Gastritis

Definition

Classification

I. Acute Gastritis

II. Chronic Gastritis

• Most common cause of chronic gastritis worldwide
• H. pylori is a gram-negative, helical, flagellated bacterium
• Infection affects the superficial mucosa initially, evolving to chronic active gastritis (neutrophils + lymphocytes + plasma cells + macrophages)
• Over 50% of the world's population is infected; 70-80% in developing countries; prevalence increases with age (up to 50% in those ≥60 years in the USA)
• Typically antrum-predominant; pangastritis with corpus involvement can occur
• Associated with increased gastric acid production (antral involvement)
• Host immune responses fail to clear the organism in most people - Sleisenger & Fordtran's GI and Liver Disease

• Autoantibodies against parietal cells and intrinsic factor
• Results in atrophy of the gastric body/oxyntic glands
• Consequences: achlorhydria/hypochlorhydria, intrinsic factor deficiency, vitamin B12 malabsorption, pernicious anaemia
• Antrum is spared - hypochlorhydria leads to high gastrin levels from antral G cells - ECL cell hyperplasia in the gastric body - microadenomas - rarely malignant carcinoid tumors
• Endoscopic surveillance may be appropriate - Bailey & Love's Surgery

• Associated with H. pylori and environmental factors
• Intestinal metaplasia develops; significant risk for gastric adenocarcinoma

III. Uncommon Forms

• Lymphocytic (varioliform) gastritis - mucosal T-lymphocyte infiltration
• Eosinophilic gastritis - eosinophil-predominant infiltrate
• Granulomatous gastritis - Crohn's disease, sarcoidosis, isolated granulomatous
• Russell body gastritis - plasma cells containing Russell bodies, often Hp-related
• Nodular (chicken-skin) gastritis - visible endoscopically; seen in Hp, Crohn's, syphilis, lymphocytic gastritis

Pathogenesis & Key Mechanisms

H. pylori

• Induces chemokines → persistent neutrophilic and chronic inflammatory infiltrate
• Despite robust host immune response, bacteria persist in most infected individuals
• Stimulates MALT (mucosa-associated lymphoid tissue) - can give rise to B-cell MALTomas (MALT lymphomas)
• Antral gastritis → hyperchlorhydria → peptic ulcer disease (gastric and duodenal)
• Pangastritis + glandular atrophy → reduced acid → gastric adenocarcinoma risk

NSAIDs and Alcohol (Erosive Gastritis)

• NSAIDs inhibit COX-1, reducing prostaglandin synthesis - disrupts the gastric mucosal barrier
• Both agents disturb the mucosa and cause erosive (erosive) gastritis

Autoimmune Mechanism

• Anti-parietal cell antibodies destroy oxyntic gland parietal cells
• Loss of acid secretion and intrinsic factor production → B12 deficiency

Complications

Clinical Features

• Correlation between histologic gastritis, clinical symptoms, and endoscopic appearances is poor
• No typical clinical manifestation
• Symptoms (when present): epigastric pain/discomfort, nausea, vomiting, bloating, early satiety
• Can be entirely asymptomatic - especially chronic gastritis - Harrison's 22E

Diagnosis

• Gold standard: Histology from endoscopic biopsies
• H. pylori testing: urea breath test (UBT), stool antigen test, serology, rapid urease test on biopsy (CLO test)
• Bloods: full blood count (anaemia), B12 levels, anti-parietal cell antibodies, anti-intrinsic factor antibodies (autoimmune gastritis)
• CT/plain films: important in phlegmonous/emphysematous gastritis (gas in gastric wall, portal venous gas)

Treatment

H. pylori Eradication

• Standard therapy: PPI + 2 antibiotics (triple therapy or bismuth-based quadruple therapy)
• Eradication achievable in up to 90% of patients
• Reinfection rate is uncommon (<0.5%) after successful eradication
• Indications include: peptic ulcer disease (primary indication), MALT lymphoma, gastric cancer risk reduction - Bailey & Love's Surgery

Erosive/NSAID Gastritis

• Discontinue offending agent
• PPIs are the mainstay of treatment and prevention

Autoimmune Gastritis

• Vitamin B12 supplementation (intramuscular injections for pernicious anaemia)
• Endoscopic surveillance given cancer/carcinoid risk

Recent Evidence

• Global H. pylori antibiotic resistance is rising, particularly in children - PMID 39710669
• Autoimmune gastritis may be more prevalent than previously thought, with a recent meta-analysis quantifying worldwide prevalence - PMID 40831008

Note: Rising antibiotic resistance patterns for H. pylori may affect first-line eradication regimen choices. Local susceptibility data should guide antibiotic selection.