Oxidant-Antioxidant Homeostasis in Gastroduodenopathies Induced by Nonsteroidal Anti-Inflammatory Drugs in Patients with Osteoarthritis Taking into Account the Pathogenic Helicobacter pylori Strains
The role of Helicobacter pylori (Hp) in pathogenetic mechanisms of gastroduodenopathies (GDP) caused by nonsteroidal anti-inflammatory drugs (NSAIDs) in patients with osteoarthritis (OA) is ambiguous. The aim of the work was to determine the changes in the oxidant-antioxidant homeostasis at GDP induced by NSAIDs in patients with OA, depending on the presence of pathogenic strains of Hp. Methods. To achieve this goal, we have examined 68 patients with OA and concomitant Hp-associated GDP induced by NSAIDs. We have determined strains of Hp in the stool, blood and biopsy samples by polymerase chain reaction. We studied the content of the products of oxidative protein modification — neutral aldehyde- and ketone dinitrophenylhydrazone (NAKDNPH), reduced glutathione (RG), the activity of glutathione peroxidase (GP) and glutathione-S-transferase (GT). Results. In all patients, there was a significant increase in the intensity of oxidative modification of proteins. However, in patients with concomitant Hp pathogenic and ulcerative strain, cag A+/vac A+ of NAKDNPH were higher by 13.55 % (p < 0.05) and 22.89 % (p < 0.05), respectively, as compared to the patients with concomitant Hp cag A+/vac A– and Hp cag A–/vac A+. The patients had a decrease in the content of RG on the background of compensatory increase in the activities of GT and GP. In the examinees with Hp pathogenic and ulcerative strains cag A+/vac A+, the content of RG was significantly lower by 16.45 and 26.66 %, respectively, as compared to the patients with associated Hp cag A+/vac A– and Hp cag A–/vac A+. GT and GP activity in patients with Hp containing strains cag A+/vac A– was somewhat higher than in patients with Hp containing strains cag A–/vac A+. Conclusion. In gastroduodenopathies, caused by NSAIDs, in patients with OA, there are significant changes in the oxidant-antioxidant homeostasis, and associated pathogenic and ulcerogenic strain Hp cag A+/vac A+ intensifies the oxidative modification of proteins on the background of dysfunction of the antioxidant defense system.
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