The aim of study was to evaluate the effect of helicobacter pylori eradication on liver fat content, liver function tests, lipid profile, homeostasis model assessment-IR (HOMA-IR) index, and anthropometric measurements (body mass index and waist circumference)in non-diabetic subjects with non-alcoholic fatty liver disease.
Helicobacter pylori (HP) antigens have been found in the liver of individuals with benign and malignant liver diseases. The role of HP in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) is controversial. This randomized double blind clinical trial was performed in non-diabetic dyspeptic patients with positive antibody to HP and the evidence of fatty liver in ultrasonography. After excluding other causes, participants with persistent elevated serum aminotransferase levels were presumed to have NAFLD. Those with NAFLD liver fat score greater than (-0.64) and positive urea breath test (UBT) were enrolled. They were randomly assigned to lifestyle modification alone or lifestyle modification plus HP eradication groups. Quadruple therapy (omeprazole, amoxicillin, bismuth subcitrate, and clarithromycin) for HP eradication was performed in two weeks. HP eradication was documented by UBT. Liver fat content, fasting serum glucose, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, triglyceride, cholesterol, high and low-density lipoprotein, HOMA-IR, and anthropometric measurements (body mass index and waist circumference) were checked at baseline and six weeks post-treatment.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
DOUBLE
Enrollment
40
Omeprazole (20 mg/BD)+ Amoxicillin (1 g/day)+ Bismuth subcitrate (240 mg/BD)+ Azithromycin (500 mg/BD)
Gastroenterology clinic, Sina hospital.
Tehran, Iran
Liver Fat Content
Primary outcome measure was changes in the liver fat content from baseline to the end of study (6 weeks post-treatment). The percent of liver fat was calculated as below: "Liver fat content (%) = 10 (-0.805 + 0.282 \* metabolic syndrome (yes = 1 / no = 0) + 0.078 \* type 2 diabetes (yes =2 / no =0) + 0.525 \* log fasting serum insulin (mU/L) + 0.521 \* log fasting serum AST (U/L) - 0.454 \* log (AST/ALT)"
Time frame: 8 weeks (6 weeks post-treatment)
Serum Alanine Aminotransferase Level
Secondary outcome measure was change in serum alanine aminotransferase concentration from baseline to the end of study
Time frame: 8 weeks
Serum Aspartate Aminotransferase Level
Secondary outcome measure was change in serum aspartate aminotransferase concentration from baseline to the end of study
Time frame: 8 weeks
Fasting Serum Glucose
Secondary outcome measure was change in fasting serum glucose concentration from baseline to the end of study
Time frame: 8 weeks
Serum Lipid Profile
Secondary outcome measure was change in serum lipid profile (including serum triglyceride, cholesterol, low-density lipoprotein, and high-density lipoprotein concentration) from baseline to the end of study
Time frame: 8 weeks
Homeostasis Model Assessment-Insulin Resistance (HOMA-IR)
Secondary outcome measure was change in HOMA-IR from baseline to the end of study
Time frame: 8 weeks
Anthropometric Measurements
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Secondary outcome measure was change in anthropometric measurements (body mass index and waist circumference) from baseline to the end of study
Time frame: 8 weeks