucosa. However, the majority of LPSs were cleared by liver filtration [10,14]. West et al demonstrated that about 40 ?0 
of an intravenous dose of LPS was cleared up by the liver filtration in animal models [13]. In addition to the filtration, hepatic and Kupffer cell (KC) uptake in the liver with detoxification played a key role in preventing high circulating levels of LPS [9]. In CHB patients, Sozinov et al observed that high incidence of Gram-negative bacteria overgrowth leads to the over production of LPS and results in higher serum levels of LPS [14]. On the other hand, several studies in.
