Published online Jan 28, 2017. doi: 10.3748/wjg.v23.i4.712
Peer-review started: September 16, 2016
First decision: September 20, 2016
Revised: November 14, 2016
Accepted: January 2, 2017
Article in press: January 3, 2017
Published online: January 28, 2017
Processing time: 127 Days and 21.8 Hours
To assess whether surrogate biomarkers of endotoxemia were correlated with the histological features of nonalcoholic fatty liver disease (NAFLD).
One hundred twenty-six NAFLD patients who had undergone percutaneous liver biopsy were enrolled. Serum lipopolysaccharide (LPS)-binding protein (LBP) and anti-endotoxin core immunoglobulin G (EndoCab IgG) antibody concentrations at the time of liver biopsy were measured using the enzyme-linked immunosorbent assays to examine for relationships between biomarker levels and histological scores.
Serum LBP concentration was significantly increased in nonalcoholic steatohepatitis (NASH) patients as compared with nonalcoholic fatty liver (NAFL) subjects and was correlated with steatosis (r = 0.38, P < 0.0001) and ballooning scores (r = 0.23, P = 0.01), but not with the severity of lobular inflammation or fibrosis. Multivariate linear regression analysis revealed that LBP was associated with steatosis score and circulating C-reactive protein, aspartate aminotransferase, and fibrinogen levels. Serum EndoCab IgG concentration was comparable between NASH and NAFL patients. No meaningful correlations were detected between EndoCab IgG and histological findings.
LBP/EndoCab IgG were not correlated with lobular inflammation or fibrosis. More accurate LPS biomarkers are required to stringently assess the contribution of endotoxemia to conventional NASH.
Core tip: This is the first study simultaneously measuring two surrogate endotoxemia markers, lipopolysaccharide-binding protein (LBP) and EndoCab IgG, in biopsy-proven nonalcoholic fatty liver disease (NAFLD) patients in order to assess for relationships with the histological features of NAFLD. Serum LBP/EndoCab IgG were not correlated with lobular inflammation or fibrosis. It remains elusive whether portal endotoxemia promotes hepatitis/fibrosis in human conventional NAFLD/nonalcoholic steatohepatitis.