The development of chronic Helicobacter pylori is affected by various factors that are characterized by a common property, i.e. the effect on the active form of Helicobacter pylori infection: both for factors that kill this form (antibiotics, bismuth preparations) and for factors that convert the active form of the bacterium into an inactive form ( proton pump inhibitors). One of these factors is the reflux of bile but there are no data on the effect of various forms of biliary dyskinesia on this process. Material and methods. On the basis of the clinical department of the problem laboratory for chronic Helicobacter pylori of Petro Mohyla Black Sea National University and the functional diagnostics of the hospital number 4 in Mykolaiv, 32 patients with biliary dyskinesia with hypotonic hypokinetic type and 30 patients with biliary dyskinesia with hypertonic hyperkinetic type were comprehensively examined. The age of patients ranged from 22 to 53 years. There were 41 men (66.1%), 21 women (33.9%). The complex examination included: step-by-step intragastric pH-metry, esophagogastroduodenoscopy according to the standard procedure, double testing for Helicobacter pylori: urease activity test and microscopy of Giems-stained smear-prints, material for which was taken during endoscopy from 4 topographic zones, and histological examination of the gastric mucosa. After conducting a comprehensive survey we performed ultrasound examination with food load. Results and discussion. When analyzing the data on the level of acidity, we noted the predominance of hypoacidness (81.3%) in patients of the 1st group, in the 2nd group it was normacidity and hyperacidity (62.3%). When performing esophagogastroduodenoscopy in patients of the 1st group, the active ulcerative process was absent, 2 (6.3%) patients had cicatricial deformity in the duodenal bulb, and 13 patients (40.6%) had bile in the stomach cavity. In 4 patients (13.3%) of the 2nd group we detected an active ulcerative process in the duodenum, in 11 (36.7%) patients we recorded cicatricial deformity, and in 2 patients (6.7%) bile was present in the stomach cavity. In all patients in 100% of cases the presence of chronic non-atrophic gastritis was confirmed in both active and inactive stages. When testing for the identification of the active form of Helicobacter pylori infection in the 1st group in the antrum, this form was absent; in the body of the stomach in the greater curvature was present in 13 (43.3%), in the minor curvature was in 28 (87.5%) cases at a concentration of (+). In the 2nd group, the active form was present in all zones in 100% of cases at a concentration of (++) - (+++). Conclusions. These results are explainable from the point of view of the influence of bile and pancreatic juice, which fall during gastric duodeno-gastric reflux, on the active form of Helicobacter pylori. If the contractile function of the gallbladder is impaired as hypotonia, bile and pancreatic juice enter the duodenum late, which leads to a violation of antroduodenal coordination and the formation of duodenal-gastric reflux. In this case, Helicobacter pylori infection becomes inactive, which cannot be fixed on the mucous membrane and is quickly washed away from the antrum mucosa in the intestine. In the body of the stomach, where the mucous due to folding is more prominent, inactive forms are less susceptible to the washing process, and active forms are more protected from the effects of reflux, especially along the lesser curvature, where contact with bile and pancreatic juice is the smallest. The decrease in the concentration of active forms on the gastric mucosa leads to a decrease in the concentration of residual ammonia in the cavity of the stomach and reduces the likelihood of the process of ulceration.
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