The formation of diseases of the gastric and duodenum in the adult population begins at school age. Among the leading risk factors for their formation are family predisposition (to peptic ulcer disease (PU), gastric cancer). The basis for their formation is gastritis, the course of which is actively influenced by cytokines. Aim. To study the characteristics of cytokine levels in blood serum in schoolchildren with gastritis and a family history of gastric cancer and peptic ulcer. A total of 179 schoolchildren with gastroenterological complaints were examined. All subjects underwent an endoscopic examination with biopsies taken from the antrum of the gastric and morphological confirmation of gastritis (Sydney classification). The presence of H. pylori was also determined by morphological method. The level of cytokines in the blood (IL-2, IL-4, IL-8, IL-18, IL- 1β, IFNα, TNFα) was determined by ELISA. The study found that schoolchildren with a burden of ulcer had a decreased IL-1β in comparison with children without aggravation (p = 0.005), and with children with a burden of cancer (p = 0.030). Also, IFNα was increased in schoolchildren with a burden of ulcerative disease (p = 0.001) and gastric cancer (p = 0.038). A decrease in IL-1β was found in children with aggravated ulcer disease, both with H. pylori infection (p = 0.048) and without it (p = 0.043). IL-1β plays an important role in the immune response to H. pylori infection. In addition, it is known that during H. pylori infection the level of IL-1β increases, which is accompanied by inhibition of gastric acidity. There was a decrease in IL-1β and an increase in IFNα in children with aggravated ulcer disease, regardless of the activity of inflammation. In addition, they observed an increase in TNFα (p = 0.04) with high gastritis activity (stage 2-3). In addition, in children with ulcer burden and high gastritis activity, IL-4 is increased (p = 0.018). Thus, in children with a family history of both peptic ulcers and gastric cancer, there are features of the association of specific cytokines with gastritis, as well as its activity and H. pylori infection.
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