Clinical manifestations and endoscopic and histological changes in children with chronic gastritis, induced by Helicobacter pylori, with different toxicity
Background. Helicobacter pylori infection is an important factor in chronic gastritis and duodenal ulcer in children. Over the past decade, different virulence of H.pylori strains has been determined, which depends on its toxicity genes. The purpose was to study the clinical manifestations, endoscopic and histological changes of the gastric mucosa in children with chronic gastritis, induced by H.pylori, with its different toxicity. Materials and methods. One hundred thirty-six children with chronic H.pylori-induced gastritis aged 7–17 years (main group) and 30 healthy children of the same age (control group) were examined clinically and instrumentally. Patients were divided into 2 groups: group IA consisted of 72 children with chronic gastritis, induced by H.pylori CagA “+”, and group IB included 64 children with chronic gastritis, induced by H.pylori CagA “–”, according to the results of determining the total IgG antibodies to CagA antigen in the blood serum or evaluating CagA in gastric mucosal biopsy specimens using polymerase chain reaction. Clinical manifestations, endoscopic and histological changes of the gastric mucosa were analyzed. Statistical processing was performed using the statistical software package Statgraphics 16.0. Results. In children with chronic gastritis, induced by H.pylori CagA “+” (group IА), the clinical manifestations of pain, abdominal and dyspeptic syndromes were not significantly different from those in patients with chronic gastritis, induced by H.pylori CagA “–” (group IB). There were no significant endoscopic changes in the form of erythematous gastropathy and antral nodularity in children with chronic gastritis, induced by both H.pylori CagA “+” and CagA “–”. Histological changes in groups IA and IB were different: children with chronic gastritis, induced by H.pylori CagA “+”, had inflammatory activity degree II and I and degree II, I, III of gastric contamination by H.pylori, while children with chronic gastritis, induced by H.pylori CagA “–”, had degree I, II activity of the gastric mucosal inflammation and stages II and I of H.pylori contamination. In children with H.pylori-induced chronic gastritis, it is advisable to diagnose toxicity of CagA “+” and CagA “–” in order to evaluate H.pylori CagA “–” child’s status. Conclusions. Clinical manifestations of H.pylori-induced chronic gastritis in children are epigastric pain, symptoms of dyspepsia, and chronic intoxication syndrome. Endoscopic manifestations are erythematous gastopathy and/or antral nodularity. In children with chronic gastritis, induced by H.pylori CagA “+” and CagA “–”, there was no significant difference in clinical and endoscopic manifestations. Histological change in gastric mucosa in chronic gastritis, induced by H.pylori, at the stage of exacerbation is diffuse lymphocytic-plasmocytic infiltration of the lamina propria of gastric mucosa with epithelial damage. In the chronic gastritis, induced with H.pylori CagA “+”, II and III degrees of H.pylori contamination predominate, in combination with degrees I and II of inflammation activity. In chronic gastritis, induced by H.pylori CagA “–”, stages II and I of H.pylori contamination predominate. In children with H.pylori-induced chronic gastritis, it is advisable to diagnose its CagA “+”toxicity in order to evaluate H.pylori CagA “–” child’s status.
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