H. pylori is involved in the development of 80% of gastric cancers and 5.5% of all malignant conditions worldwide. Its persistence within the host’s stomach causes chronic inflammation, which is a well-known hallmark of carcinogenesis. A wide range of cytokines was reported to be involved in the initiation and long-term persistence of this local and systemic inflammation. IL-8 was among the first cytokines described to be increased in patients with H. pylori infection. Although, this cytokine was initially identified to exert a chemoattracting effect that represents a trigger for the activation of inflammatory cells within H.-pylori-infected mucosa, more recent studies failed in encountering any association between IL-8 and H. pylori infection. IL-6 is a multifunctional, pleiotropic and multipotent cytokine involved in mediating the interaction between innate and adaptive immunity with a dichotomous role acting as both a proinflammatory and an anti-inflammatory cytokine depending on the signaling pathway. IL-1α functions as a promoter of angiogenesis and vascular endothelial cell proliferation in gastric carcinoma since it is closely related to H.-pylori-induced inflammation in children. IL-1β is an essential trigger and enhancer of inflammation. The association between a low IL-1β level and an increased TNF-α level might be considered a risk factor for peptic ulcer disease in the setting of H. pylori infection. IL-10 downregulates both cytotoxic inflammatory responses and cell-mediated immune responses. H. pylori uses the immunosuppressive role of IL-10 to favor its escape from the host’s immune system. TGFβ is a continuous inflammatory mediator that promotes the adherence of H. pylori to the host’s cells and their subsequent colonization. The role of H.-pylori-induced inflammatory responses in the onset of gastric carcinogenesis seems to represent the missing puzzle piece for designing effective preventive and therapeutic strategies in patients with H.-pylori-associated gastric cancer.

Helicobacter pylori infection is one of the main causes of dyspepsia, but it is not the only cause. Esophageal inlet patches are areas of heterotopic gastric mucosa within the esophagus and are commonly located in the cervical part of the esophagus. We report the case of a 16-year-old female, previously known to display symptoms of anxiety, who was admitted to our clinic for dyspeptic symptoms lasting for approximately 1 month in spite of the treatment with proton pump inhibitors. The clinical exam revealed only abdominal tenderness in the epigastric area, while routine laboratory tests showed no abnormalities. The upper digestive endoscopy revealed a well-circumscribed salmon-pink-colored oval lesion of approximately 10 mm in the cervical esophagus, along with hyperemia of the gastric mucosa and biliary reflux. The histopathological exam established the diagnosis of esophageal inlet patch with heterotopic antral-type gastric mucosa and also revealed regenerative changes within the gastric mucosa. We continued to treat the patient with proton pump inhibitors, as well as ursodeoxycholic acid, with favorable evolution. Although rare or underdiagnosed, esophageal inlet patches should never be underestimated and all gastroenterologists should be aware of their presence when performing an upper digestive examination in a patient with dyspeptic symptoms.

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.