Related Experiment Video
Updated: Jul 29, 2025

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
Published on: March 7, 2025
RELATIONSHIP OF HELICOBACTER PYLORI CAGA AND VACA STATUS TO MORPHOLOGICAL CHANGES OF GASTRIC MUCOSA AND PRIMARY
Liliia M Nikulina1, Galyna A Solovyova2, Igor A Svintsitskyi1
1BOGOMOLETS NATIONAL MEDICAL UNIVERSITY, KYIV, UKRAINE.
Objective:
The aim: To investigate the relation of H. pylori CagA and VacA status to morphological changes of gastric mucosa and primary clarithromycin resistance rate in patients with chronic gastritis.
Patients And Methods:
Materials and methods: A cross-sectional study was conducted between May 2021 and January 2023, involving 64 patients with H. pylori-associated chronić gastritis. The patients were assigned to two groups according to the H. pylori virulence factors (CagA and VacA) status. The grades of inflammation, activity, atrophy, and metaplasia were determined according to the Houston-updated Sydney system. The identification of H. pylori genetic markers of antibiotic resistance and pathogenicity was performed by the polymerase chain reaction using paraffin stomach biopsies.
Results:
Results: Patients with CagA- and VacA-positive H. pylori strains had significantly higher grades of inflammation both in the antrum and in the corpus of the stomach, activity of gastritis in the antrum, higher incidence and grade of atrophy in the antrum. Primary resistance to clarithromycin was significantly more prevalent in patients with CagA- and VacA-negative H. pylori strains (58.3% vs. 11.5%, p=0.002).
Conclusion:
Conclusions: Positive CagA and VacA status is related to more severe histopathological changes of gastric mucosa. In contrast, the rate of primary clarithromycin resistance is higher in patients CagA- and VacA-negative H. pylori strains.
More Related Videos
Related Concept Videos
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
Mucosal Barrier of the Stomach
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...

