Helicobacter pylori—The Bridge between Local and Systemic Inflammation in Children

Abstract

Helicobacter pylori (H. pylori)-associated inflammatory status is no longer a debatable topic in children. The aim of our study was to to compare the inflammatory status in pediatric patients with H. pylori gastritis and non-H. pylori gastritis versus control group. We performed a prospective study on 68 children with dyspeptic symptoms which were divided into 3 groups: 14 children with H. pylori gastritis (group 1), 26 children with non-H. pylori gastritis (group 2) and 28 children with no pathological findings—control group (group 3). Several laboratory parameters, histopathological and immunohistochemistry tests were performed in all children for detecting inflammatory status. We noticed a significant difference in terms of rural area between the three groups (p = 0.0404). Comparing the laboratory parameters between the three groups, we noticed significant differences in terms of serological tests (p = 0094), and NLR (p = 0.0253), the latter being significantly higher in children with H. pylori-induced gastritis as compared to those with non-H. pylori gastritis (0.0107). According to the Dunn’s Multiple Comparison Test, we noticed a significantly elevated neutrophil level in children with H. pylori-induced gastritis when compared to non-H. pylori gastritis group (p = 0.0146), as well as a significantly increased eosinophil count in patients with non-H. pylori gastritis as compared to control group (p = 0.0417). The immunohistochemistry method pointed out no significant variation concerning interleukin (IL 6) between children with gastritis and control group [RR = 1.283, IC (95%): 0.9404–1.751, p = 0.0988]. Additionally, children with gastritis regardless of the etiology have a significant risk of associating increased gastric expression of tumor necrosis factor alpha (TNF α) [RR = 3.967; CI (95%): 1.283–12.263; p = 0.0063]. Moreover, TNF α was significantly associated with presence of H. pylori gastritis (p = 0.0002). The early detection of local inflammation triggered by this infection might preempt gastric carcinogenesis, while identifying H. pylori-induced systemic inflammation lowers the risk of severe extraintestinal manifestations.