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in the
pathogenesis of non-alcoholic steatohepatitis
a Department of
Gastroenterology, Queen Elizabeth Hospital, Adelaide, South Australia,
Australia, b Department of
Histopathology, Queen Elizabeth Hospital, Adelaide, South Australia,
Australia, c Department of
Biochemistry, Repatriation General Hospital, Adelaide, South Australia,
Australia
Correspondence to: A J Wigg, Unit of Gastroenterology and Hepatology, Flinders Medical Centre, Bedford Park, 5042, South Australia, Australia. alan.wigg{at}flinders.edu.au
Accepted for publication 18 July 2000
BACKGROUND
Small
intestinal bacterial overgrowth may contribute to the development of
non-alcoholic steatohepatitis, perhaps by increasing intestinal
permeability and promoting the absorption of endotoxin or other enteric
bacterial products.
AIMSTo investigate
the prevalence of small intestinal bacterial overgrowth, increased
intestinal permeability, elevated endotoxin, and tumour necrosis factor
(TNF-) levels in patients with non-alcoholic steatohepatitis and
in control subjects.
PATIENTS AND
METHODSTwenty two patients with non-alcoholic
steatohepatitis and 23 control subjects were studied. Small intestinal
bacterial overgrowth was assessed by a combined
14C-D-xylose and lactulose breath test.
Intestinal permeability was assessed by a dual lactulose-rhamnose sugar
test. Serum endotoxin levels were determined using the limulus
amoebocyte lysate assay and TNF- levels using an ELISA.
RESULTSSmall
intestinal bacterial overgrowth was present in 50% of patients with
non-alcoholic steatosis and 22% of control subjects (p=0.048). Mean
TNF- levels in non-alcoholic steatohepatitis patients and control
subjects were 14.2 and 7.5 pg/ml, respectively (p=0.001). Intestinal
permeability and serum endotoxin levels were similar in the two groups.
CONCLUSIONSPatients
with non-alcoholic steatohepatitis have a higher prevalence of small
intestinal bacterial overgrowth, as assessed by the
14C-D-xylose-lactulose breath test, and higher
TNF- levels in comparison with control subjects. This is not
accompanied by increased intestinal permeability or elevated endotoxin levels.
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