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Syndrome of dyspepsia in patients with connective tissue dysplasia: mechanisms prospects for рathogenetic treatment

https://doi.org/10.31146/1682-8658-ecg-240-8-76-83

Abstract

Objective: To determine the changes in organs and systems associated with connective tissue dysplasia (CTD) that affect gastric acid production in patients with CTD presenting symptoms of dyspepsia. Materials and Methods: A randomized controlled cross-sectional comparative study was conducted involving a total of 151 participants using a cross-sectional design. Inclusion criteria included presence of dyspeptic symptoms, absence of severe organic pathology capable of manifesting as dyspeptic symptoms (fever, hematemesis, anemia, leukocytosis, elevated ESR, melena), peptic ulcers or erosions in the stomach and duodenum mucosa, age between 18 to 29 years old, no history of Helicobacter pylori eradication therapy, discontinuation of medications affecting gastric acidity according to their half-life period, informed consent for participation in the study. All enrolled subjects underwent general clinical examination (collection of complaints, medical history, physical examination), screening for CTD, assessment of vegetative vascular reactivity (“Nerosoft,” Russia). Since there are no clear reference values for gastric acid-producing function, two additional groups without dyspepsia were formed using the same inclusion criteria except for the presence of dyspeptic symptoms. The research cohort consisted of four groups: Group 1-42 patients with dyspepsia and CTD; Group 2-36 patients with dyspepsia but no CTD; Group 3-37 patients with CTD but no dyspeptic complaints; Group 4-37 healthy volunteers free from both CTD and dyspeptic symptoms. All four groups received comprehensive clinical evaluation including symptom questionnaires using the Gastrointestinal Symptom Rating Scale (GSRS), 24-hour pH-metry (“Gastronscan-24,” Fryazino, Moscow Region, Russia), measurement of serum levels of pepsinogens I and II, gastrin-17, anti-H. pylori IgG antibodies (“Vector-Best,” Novosibirsk, Russia), endoscopic laser Doppler flowmetry (“LAKK-2,” Russia). Results: Among patients with CTD experiencing dyspeptic symptoms, postprandial distress syndrome occurred in 77% of cases. Clinico-functional markers specific to biliary type dysfunction include reflux-gastritis (17.8%) and gallbladder deformation (30%). Markers indicative of hypoacid condition include impaired microcirculation in the gastric wall (26.2%), gastropathy (gastric ptosis, 42%), thoracic cage deformities (23%), hypergastrinemia (25.6%). Conclusion: Decreased gastric acid secretion in patients with CTD is caused by two primary mechanisms. The most common factor involves disturbed gastric motility leading to duodenogastric reflux, resulting in bile entering the stomach and disrupting its secretory activity. In some patients, this process progresses to atrophic changes in the gastric mucosa accompanied by true deficiency in hydrochloric acid production. Both mechanisms significantly reduce the stomach's ability to produce acid, thereby influencing digestive processes and gastrointestinal protective properties.

About the Authors

M. Yu. Rozhkova
Omsk State Medical University
Russian Federation


G. I. Nechaeva
Omsk State Medical University
Russian Federation


I. A. Viktorova
Omsk State Medical University
Russian Federation


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For citations:


Rozhkova M.Yu., Nechaeva G.I., Viktorova I.A. Syndrome of dyspepsia in patients with connective tissue dysplasia: mechanisms prospects for рathogenetic treatment. Experimental and Clinical Gastroenterology. 2025;(8):76-83. (In Russ.) https://doi.org/10.31146/1682-8658-ecg-240-8-76-83

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