Helicobacter pylori infection development can be influenced by various factors: a decrease in the immunity level and the acidity level of gastric juice in stress, a decrease in the acidity level when taking drugs that block the production of hydrochloric acid; reception of antibacterial drugs; vomiting, drugs containing pancreatic enzymes. These enzymes enter the stomach and duodenogastric reflux. 120 patients with chronic non-atrophic gastritis with dyskinesia of the bile ducts in the hypokinetic hypotonic type (the main group) and 113 patients were systematically examined on the basis of clinical department of the problem laboratory on chronic helikobacteriosis of the Black Sea National University named after Peter Mohyla and the department of functional diagnostics of the 4th city Mykolaiv hospital. Patients with chronic non-atrophic gastritis, whose gallbladder function was in normal condition (control group). The complex examination included: step-by-step intragastric pH-metry, esophagogastroduodenoscopy according to the standard procedure, double testing for HP: 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. Before the patients underwent a comprehensive examination, they underwent ultrasound – a diagnosis of the abdominal cavity with the definition of the gallbladder function according to the generally accepted technique. When analyzing the acidity level, it was revealed that in the patients of the main group in 73.4% of cases the acidity was low, while in the control group low acidity was noted in 46% of cases; in 100% of cases, the presence of chronic non-atrophic gastritis was confirmed in both active and inactive stages of varying severity; Helicobacter pylori infection was detected in 100% cases both in active and inactive form with degree of colonization of the gastric mucosa from (+) to (+++). When carrying out EGDS, an active ulcerative process was detected in the duodenum in 9 (3.9%), 24 (10.3%) patients had cicatricle deformation of different severity. The frequency of duodenogastric reflux in patients of the main group was 10%, while in the control group 3.5%. Thus, a more frequent (2.8 times) detection of duodenogastric reflux in patients of the main group indicates the role of the gallbladder dysfunction in the reflux formation. Given the negative effect of bile on the active forms of Helicobacter pylori infection, attention should be paid to the localization of inactive forms of HP-infection on the stomach mucosa in the presence of duodenogastric reflux in patients, which will become the prospect of further research.
Keywords: chronic non-atrophic gastritis, duodenogastric reflux, biliary dyskinesia
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