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Increased risk of NASH in patients carrying the C(−159)T polymorphism in the CD14 gene promoter region
  1. P Brun1,
  2. I Castagliuolo2,
  3. A R Floreani3,
  4. A Buda3,
  5. L Blasone3,
  6. G Palù4,
  7. D Martines5
  1. 1Department of Histology, Microbiology, and Medical Biotechnologies, and Department of Gastroenterological Sciences, University of Padua, Italy
  2. 2Department of Histology, Microbiology, and Medical Biotechnologies, University of Padua, Italy
  3. 3Department of Gastroenterological Sciences, University of Padua, Italy
  4. 4Department of Histology, Microbiology, and Medical Biotechnologies, University of Padua, Italy
  5. 5Department of Gastroenterological Sciences, University of Padua, Italy
  1. Correspondence to:
    Dr I Castagliuolo
    University of Padua, School of Pharmacy, Department of Histology, Microbiology, and Medical Biotechnology, Via A Gabelli 63. Padua, 35121 Italy; ignazio.castagliuolo{at}unipd.it

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Non-alcoholic fatty liver (NAFL) is a common hepatic disorder that progresses to non-alcoholic steatohepatitis (NASH) in only 20% of patients. Whereas polymorphisms in genes involved in fat metabolism confer susceptibility to NAFL,1 the risk factors involved in the progression of the disease to NASH are not known. A possible role for intestinal derived bacterial endotoxins in the progression from NAFL to NASH is gaining increasing interest in view of recent experimental data. Thus NASH patients show a higher prevalence of small intestinal bacterial overgrowth (SIBO) and, in animal models of SIBO, hepatitis is improved following antibiotic treatment.2,3 Furthermore, we have recently observed that increased intestinal mucosal permeability, such as that observed in obese C57BL/6Job/ob mice, leads to higher lipopolysaccharide (LPS) levels in …

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