title: Dynamic changes of lipopolysaccharide levels in different phases of acute on chronic hepatitis B liver failure.
abstract: BACKGROUND
  High serum levels of lipopolysaccharide (LPS) with LPS-MD-2/TLR4 complex activated NF-kb and cytokine cause hepatic necrosis in animal models. We investigated the dynamic changes of LPS levels in patients with acute on chronic hepatitis B liver failure (ACHBLF).
  
  
  METHODS
  We enrolled ACHBLF patients for a 12-week study. Patients' LPS levels were measured along with 10 healthy controls. Patients on supportive care and recovered without intervention(s) were analyzed. Patients' LPS levels during the disease progression phase, peak phase, and remission phase were compared with healthy controls.
  
  
  RESULTS
  Among 30 patients enrolled, 25 who received interventions or expired during the study period were excluded from the analysis, five patients on supportive care who completed the study were analyzed. Significant abnormal distributions of LPS levels were observed in patients in different phases (0.0168±0.0101 in progression phase; 0.0960±0.0680 in peak phase; 0.0249±0.0365 in remission phase; and 0.0201±0.0146 in controls; respectively, p<0.05). The highest level of LPS was in the peak phase and significantly elevated when compared to controls (0.0201±0.0146 vs. 0.0960±0.0680, p = 0.007). There were no statistically significant differences in LPS levels between healthy controls and subjects in the progression phase or remission phase. Dynamic changes of LPS were correlated with MELD-Na in the progression phase (p = 0.01, R = 0.876) and in the peak phase (p = 0.000, R = -1.00).
  
  
  CONCLUSIONS
  Significant abnormal distributions of LPS levels were observed in ACHBLF with the highest level in the peak phase. The dynamic changes of LPS were correlated with disease severity and suggested LPS causing secondary hepatic injury.
authors.affiliation: Division of Liver Diseases, Department of Medicine, The Mount Sinai Medical Center, Mount Sinai School of Medicine, New York, New York, United States of America.
authors.forename: Calvin
authors.initials: C
authors.lastname: Pan
authors.forename: Yurong
authors.initials: Y
authors.lastname: Gu
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Yubao
authors.initials: Y
authors.lastname: Zheng
authors.forename: Liang
authors.initials: L
authors.lastname: Peng
authors.forename: Hong
authors.initials: H
authors.lastname: Deng
authors.forename: Youming
authors.initials: Y
authors.lastname: Chen
authors.forename: Lubiao
authors.initials: L
authors.lastname: Chen
authors.forename: Sui
authors.initials: S
authors.lastname: Chen
authors.forename: Min
authors.initials: M
authors.lastname: Zhang
authors.forename: Zhiliang
authors.initials: Z
authors.lastname: Gao
mesh_terms: D000818:Animals; D001931:Brain Mapping / Q000379:methods; D004195:Disease Models, Animal; D004566:Electrodes; D005246:Feedback; D019694:Hepatitis B, Chronic / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000378:metabolism*; D008099:Liver / Q000473:pathology; D017114:Liver Failure, Acute / Q000378:metabolism / Q000821:virology*; D008297:Male; D009474:Neurons / Q000378:metabolism; D009991:Oscillometry / Q000379:methods; D017397:Prefrontal Cortex / Q000502:physiology; D051381:Rats; D020318:Rats, Long-Evans; D015203:Reproducibility of Results; D013788:Thalamus / Q000378:metabolism*
chemical_list: D008070:Lipopolysaccharides