Abstract
The aim of the study was to investigate the characteristics of inflammatory gastroduodenal diseases in children, associated with CagA-positive strains of H. pylori. We observed 283 children aged 7 to 17 years with chronic gastroduodenal pathology in exacerbation stage; endoscopic examination of the esophagus, stomach and duodenum was performed, total Ig M, A, G to Ag SagA H. pylori protein in blood serum by ELISA was determined. The study group included 156 patients infected with cytotoxic CagA (+) strains of H. pylori (H. pylori-positive status), comparison group - 59 (20,9%) patients with H. pylori-negative status. It was shown that 55.1% of patients observed were infected with cytotoxic CagA (+) strains of H. pylori. The intensity of clinical symptoms and the severity of inflammatory changes in stomach and duodenum mucosa in children with H. pylori infection is associated with cytotoxic strains of CAG A H. pylori. Presence of extensive gastritis (34,6%; p<0,05), lymphoid hyperplasia (16,0%; p <0,05), turbid mucus in the gastric lumen are the special features of endoscopic changes in children with H. pylori-positive status.
Highlights
Particularities of gastroduodenal pathology in children, associated with cytotoxic CAGA-positive strains of Helicobacter pylori
Ɇɚɤɫɢɦɚɥɶɧɚ ɩɢɬɨɦɚ ɜɚɝɚ ɡɚɝɨɫɬɪɟɧɶ ɭ ɝɪɭɩɿ ɞɿɬɟɣ ɡ ɩɨɡɢɬɢɜɧɢɦ ɇ. pylori-ɫɬɚɬɭɫɨɦ ɪɟɽɫɬɪɭɜɚɥɚɫɹ ɜɡɢɦɤɭ (41,0%), ɚ ɭ ɞɿɬɟɣ ɡ ɧɟɝɚɬɢɜɧɢɦ ɇ. pylori ɫɬɚɬɭɫɨɦ – ɜɨɫɟɧɢ (Ȥ2 =3,81; P= 0,05). ɉɪɚɤɬɢɱɧɨ ɡ ɨɞɧɚɤɨɜɨɸ ɱɚɫɬɨɬɨɸ ɡɚɝɨɫɬɪɟɧɧɹ ɯɟɥɿɤɨɛɚɤɬɟɪɧɨʀ ɿɧɮɟɤɰɿʀ ɡɭɫɬɪɿɱɚɥɢɫɹ ɧɚɜɟɫɧɿ (25%), ɜɥɿɬɤɭ (18%) ɿ ɜɨɫɟɧɢ (16%). ɍ ɝɪɭɩɿ ɩɨɪɿɜɧɹɧɧɹ ɧɚɣɛɿɥɶɲɚ ɱɚɫɬɨɬɚ ɡɚɝɨɫɬɪɟɧɶ ɜɿɞɡɧɚɱɚɥɚɫɹ ɜ ɨɫɿɧɧɶɨ-ɡɢɦɨɜɿ ɩɟɪɿɨɞɢ (30,51%, 28,81% ɜɿɞɩɨɜɿɞɧɨ), ɦɿɧɿɦɚɥɶɧɚ – ɧɚɜɟɫɧɿ ɬɚ ɜɥɿɬɤɭ (20,34%)
2. ȱɧɬɟɧɫɢɜɧɿɫɬɶ ɤɥɿɧɿɱɧɢɯ ɨɡɧɚɤ ɿ ɬɹɠɤɿɫɬɶ ɡɚɩɚɥɶɧɢɯ ɡɦɿɧ ɭ ɫɥɢɡɨɜɿɣ ɨɛɨɥɨɧɰɿ ɲɥɭɧɤɚ ɿ ɞɜɚɧɚɞɰɹɬɢɩɚɥɨʀ ɤɢɲɤɢ ɩɪɢ ɯɟɥɿɤɨɛɚɤɬɟɪɧɿɣ ɿɧɮɟɤɰɿʀ ɭ ɞɿɬɟɣ ɚɫɨɰɿɣɨɜɚɧɚ ɡ ɰɢɬɨɬɨɤɫɢɱɧɢɦɢ ɲɬɚɦɚɦɢ ɋɚg A H. pylori
Summary
ȾɁ «Ⱦɧɿɩɪɨɩɟɬɪɨɜɫɶɤɚ ɦɟɞɢɱɧɚ ɚɤɚɞɟɦɿɹ ɆɈɁ ɍɤɪɚʀɧɢ» ɤɚɮɟɞɪɚ ɮɚɤɭɥɶɬɟɬɫɶɤɨʀ ɩɟɞɿɚɬɪɿʀ ɬɚ ɦɟɞɢɱɧɨʀ ɝɟɧɟɬɢɤɢ ɜɭɥ. Ɉɫɨɛɟɧɧɨɫɬɢ ɝɚɫɬɪɨɞɭɨɞɟɧɚɥɶɧɨɣ ɩɚɬɨɥɨɝɢɢ ɭ ɞɟɬɟɣ, ɚɫɫɨɰɢɢɪɨɜɚɧɧɨɣ ɫ ɰɢɬɨɬɨɤɫɢɱɟɫɤɢɦɢ CAGA-ɩɨɡɢɬɢɜɧɵɦɢ ɲɬɚɦɦɚɦɢ Helicobacter pylori. Ɐɟɥɶɸ ɢɫɫɥɟɞɨɜɚɧɢɹ ɛɵɥɨ ɢɡɭɱɟɧɢɟ ɨɫɨɛɟɧɧɨɫɬɟɣ ɬɟɱɟɧɢɹ ɜɨɫɩɚɥɢɬɟɥɶɧɵɯ ɡɚɛɨɥɟɜɚɧɢɣ ɝɚɫɬɪɨɞɭɨɞɟɧɚɥɶɧɨɣ ɡɨɧɵ ɭ ɞɟɬɟɣ, ɚɫɫɨɰɢɢɪɨɜɚɧɧɵɯ ɫ CagȺ-ɩɨɡɢɬɢɜɧɵɦɢ ɲɬɚɦɦɚɦɢ ɇ. Ɉɨɞ ɧɚɛɥɸɞɟɧɢɟɦ ɧɚɯɨɞɢɥɢɫɶ 283 ɪɟɛɟɧɤɚ ɜ ɜɨɡɪɚɫɬɟ ɨɬ 7 ɞɨ 17 ɥɟɬ ɫ ɯɪɨɧɢɱɟɫɤɨɣ ɝɚɫɬɪɨɞɭɨɞɟɧɚɥɶɧɨɣ ɩɚɬɨɥɨɝɢɟɣ ɜ ɫɬɚɞɢɢ ɨɛɨɫɬɪɟɧɢɹ; ɩɪɨɜɟɞɟɧɨ ɷɧɞɨɫɤɨɩɢɱɟɫɤɨɟ ɢɫɫɥɟɞɨɜɚɧɢɟ ɩɢɳɟɜɨɞɚ, ɠɟɥɭɞɤɚ ɢ ɞɜɟɧɚɞɰɚɬɢɩɟɪɫɬɧɨɣ ɤɢɲɤɢ (ȾɉɄ), ɨɩɪɟɞɟɥɟɧɢɟ ɜ ɫɵɜɨɪɨɬɤɟ ɤɪɨɜɢ ɫɭɦɦɚɪɧɵɯ Ig Ɇ, A,G ɤ Ag ɋɚgȺ ɛɟɥɤɚ ɇ. Ȼ ɨɫɧɨɜɧɭɸ ɝɪɭɩɩɭ ɜɨɲɥɢ 156 ɩɚɰɢɟɧɬɨɜ, ɢɧɮɢɰɢɪɨɜɚɧɧɵɯ ɰɢɬɨɬɨɤɫɢɱɟɫɤɢɦɢ CagA (+) ɲɬɚɦɦɚɦɢ ɇ. Pylori-ɫɬɚɬɭɫ ɩɨɥɨɠɢɬɟɥɶɧɵɣ), ɜ ɝɪɭɩɩɭ ɫɪɚɜɧɟɧɢɹ - 59 (20,9%) ɩɚɰɢɟɧɬɨɜ ɫ ɨɬɪɢɰɚɬɟɥɶɧɵɦ ɇ. Ɉɨɤɚɡɚɧɨ, ɱɬɨ 55,1% ɛɨɥɶɧɵɯ ɞɟɬɟɣ, ɧɚɯɨɞɢɜɲɢɯɫɹ ɩɨɞ ɧɚɛɥɸɞɟɧɢɟɦ, ɢɧɮɢɰɢɪɨɜɚɧɵ ɰɢɬɨɬɨɤɫɢɱɟɫɤɢɦɢ CagA (+) ɲɬɚɦɦɚɦɢ ɇ. Ɂɧɬɟɧɫɢɜɧɨɫɬɶ ɤɥɢɧɢɱɟɫɤɢɯ ɩɪɢɡɧɚɤɨɜ ɢ ɬɹɠɟɫɬɶ ɜɨɫɩɚɥɢɬɟɥɶɧɵɯ ɢɡɦɟɧɟɧɢɣ ɜ ɫɥɢɡɢɫɬɨɣ ɠɟɥɭɞɤɚ ɢ ɞɭɨɞɟɧɭɦ ɩɪɢ ɯɟɥɢɤɨɛɚɤɬɟɪɧɨɣ ɢɧɮɟɤɰɢɢ ɭ ɞɟɬɟɣ ɚɫɫɨɰɢɢɪɨɜɚɧɚ ɫ ɰɢɬɨɬɨɤɫɢɱɟɫɤɢɦɢ ɲɬɚɦɦɚɦɢ ɋɚg A H. pylori. Ʉ ɨɫɨɛɟɧɧɨɫɬɹɦ ɷɧɞɨɫɤɨɩɢɱɟɫɤɢɯ ɢɡɦɟɧɟɧɢɣ ɋɈɀ ɢ ȾɉɄ ɭ ɞɟɬɟɣ ɩɨɥɨɠɢɬɟɥɶɧɵɦ ɇ. pylori-ɫɬɚɬɭɫɨɦ ɨɬɧɨɫɹɬɫɹ ɧɚɥɢɱɢɟ ɪɚɫɩɪɨɫɬɪɚɧɟɧɧɨɝɨ ɝɚɫɬɪɢɬɚ (34,6%; p
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