Chronic gastritis

Etiology and pathogenesis

Chronic inflammation of the gastroduodenal zone is a multifactorial process, where the bacterium Helicobacter pylori plays the main role. It is an anthroponotic infection transmitted via the fecal-oral or oral-oral route (especially through shared utensils or saliva within the family).

The most important virulence factor of the pathogen is the enzyme urease. The bacterium uses it to break down urea contained in the gastric secretion into ammonia and carbon dioxide. Ammonia locally neutralizes acid, allowing the bacterium to survive, while simultaneously damaging the mucous membrane.

Pathogenesis develops at two levels:

1. Systemic: failures in nervous and hormonal regulation, imbalance of neuropeptides of the APUD system.
2. Local: disruption of the balance between aggressive factors (acid, pepsin) and mucosal defense factors, which leads to impaired epithelial regeneration.

Classification by etiopathogenesis

Modern diagnosis is based on the Sydney system (and its domestic modifications). Three key forms of the disease are distinguished:

• Type A (autoimmune): Develops against the background of other autoimmune pathologies (vitiligo, type 1 diabetes). The body produces autoantibodies to its own gastric glands. The body of the stomach is affected, secretion drops sharply.
• Type B (infectious): The most common variant associated with H. pylori. The detection rate of the pathogen increases with age (from 20% in preschoolers to 70% in adolescents). During endoscopy, it often presents a specific "cobblestone pavement" pattern in the antrum.
• Type C (reactive/chemical): Caused by constant irritation of the mucosa. The main causes are bile reflux during duodenogastric reflux or NSAID intake. This form accounts for 10–15% of cases in pediatrics.

Clinical presentation

The disease proceeds with alternating exacerbations and remissions (when there are no complaints, but morphological defects persist). Symptoms strongly depend on which part is affected.

In addition to local symptoms, asthenovegetative syndrome is almost always present: blood pressure lability, insomnia, sweating, cephalalgia, and irritability.

Treatment and Prevention

Therapy is selected individually depending on the stage and acidity (Diet No. 1 for hyperacid and No. 2 for hypoacid states).

The basis of infectious gastritis treatment is eradication therapy (elimination of Helicobacter with an efficiency of at least 80%):

• Primary regimen (triple): proton pump inhibitor (PPI) + 2 antibiotics (amoxicillin, clarithromycin).
• Repeat course (quadruple therapy): PPI + bismuth tripotassium dicitrate + 2 antibiotics.

After eradication, restoration of motility (prokinetics), reduction of acid aggression (antacids), and correction of microbiota (pre- and probiotics) are required. Children with chronic gastritis are subject to dispensary registration with a gastroenterologist. In critical seasons (autumn, spring), a prophylactic anti-relapse course lasting 3–4 weeks is carried out.

Class and exam questions

What else to study on this topic

• Features of the Sydney classification system and its histological criteria.
• The role of the APUD system in the pathogenesis of gastroduodenal diseases.
• Invasive and non-invasive (breath tests, stool antigen) diagnostic methods for H. pylori.
• Differential diagnosis of peptic ulcer disease, GERD, and functional dyspepsia.
• Principles of diet prescription (Pevzner diet No. 1 and No. 2) in various forms of secretory dysfunction.

Other topics in "Chapter 7. Digestive System Diseases"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.