Explain chronic gastritis due to h pylori 2nd mbbs pathology ROBBINS
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Chronic gastritis due to Helicobacter pylori (Type B gastritis)
Definition
H. pylori gastritis is the commonest form of chronic gastritis. It is a persistent inflammation of gastric mucosa caused by colonization with Helicobacter pylori, a curved/spiral, gram-negative, microaerophilic bacillus.
It usually begins in the antrum and may later extend to the body and fundus, producing multifocal atrophic gastritis.
Robbins & Kumar Basic Pathology, p. 497.
Robbins & Kumar Basic Pathology, p. 497.
Etiology and epidemiology
- Infection is generally acquired in childhood and, without eradication, may persist lifelong.
- Associated with overcrowding, poor sanitation, and lower socioeconomic conditions.
- Many infected people are asymptomatic.
- It is strongly associated with:
- Chronic active gastritis
- Duodenal and gastric peptic ulcer disease
- Gastric adenocarcinoma
- Gastric MALT lymphoma
Pathogenesis
The organism lives within the mucus layer overlying foveolar epithelial cells, especially in the antrum. It usually does not deeply invade the gastric mucosa. Disease results from bacterial virulence factors plus the host inflammatory response.
Virulence factors and their effects
| Factor | Role in disease |
|---|---|
| Flagella | Allow movement through the viscous gastric mucus toward the less acidic mucosal surface. |
| Urease | Converts urea to ammonia, raising the local pH and allowing bacterial survival in acid. Ammonia and related products also contribute to epithelial injury. |
| Adhesins | Promote attachment to gastric surface epithelial cells. |
| CagA/CagE-associated factors | Stimulate epithelial release of cytokines, especially IL-8, causing neutrophil recruitment and persistent inflammation. |
| Host immune response | Chronic T-cell, B-cell, plasma-cell, and macrophage response damages the mucosa but commonly fails to eliminate the organism. |
Sequence of events
- H. pylori colonizes the antral mucus layer.
- Bacterial products and epithelial cytokines recruit neutrophils and mononuclear inflammatory cells.
- Antral inflammation reduces somatostatin-mediated inhibition of G cells.
- Gastrin secretion rises, causing increased acid output in antral-predominant disease.
- Increased acid predisposes to duodenal peptic ulceration.
- In some patients, infection spreads to corpus/body mucosa.
- Long-standing inflammation causes gland loss, atrophy, and intestinal metaplasia, increasing risk of gastric adenocarcinoma.
Morphology
Gross appearance
Early disease may show little or no gross abnormality. With persistent inflammation, the mucosa may become erythematous, nodular, thickened, or have prominent rugal folds.
Microscopy: chronic active gastritis
The characteristic lesion is chronic active gastritis.
Location of organism
- Curved bacilli lie in the mucus layer:
- Over the surface foveolar epithelium
- In the neck region of gastric glands
- Usually best detected by:
- H&E stain
- Giemsa stain
- Immunohistochemistry
Inflammatory infiltrate
- Chronic inflammation: lymphocytes, plasma cells, macrophages in the lamina propria.
- Activity: neutrophils infiltrating lamina propria and epithelium.
- Neutrophils may enter gastric pits and form pit abscesses.
- Lymphoid aggregates with germinal centers are common, representing acquired gastric MALT.
Chronic mucosal injury
Long-standing infection may cause:
- Glandular atrophy
- Intestinal metaplasia with goblet cells and absorptive-type columnar cells
- Regenerative foveolar hyperplasia
- Hyperplastic or inflammatory polyps
Robbins & Kumar Basic Pathology, p. 497.
Patterns and consequences
1. Antral-predominant gastritis
- Common initial pattern
- Increased gastrin and increased acid secretion
- Predisposes chiefly to duodenal ulcer
2. Multifocal atrophic gastritis or pangastritis
- Involves antrum and body
- Leads to loss of parietal-cell function, atrophy, and intestinal metaplasia
- Associated with:
- Gastric ulcer
- Gastric adenocarcinoma, particularly intestinal-type/non-cardia cancer
3. MALT lymphoma
Chronic antigenic stimulation produces acquired MALT in the stomach. This can progress to extranodal marginal-zone B-cell lymphoma of MALT type. Early lesions may regress after H. pylori eradication.
Clinical features
Often asymptomatic. When symptomatic, patients may have:
- Dyspepsia
- Epigastric discomfort or pain
- Nausea
- Occasional vomiting
Hematemesis is uncommon in uncomplicated chronic gastritis. Symptoms frequently arise from associated peptic ulcer disease rather than gastritis itself.
Diagnosis
- Endoscopic biopsy: Histology demonstrates chronic active gastritis and organisms.
- Special stains: Giemsa, Warthin-Starry, or immunohistochemistry.
- Rapid urease test on biopsy.
- Urea breath test.
- Stool antigen test.
- PCR/culture in selected settings.
Antral biopsies are particularly useful because H. pylori has a predilection for gastric foveolar epithelium and is usually concentrated in the antrum.
Treatment principle
Eradication requires a proton-pump inhibitor plus antibiotics. Successful eradication heals inflammation, reduces ulcer recurrence, and lowers the risk of MALT lymphoma and progression along the atrophy-metaplasia-dysplasia-carcinoma pathway.
Important distinction: H. pylori vs autoimmune gastritis
| Feature | H. pylori gastritis | Autoimmune gastritis |
|---|---|---|
| Traditional name | Type B | Type A |
| Main site | Antrum initially, then multifocal/pangastritis | Body and fundus |
| Antrum | Typically involved | Typically spared |
| Acid secretion initially | Often increased | Markedly decreased or absent |
| Main complications | Duodenal ulcer, gastric ulcer, adenocarcinoma, MALT lymphoma | Pernicious anemia, gastric neuroendocrine tumor, adenocarcinoma |
| Histology | Chronic active inflammation with neutrophils; lymphoid aggregates; organisms in mucus | Oxyntic gland atrophy; parietal cell loss; no organisms |
One-line exam summary
Chronic H. pylori gastritis is an antral-predominant chronic active gastritis characterized by organisms in surface mucus, neutrophilic activity, lymphoplasmacytic infiltrate and lymphoid aggregates; persistent infection may cause peptic ulcer disease, multifocal atrophy, intestinal metaplasia, gastric adenocarcinoma, and MALT lymphoma.
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