Release of α-Glutathione s-Transferase (α-GST) and Hepatocellular Damage Induced by Helicobacter pylori and Eradication Treatment

Helicobacter pylori (H. pylori) is a gram negative, spiral, microaerophylic bacterium that infects the stomach of more than 50% of the human population worldwide. H. pylori is well recognized as a critical factor in the majority of patients with peptic ulcer disease and successful treatment results in cure of the disease. On the other hand, H. pylori infection has been associated with several extra-intestinal diseases such as hepatic encephalopathy. In this study, a triple treatment was used in management and eradication of H. pylori infection. We hypothesized that H. pylori infection and/or eradication treatment increased the releasing of 28;“-glutathione S-transferase (28;“-GST). We also investigated whether 28;-GST is a more sensitive marker than aminotransferases (traditional liver function tests) for hepatocellular damage. However, we did not find any association between both H. pylori infection and eradication treatment and 28;“-GST levels. According to our data, eradication treatment did not cause hepatocellular damage.