Definition/General
Introduction:
Gastric hypertrophic gastritis is characterized by enlarged gastric folds and mucosal thickening
It may be localized or diffuse
It can cause protein-losing gastropathy
It requires differentiation from Menetrier disease and malignancy.
Origin:
Results from chronic inflammatory stimulation
May be associated with H
pylori infection
Hypergastrinemia can cause hypertrophy
Autoimmune mechanisms may be involved
Represents adaptive response to chronic injury.
Classification:
Diffuse hypertrophic gastritis: involves entire stomach
Localized hypertrophic gastritis: segmental involvement
Associated with H
pylori infection
Autoimmune type
Idiopathic hypertrophic gastropathy.
Epidemiology:
Uncommon condition (1-2% of gastritis cases)
Male predominance (2:1 ratio)
Middle-aged adults (40-60 years)
Higher prevalence with H
pylori infection
Associated with hypergastrinemic states.
Clinical Features
Presentation:
Epigastric pain (most common)
Nausea and vomiting
Protein-losing gastropathy (hypoproteinemia, edema)
Early satiety and bloating
Iron deficiency anemia
Weight loss (severe cases).
Symptoms:
Abdominal pain (postprandial)
Dyspepsia and indigestion
Peripheral edema (protein loss)
Diarrhea (protein-losing enteropathy)
Fatigue and weakness
Loss of appetite.
Risk Factors:
H
pylori infection (major risk factor)
Hypergastrinemia
Autoimmune gastritis
Chronic NSAID use
Zollinger-Ellison syndrome
Family history (rare familial cases).
Screening:
Upper endoscopy (enlarged folds >5mm)
Endoscopic ultrasonography
H
pylori testing
Serum protein levels
Gastrin levels
24-hour gastric pH monitoring.
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Gross Description
Appearance:
Markedly enlarged gastric folds (>5mm thickness)
Cobblestone appearance
Cerebriform pattern of mucosal folds
Mucosal edema and congestion
Increased rugal height
Surface may appear granular.
Characteristics:
Diffuse fold enlargement
Corpus and fundus involvement predominant
Mucosal thickening and edema
Preserved peristalsis (vs
malignancy)
Soft, pliable folds on palpation.
Size Location:
Corpus-fundus predominance (60-70% cases)
May involve entire stomach
Antral involvement less common
Greater curvature predilection
Concurrent duodenal involvement possible.
Multifocality:
Diffuse involvement most common
Patchy distribution possible
Progressive extension over time
Asymmetric involvement
May spare antrum initially.
Microscopic Description
Histological Features:
Marked foveolar hyperplasia
Cystic dilatation of gastric glands
Chronic inflammation in lamina propria
Edema and vascular congestion
Surface epithelial erosions
Mucin hypersecretion.
Cellular Characteristics:
Hyperplastic surface epithelium
Enlarged mucous cells
Chronic inflammatory infiltrate
Lymphocytes and plasma cells
Eosinophils may be present
Increased mitotic activity.
Architectural Patterns:
Elongated and tortuous crypts
Cystic gland dilatation
Lamina propria expansion
Submucosal edema
Preserved glandular architecture
Mucin pooling in expanded crypts.
Grading Criteria:
Fold thickness: mild (5-7mm), moderate (7-10mm), severe (>10mm)
Foveolar hyperplasia grade: 1-3
Inflammation grade: 0-3
Glandular dilatation: minimal, moderate, marked.
Immunohistochemistry
Positive Markers:
MUC5AC (surface mucin, increased)
Ki-67 (increased proliferation)
MUC6 (pyloric gland mucin)
PAS stain (mucin demonstration)
Gastrin (G-cells, if hyperplastic).
Negative Markers:
p53 (usually negative, excludes dysplasia)
CDX2 (excludes intestinal metaplasia)
Chromogranin A (normal neuroendocrine cells)
Cancer markers (excludes malignancy).
Diagnostic Utility:
Demonstrates mucin hypersecretion
Assesses proliferative activity
Excludes dysplasia and malignancy
Evaluates gastrin cell hyperplasia
Confirms benign nature.
Molecular Subtypes:
H
pylori-associated: inflammatory pattern
Hypergastrinemic type: ECL cell changes
Autoimmune type: corpus predominant
Idiopathic type: isolated finding.
Molecular/Genetic
Genetic Mutations:
EGFR overexpression (growth factor pathway)
TGF-α upregulation
Gastrin receptor upregulation
COX-2 overexpression
Growth factor pathway alterations.
Molecular Markers:
Elevated gastrin (secondary hypergastrinemia)
Increased TGF-α
EGFR expression
PGE2 elevation
Inflammatory mediator upregulation.
Prognostic Significance:
H
pylori-associated: reversible with eradication
Protein-losing gastropathy: significant morbidity
Response to treatment varies
Malignant transformation rare but reported.
Therapeutic Targets:
H
pylori eradication (if present)
Proton pump inhibitors
Octreotide (severe protein loss)
Anti-inflammatory agents
Nutritional support
Surgery (refractory cases).
Differential Diagnosis
Similar Entities:
Menetrier disease
Gastric adenocarcinoma (linitis plastica)
Lymphoma
Zollinger-Ellison syndrome
Reactive gastropathy
Gastric varices.
Distinguishing Features:
Hypertrophic gastritis: inflammatory infiltrate, H
pylori association
Menetrier: protein loss, foveolar hyperplasia
Cancer: malignant cells, rigid folds
Lymphoma: lymphoid infiltrate, monoclonality.
Diagnostic Challenges:
Distinguishing from Menetrier disease
Excluding underlying malignancy
Adequate tissue sampling
Correlation with clinical findings
Assessment of protein loss.
Rare Variants:
Familial hypertrophic gastropathy
Drug-induced hypertrophy
Association with polyposis syndromes
Concurrent with other gastric diseases
Pediatric cases.
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 [site], [number] fragments
Diagnosis
Hypertrophic gastritis
Mucosal Changes
Mucosal thickening with foveolar hyperplasia and cystic gland dilatation
Inflammation
Chronic inflammation: [grade], predominantly lymphoplasmacytic
Architecture
Glandular architecture: [preserved/altered], cystic dilatation: [present/absent]
Dysplasia
Dysplasia: [absent/present]
Special Studies
PAS stain: [positive for mucin]
H. pylori: [present/absent]
Ki-67: [result]
Recommendations
Clinical correlation, H. pylori testing, protein levels assessment
Final Diagnosis
Hypertrophic gastritis with [degree] mucosal thickening