Definition/General
Introduction:
Helicobacter pylori gastritis is a chronic bacterial infection of the gastric mucosa caused by H
pylori
It represents the most common cause of chronic gastritis worldwide
It is associated with peptic ulcer disease and gastric malignancy
It affects over 50% of global population.
Origin:
Caused by Helicobacter pylori, a gram-negative, spiral-shaped bacterium
Colonizes the gastric antrum preferentially in acidic environment
Produces urease enzyme and various virulence factors
CagA and VacA are major pathogenicity factors
Induces chronic inflammatory response.
Classification:
Classified by Sydney system: activity, chronicity, atrophy, intestinal metaplasia
Based on distribution: antral-predominant (most common)
Corpus-predominant (hypochlorhydria)
Pangastric (severe infection)
Activity graded by neutrophil infiltration.
Epidemiology:
Prevalence: 70-80% in developing countries
30-40% in developed countries
Higher in India (60-80% adults)
Acquisition in childhood (80% cases)
Family clustering common
Associated with low socioeconomic status.
Clinical Features
Presentation:
Often asymptomatic (70-80% cases)
Dyspepsia (most common symptom)
Epigastric pain and discomfort
Peptic ulcer symptoms (10-15% patients)
Early satiety and bloating
Nausea and occasional vomiting.
Symptoms:
Epigastric pain (burning sensation)
Dyspepsia and indigestion
Peptic ulcer disease (duodenal 10x, gastric 3x increased risk)
Post-prandial discomfort
Loss of appetite
Iron deficiency anemia (chronic cases).
Risk Factors:
Low socioeconomic status
Overcrowded living conditions
Poor sanitation and hygiene
Contaminated water and food
Family history of H
pylori infection
Childhood acquisition
Immunocompromised states.
Screening:
Urea breath test (gold standard for active infection)
Stool antigen test
Serology (IgG antibodies)
Endoscopic biopsy with histology
Rapid urease test (CLO test)
PCR for antibiotic resistance.
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Gross Description
Appearance:
Antral erythema and edema (early changes)
Nodular gastritis (lymphoid follicle hyperplasia)
Mucosal irregularity and friability
Erosions may be present
Associated peptic ulcers in some cases.
Characteristics:
Antral-predominant involvement initially
Mucosal edema and hyperemia
Cobblestone appearance (severe cases)
Loss of normal mucosal pattern
Surface irregularities
Lymphoid nodularity.
Size Location:
Antral involvement (initial and predominant)
May extend to incisura angularis
Corpus involvement in severe cases
Pyloric channel commonly affected
Fundus relatively spared initially.
Multifocality:
Multifocal distribution pattern
Initially antral, spreading proximally
Skip lesions may occur
Progressive involvement over years
Association with duodenal ulcers
May coexist with gastric ulcers.
Microscopic Description
Histological Features:
Chronic inflammation with lymphocytes and plasma cells
Neutrophilic infiltrate (activity marker)
Lymphoid follicles with germinal centers
Surface epithelial damage
H
pylori organisms on surface and in crypts.
Cellular Characteristics:
Surface epithelial degeneration
Chronic inflammatory cells in lamina propria
Neutrophils in surface epithelium and crypts
Lymphoid follicles may be prominent
Increased mitotic activity
Mucin depletion.
Architectural Patterns:
Surface foveolar hyperplasia
Crypt elongation and distortion
Lymphoid follicle formation
Preserved glandular architecture (early stages)
Progressive atrophy (chronic cases)
Intestinal metaplasia (long-term).
Grading Criteria:
Sydney system: Activity (neutrophil grade 0-3)
Chronic inflammation (lymphocyte grade 0-3)
Atrophy (gland loss grade 0-3)
Intestinal metaplasia (grade 0-3)
H
pylori density (grade 0-3).
Immunohistochemistry
Positive Markers:
Anti-H
pylori antibodies (specific identification)
Giemsa stain (highlights organisms)
Warthin-Starry stain (silver stain)
Ki-67 (increased proliferation)
CD68 (macrophages)
CD20 (B-cell lymphoid follicles).
Negative Markers:
CagA protein (not routinely used)
VacA protein (research tool)
Gastrin (may be elevated systemically)
Pepsinogen I (may be decreased)
MUC5AC (may be depleted).
Diagnostic Utility:
Organism identification when morphology unclear
Confirms active infection
Distinguishes from other spiral organisms
Evaluates bacterial density
Assesses inflammatory response
Monitors treatment response.
Molecular Subtypes:
CagA-positive strains (more virulent, 60-70% cases)
CagA-negative strains (less aggressive)
VacA-positive strains (vacuolating cytotoxin)
Mixed genotype infections possible.
Molecular/Genetic
Genetic Mutations:
CagA gene (cytotoxin-associated gene A)
VacA gene (vacuolating cytotoxin A)
BabA gene (blood group antigen-binding adhesin)
IceA gene (induced by contact with epithelium)
OipA gene (outer inflammatory protein).
Molecular Markers:
Urease gene complex (ureA, ureB, ureC)
16S rRNA gene (species identification)
23S rRNA mutations (clarithromycin resistance)
gyrA mutations (quinolone resistance)
rdxA mutations (metronidazole resistance).
Prognostic Significance:
CagA-positive strains: higher ulcer risk, gastric cancer risk
VacA s1/m1 genotype: more severe disease
Antibiotic resistance: treatment failure
IL-1β polymorphisms: host susceptibility
Duration of infection: atrophy development.
Therapeutic Targets:
Triple therapy: PPI + clarithromycin + amoxicillin
Bismuth quadruple therapy: PPI + bismuth + tetracycline + metronidazole
Sequential therapy
Concomitant therapy
Resistance testing guided therapy.
Differential Diagnosis
Similar Entities:
Reactive gastropathy (NSAIDs, bile reflux)
Autoimmune gastritis (corpus-predominant)
Lymphocytic gastritis (intraepithelial lymphocytes)
Granulomatous gastritis
Eosinophilic gastritis
MALT lymphoma.
Distinguishing Features:
H
pylori gastritis: antral-predominant, neutrophilic activity, organisms visible
Reactive: surface changes, no organisms
Autoimmune: corpus involvement, parietal cell loss
Lymphocytic: >20 IEL/100 epithelial cells
MALT lymphoma: lymphoepithelial lesions.
Diagnostic Challenges:
Identifying H
pylori organisms in routine H&E
Distinguishing from other spiral organisms
Post-treatment changes
Patchy distribution sampling
Antibiotic resistance assessment
Correlation with clinical symptoms.
Rare Variants:
Hemorrhagic gastropathy (severe acute infection)
Follicular gastritis (prominent lymphoid follicles)
Varioliform gastritis (aphthoid erosions)
Giant fold gastropathy (Menetrier-like changes).
Sample Pathology Report
Template Format
Sample Pathology Report
Complete Report: This is an example of how the final pathology report should be structured for this condition.
Specimen Information
Gastric biopsy from [antrum/corpus], [number] fragments
Diagnosis
Chronic active gastritis with H. pylori infection
H. Pylori Status
H. pylori: [positive/negative], density: [mild/moderate/severe]
Activity Grade
Activity (neutrophilic infiltrate): Grade [0-3]
Chronic Inflammation
Chronic inflammation: Grade [0-3]
Atrophy
Atrophy: Grade [0-3]
Intestinal Metaplasia
Intestinal metaplasia: Grade [0-3]
Special Studies
Giemsa stain: [positive/negative for H. pylori]
Rapid urease test: [positive/negative]
[other study]: [result]
Recommendations
Recommend H. pylori eradication therapy and follow-up
Final Diagnosis
Chronic active gastritis with H. pylori infection (Sydney system grades provided)