Gastritis

Classification

• Acute H. pylori infection
• Other acute infectious gastritides: bacterial (non-HP), H. heilmannii, phlegmonous, mycobacterial, syphilitic, viral, parasitic, fungal

• Type A: Autoimmune, body-predominant
• Type B: H. pylori-related, antral-predominant
• Indeterminate

• Harrison's, Table 335-10

Topographic Patterns of Chronic Gastritis

Fig. 52.2 - Sleisenger & Fordtran's Gastrointestinal and Liver Disease, p. 910

Etiology and Pathophysiology

1. H. pylori Gastritis (Most Common Cause of Chronic Gastritis)

• Infects superficial layers of gastric mucosa, initially causing diffuse antral gastritis
• Induces persistent neutrophilic + chronic inflammatory infiltrate (lymphocytes, plasma cells)
• cag pathogenicity island (cag PAI): strains expressing CagA are associated with more severe disease and higher cancer risk
• Activates NF-κB in gastric epithelial cells → upregulation of IL-8 and other pro-inflammatory cytokines
• Urease produces NH3 from urea, damaging mucosal cells
• Oxidative stress via reactive oxygen species contributes to DNA damage
• Induces MALT (mucosa-associated lymphoid tissue), which can give rise to B-cell lymphomas (MALTomas)

• Antral-predominant → can progress to pangastritis with glandular atrophy → intestinal metaplasia → dysplasia → gastric adenocarcinoma (Correa cascade)
• H. pylori gastritis with antral predominance → increased acid → predisposes to peptic ulcer disease (duodenal)
• Pangastritis with atrophy → reduced acid → predisposes to gastric ulcer and cancer
• Robbins & Cotran, p. 720; Bailey & Love's Surgery 28th Ed., p. 1177

2. Autoimmune Atrophic Gastritis (Type A)

• Circulating anti-parietal cell and anti-intrinsic factor antibodies
• Affects the gastric body/corpus (oxyntic glands), sparing the antrum
• Loss of parietal cells → achlorhydria + loss of intrinsic factor
• Loss of intrinsic factor → vitamin B12 malabsorption → pernicious anaemia if untreated
• Achlorhydria → hypergastrinaemia (antral G-cells overactivated) → ECL cell hyperplasia → possible carcinoid tumors
• Associated with gastric cancer risk; endoscopic surveillance may be warranted
• Bailey & Love's, p. 1177; Robbins & Cotran, p. 720

3. NSAIDs and Alcohol

• NSAIDs inhibit COX-1 → reduce prostaglandin synthesis → impair mucosal protective mechanisms → erosive/chemical gastritis
• One of the most common causes of acute/erosive gastritis in clinical practice
• Robbins & Cotran, p. 719

4. Acute Infectious (Phlegmonous / Emphysematous Gastritis)

• Phlegmonous gastritis: infection of gastric submucosa and muscularis propria by invasive organisms (gram-negative bacilli, anaerobes, streptococci, fungi). Often spares the mucosa.
• Emphysematous gastritis: severe form with gas-producing organisms (Clostridium perfringens, E. coli, S. aureus); gas visible in gastric wall and portal venous system on CT/plain films
• Risk factors: heavy alcohol intake, recent GI surgery, corrosive ingestion, AIDS, immunosuppression, diabetes
• Presentation: septic appearance, acute upper abdominal pain, peritonitis, fever, hypotension
• Can be fatal; may progress to gastric gangrene
• Sleisenger & Fordtran's, p. 909

5. Reflux Gastritis

• Caused by enterogastric bile reflux
• Histologically distinct from other types
• Common after gastric surgery; occasionally occurs without prior surgery
• Bailey & Love's, p. 1177

Clinical Features

Complications

• Robbins & Cotran, p. 720

Diagnosis

• Gold standard: Mucosal biopsy at endoscopy with histopathology
• H. pylori testing:
  • Non-invasive: urea breath test (UBT), stool antigen test, serology (less reliable for active infection)
  • Invasive: rapid urease test (RUT), histology, culture from endoscopic biopsy
• Autoimmune gastritis: serum anti-parietal cell antibodies, anti-intrinsic factor antibodies, low vitamin B12, elevated gastrin, low pepsinogen I
• Imaging (CT/plain films): useful in emphysematous gastritis (gas in gastric wall, portal venous gas)
• Sleisenger & Fordtran's, p. 909; Tietz Textbook of Laboratory Medicine

Management

H. pylori Eradication

• Triple therapy (7-14 days): PPI + clarithromycin + amoxicillin (or metronidazole)
• Bismuth quadruple therapy: PPI + bismuth + metronidazole + tetracycline (preferred where clarithromycin resistance is high)
• Concomitant / sequential therapy in areas of high resistance
• Confirm eradication with UBT or stool antigen test ≥4 weeks after completing therapy

Acid Suppression

• PPIs (omeprazole, pantoprazole, etc.): mainstay for symptom relief and mucosal healing
• H2-receptor antagonists (ranitidine, famotidine): second-line

NSAID-Induced Gastritis

• Discontinue or minimize NSAID use
• PPI co-prescription when NSAIDs cannot be stopped
• Switch to COX-2 selective inhibitor (lower GI risk)

Autoimmune Atrophic Gastritis

• Lifelong vitamin B12 supplementation (IM or oral)
• Monitor for pernicious anaemia, iron deficiency
• Endoscopic surveillance for gastric dysplasia/cancer

Phlegmonous/Emphysematous Gastritis

• Broad-spectrum IV antibiotics
• Surgical intervention if necrosis, perforation, or failure to respond to antibiotics
• Supportive ICU care for septic patients

Recent Evidence

• A 2024 systematic review and meta-analysis (PMID: 39575409) on H. pylori prevalence in China (2014-2023) highlights the ongoing high burden of infection, particularly important given gastric cancer rates.
• A 2025 meta-analysis (PMID: 40822578) examines interactions between H. pylori and the gut microbiome, suggesting microbiome disruption may contribute to clinical outcomes beyond the stomach itself.
• A 2025 systematic review (PMID: 40532847) on emphysematous gastritis provides updated characterization of this rare but potentially fatal form.