Definition/General
Introduction:
Chronic gastritis is persistent inflammation of gastric mucosa
It is characterized by chronic inflammatory infiltrate
Most commonly caused by Helicobacter pylori infection
Can progress to atrophy and metaplasia.
Origin:
Results from persistent mucosal injury
H
pylori infection most common cause (90%)
Autoimmune mechanisms (pernicious anemia)
Chemical injury (NSAIDs, bile reflux)
Environmental factors (diet, smoking).
Classification:
H
pylori gastritis (antrum-predominant vs pangastric)
Autoimmune gastritis (body-predominant)
Chemical gastropathy (reactive)
Lymphocytic gastritis
Eosinophilic gastritis
Granulomatous gastritis.
Epidemiology:
Very common worldwide (>50% adults)
H
pylori prevalence varies by region (developing countries 70-90%)
Age-related increase
Socioeconomic factors important
Declining prevalence in developed countries.
Clinical Features
Presentation:
Often asymptomatic in early stages
Dyspepsia (40-50%)
Epigastric pain (30-40%)
Nausea (20-30%)
Early satiety
Bloating and fullness
Loss of appetite.
Symptoms:
Upper abdominal discomfort
Postprandial pain
Heartburn and acid reflux
Iron deficiency anemia (chronic bleeding)
B12 deficiency (autoimmune gastritis)
Weight loss in severe cases.
Risk Factors:
H
pylori infection (strongest risk)
NSAIDs use
Alcohol consumption
Smoking
Dietary factors (high salt, low antioxidants)
Family history (autoimmune)
Age >40 years.
Screening:
H
pylori testing: serology, stool antigen, breath test
Upper endoscopy with biopsy
Serum gastrin levels
Vitamin B12 and folate
Intrinsic factor antibodies
Parietal cell antibodies.
Master Chronic Gastritis Pathology with RxDx
Access 100+ pathology videos and expert guidance with the RxDx app
Gross Description
Appearance:
Mucosal erythema and hyperemia
Mucosal edema and thickening
Erosions and shallow ulcerations
Nodular appearance (lymphoid hyperplasia)
Atrophic mucosa in advanced cases.
Characteristics:
Loss of rugal folds in atrophic gastritis
Granular mucosa
Increased friability
Patchy distribution common
Antral involvement in H
pylori.
Size Location:
H
pylori gastritis: Antrum-predominant initially, may become pangastric
Autoimmune gastritis: Body and fundus predominant
Chemical gastropathy: Antrum mainly
Patchy vs diffuse involvement.
Multifocality:
Multifocal involvement common
Skip lesions possible
Progression pattern: antrum → incisura → body
Environmental metaplasia at antral-body junction.
Microscopic Description
Histological Features:
Chronic inflammatory infiltrate (lymphocytes, plasma cells)
Increased intraepithelial lymphocytes
Surface epithelial damage
Lymphoid follicles with germinal centers
Intestinal metaplasia (complete and incomplete).
Cellular Characteristics:
Lymphocytes and plasma cells in lamina propria
Neutrophils in active inflammation
Surface epithelial flattening
Loss of mucin
Regenerative epithelial changes
Intraepithelial lymphocytes >20/100 epithelial cells.
Architectural Patterns:
Glandular atrophy and loss
Intestinal metaplasia: goblet cells, absorptive cells
Pseudopyloric metaplasia
Foveolar hyperplasia
Lymphoid aggregates
Fibrosis in severe cases.
Grading Criteria:
Sydney System grading: Chronic inflammation (0-3)
Activity (neutrophils, 0-3)
Atrophy (0-3)
Intestinal metaplasia (0-3)
H
pylori density (0-3)
Each scored as none, mild, moderate, severe.
Immunohistochemistry
Positive Markers:
H
pylori immunostain for organism identification
Ki-67 shows increased proliferation
p53 expression in dysplasia
CDX2 positive in intestinal metaplasia
MUC2 in goblet cells.
Negative Markers:
Generally not required for diagnosis
Cytokeratin pattern changes in metaplasia
Chromogranin in neuroendocrine cells.
Diagnostic Utility:
H
pylori immunostain increases detection sensitivity
CDX2 and MUC2 confirm intestinal metaplasia
Ki-67 assesses proliferative activity
p53 identifies dysplasia.
Molecular Subtypes:
CagA-positive H
pylori more virulent
VacA cytotoxin variants
Autoimmune gastritis: intrinsic factor deficiency
Genetic polymorphisms affect susceptibility.
Molecular/Genetic
Genetic Mutations:
TP53 mutations in dysplasia/carcinoma progression
APC mutations in intestinal-type carcinoma
CDH1 mutations in diffuse-type carcinoma
Microsatellite instability (MLH1 hypermethylation).
Molecular Markers:
Methylation changes (CpG island methylator phenotype)
Loss of CDH1 expression
p16 hypermethylation
Telomerase activation
Inflammatory cytokines (IL-1β, TNF-α).
Prognostic Significance:
Atrophy and metaplasia increase cancer risk
Incomplete intestinal metaplasia higher risk than complete
H
pylori eradication may reverse inflammation
Genetic background influences progression.
Therapeutic Targets:
H
pylori eradication: triple/quadruple therapy
Proton pump inhibitors
Antioxidants (vitamin C, E)
Probiotics
Dietary modifications
NSAIDs cessation.
Differential Diagnosis
Similar Entities:
Peptic ulcer disease
Gastric adenocarcinoma (early)
MALT lymphoma
Reactive gastropathy
Ménétrier disease
Zollinger-Ellison syndrome.
Distinguishing Features:
Chronic gastritis: Chronic inflammation, no mass
Carcinoma: Dysplastic epithelium, mass lesion
MALT lymphoma: Monoclonal B-cells, lymphoepithelial lesions
Reactive gastropathy: Foveolar hyperplasia, minimal inflammation.
Diagnostic Challenges:
Distinguishing severe atrophy from early carcinoma
Identifying dysplasia in inflamed mucosa
Determining H
pylori status after PPI therapy
Sampling adequacy for patchy lesions.
Rare Variants:
Lymphocytic gastritis (>20 IELs/100 epithelial cells)
Collagenous gastritis
Eosinophilic gastritis
Granulomatous gastritis
Hypertrophic gastropathy.
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
Gastric biopsy from [antrum/body/fundus]
Sydney System
Chronic inflammation: [grade], Activity: [grade], Atrophy: [grade], Metaplasia: [grade], H. pylori: [grade]
H. pylori
H. pylori organisms: [present/absent] [by H&E/immunostain]
Features
Chronic inflammation with [describe pattern and severity]
Diagnosis
Chronic [active/inactive] gastritis, [mild/moderate/severe], [H. pylori positive/negative]