Oxidative stress and the importance of H. pylori eradication in patients with functional dyspepsia

Abstract

Background: To investigage the thiol and disulphide levels in Helicobacter pylori -positive patients with non-ulcer dyspepsia and investigate the change in these levels with eradication therapy. Methods: This is a prospective observational study. A total of 320 patients diagnosed with dyspepsia according to Rome IV criteria were included in the study. First, blood samples were drawn from patients to determine their serum thiol and disulphide levels. Endoscopic biopsy was performed on all patients and the biopsy specimens obtained were examined pathologically. Patients positive for H. pylori were administered eradication therapy. Blood samples were drawn from these patients for the second time, and their serum thiol and disulphide levels were measured. The thiol–disulfide levels of the patients who were successful in H. pylori eradication treatment, with those who were not, were compared before and after the treatment. Results: The mean plasma disulphide level decreased significantly from 14.0 ± 6.6 to 10.9 ± 5.9 μmol/L in H. pylori -positive patients that responded to the H. pylori eradication treatment ( P = 0.033). On the other hand, there was an insignificant increase in the mean serum thiol level (341.4 ± 30.5 vs. 342.6 ± 29.8 μmol/L; P = 0.273) and an insignificant decrease in the mean serum disulphide level (15.2 ± 2.5 vs. 14.8 ± 2.3 μmol/L; P = 0.163) in H. pylori -positive patients that did not respond to the H. pylori eradication treatment. Conclusion: The inflammation caused by H. pylori shifted the thiol–disulphide equilibrium in the cell redox system towards the direction of disulphide. The study findings suggest that the restoration of the said hemostatic balance with eradication therapy relieved the organism from oxidative stress.

Reactive Oxygen Species and H. pylori Infection: A Comprehensive Review of Their Roles in Gastric Cancer Development

“…As excess ROS accumulate, they can damage cellular components such as membranes, proteins, and DNA, which can be detrimental to cancerous and noncancerous cells [ 20 ]. Various research studies have shown that H. pylori infection induces ROS generation and oxidative stress, which can lead to GC [ 21 , 22 ]. In this study, we discuss the pathology of ROS generation in H. pylori -mediated gastric carcinogenesis (see Figure 1 ).…”

High-Salt Diet Exacerbates H. pylori Infection and Increases Gastric Cancer Risks

“…H. pylori strains containing CagA and VacA are able to invade and destroy gastric epithelial cells and stimulate cell proliferation towards dysplasia [ 72 , 73 ]. Processes that activate the immune and antioxidant systems of the host organism are inhibited once H. pylori inhibits gastric cells [ 74 ]. Specifically, CagA H. pylori strains continue to contribute to the toxic environment of free radical ions, through the expression of spermine oxidase (SMO), and give rise to hydrogen peroxide.…”

Analysis of Network Pharmacological Efficacy and Therapeutic Effectiveness in Animal Models for Functional Dyspepsia of Foeniculi fructus

“…Functional dyspepsia is characterized as a clinical syndrome where individuals experience recurring or persistent discomfort or pain in the upper abdomen, without any identifiable organic disorders underlying the symptoms [ 1 ]. In patients with functional dyspepsia, antagonists of histamine H 2 receptors [ 2 ], inhibitors of proton pumps [ 3 ], or eradication with Helicobacter pylori have shown limited benefits [ 4 ], and the outcomes of controlled trials were generally unsatisfactory. Additionally, pharmacological agents (such as cisapride), despite their limited effectiveness, pose the risk of potential side effects such as arrhythmia, cardiovascular disease, headaches, and abdominal pain.…”