Abstract

Comparison of Insulin Resistance between Nonalcoholic Fatty Liver Disease Patients with and those without Helicobacter pylori Infection

Aim/background: Insulin resistance [IR] is the key pathophysiological mechanism for nonalcoholic fatty liver disease [NAFLD] and nonalcoholic steatohepatitis [NASH]. Recent studies have disclosed the relationship between Helicobacter pylori (H. pylori) infection and IR. This study aimed to evaluate the differences in IR between NAFLD patients with and those without H. pylori infection.
Patients and method: From January 2011 to December 2012, patients with pathologic proof of NAFLD were included. All patients received a C14 urea breath test for H. pylori infection evaluation. Serum samples were taken for homeostasis model assessment of insulin resistance [HOMA-IR], lipid profile, inflammatory cytokine and adipokine studies. Patients with H. pylori infection received standard triple eradication. Serum samples were then subjected to HOMA-IR three and six months after eradication therapy.
Results: Eleven patients with both NAFLD and H. pylori infection and 18 patients with only NAFLD were included into this study. There were no significant differences between the two groups in demographic, laboratory or histological data. The only difference was mean HDL value. Patients with H. pylori infection had higher mean HDL values than patients without H. pylori infection [50.1 ± 8.8 vs. 38.8 ± 9.7 mg/dL, p=0.004]. The serial values of HOMA-IR from patients with H. pylori infection following H. pylori eradication 0, 3 or 6 months later did not reveal an increasing or decreasing trend following H. pylori eradication treatment. Conclusion: There were no significant differences in HOMA-IR values between NAFLD patients regardless of whether they had H. pylori infection. For patients with NAFLD and H. pylori infection, the HOMA-IR value was not affected by H. pylori eradication treatment.


Author(s):

Chen Li-Wei,Chang Liang-Che,Chien Rong-Nan,Chen Chih-Hung,Kuo Sheng-Fong,Chang Jia-Jang,Hu Ching-Chih



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