Gastritis

1. Clinical Overview

Summary

Gastritis is defined as inflammation of the gastric mucosa, representing a spectrum of histopathological and clinical entities rather than a single disease. [1] It is classified according to temporal course (acute vs chronic), topographical distribution (antral, fundal, pangastric), and underlying aetiology (H. pylori, autoimmune, chemical, granulomatous). [2]

The most clinically significant forms are Type B (bacterial) gastritis caused by Helicobacter pylori infection and Type A (autoimmune) gastritis associated with parietal cell antibodies. [3] Chronic gastritis represents a critical precursor lesion in the Correa cascade towards gastric adenocarcinoma, particularly when associated with atrophy and intestinal metaplasia. [4]

Key Facts

Clinical Pearls

• Type A = Autoimmune = Antibodies = Body/fundus = B12 deficiency (mnemonic)
• Type B = Bacterial = Base (antrum) = H. pylori (mnemonic)
• Type C = Chemical = Caused by drugs/bile (mnemonic)
• Achlorhydria in Type A: Increased gastric pH → iron malabsorption + B12 deficiency + compensatory hypergastrinaemia
• H. pylori: Responsible for >90% of non-NSAID peptic ulcers and WHO Class I carcinogen for gastric cancer [5]
• Sydney System: Gold standard histopathological classification incorporating topography, morphology, and aetiology [6]
• OLGA/OLGIM staging: Operative Link for Gastritis Assessment staging systems risk-stratify gastric cancer risk based on atrophy/metaplasia extent and distribution [7]

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2. Epidemiology

Global Prevalence

Helicobacter pylori-Associated Gastritis

• Global prevalence: Approximately 50% of the world's population infected with H. pylori [8]
• Regional variation: >70% in developing countries, 20-40% in developed nations
• Age-related: Cohort effect with declining prevalence in younger generations in Western countries
• Socioeconomic gradient: Higher prevalence associated with childhood overcrowding, poor sanitation, and lower socioeconomic status

Autoimmune Gastritis

• Overall prevalence: 0.5-2% in general population, increasing with age [9]
• Female predominance: 3:1 female-to-male ratio
• Association with other autoimmune conditions:
  • Autoimmune thyroid disease (30% of cases)
  • Type 1 diabetes mellitus (10-15%)
  • Vitiligo, Addison's disease (5-10%)
• Geographical distribution: More common in Northern European populations

Chronic Atrophic Gastritis

• Worldwide prevalence: 20-30% in populations >50 years old [10]
• High-risk regions: East Asia (Japan, Korea, China), South America (Chile), Eastern Europe
• Gastric cancer correlation: Atrophic gastritis present in >80% of patients with gastric adenocarcinoma

Risk Factors

Demographics

• Age: Autoimmune gastritis typically presents in 5th-7th decade; H. pylori acquisition usually in childhood
• Sex: Autoimmune gastritis shows female predominance; H. pylori gastritis equal distribution
• Ethnicity: Gastric cancer risk from atrophic gastritis highest in East Asian, Hispanic, and African populations
• Comorbidities: Chronic kidney disease, cirrhosis, and HIV infection associated with higher H. pylori prevalence

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3. Pathophysiology

Normal Gastric Mucosal Defence

The gastric mucosa maintains homeostasis through:

• Mucus-bicarbonate barrier: Prostaglandin-stimulated secretion creates pH gradient from luminal acid (pH 1-2) to epithelial surface (pH 6-7)
• Epithelial tight junctions: Prevent back-diffusion of H+ ions
• Mucosal blood flow: Delivers bicarbonate and oxygen, removes H+ ions
• Epithelial renewal: Complete regeneration every 3-5 days
• Prostaglandins (PGE2, PGI2): Critical for mucus secretion, bicarbonate production, and mucosal blood flow

Type A (Autoimmune) Gastritis

Genetic Predisposition (HLA-DR3, DR5, PTPN22 polymorphisms)
                    ↓
Environmental Trigger (? molecular mimicry with H+/K+-ATPase)
                    ↓
Production of Autoantibodies:
├─ Anti-parietal cell antibodies (90% of cases) → Target H+/K+-ATPase
└─ Anti-intrinsic factor antibodies (70% of cases) → Neutralizing or blocking
                    ↓
Progressive Destruction of Parietal Cells (Corpus and Fundus)
                    ↓
        ┌───────────┴───────────┐
        ↓                       ↓
↓ Acid Production          ↓ Intrinsic Factor
(Achlorhydria/Hypochlorhydria)  Production
        ↓                       ↓
Compensatory                B12 Malabsorption
Hypergastrinaemia               ↓
(Gastrin >500-1000 pg/mL)   Pernicious Anaemia
        ↓                   (Megaloblastic)
Enterochromaffin-like (ECL)     ↓
Cell Hyperplasia            Neurological Sequelae
        ↓                   (Subacute combined
Gastric Carcinoid Risk      degeneration of cord)
(Type I - indolent)
        ↓
↑ Gastric pH → ↓ Iron Absorption
        ↓
Iron Deficiency Anaemia
        ↓
Combined Iron + B12 Deficiency
(Dimorphic Blood Film)

Key Molecular Mechanisms: [11]

• Th1-mediated immune response: IFN-γ and TNF-α drive chronic inflammation
• Epithelial atrophy: Loss of chief cells and parietal cells with pseudopyloric metaplasia
• Intestinal metaplasia: Chronic inflammation → CDX2 upregulation → intestinal phenotype (incomplete type carries higher cancer risk)

Type B (Helicobacter pylori) Gastritis

H. pylori Colonization (typically in childhood)
        ↓
Antral-predominant Gastritis (initial phase)
        ↓
Virulence Factors:
├─ Urease: Ammonia production → neutralizes gastric acid → creates niche
├─ CagA (cytotoxin-associated gene A): Injected via Type IV secretion system
│  └─ Dysregulates cell signaling, proliferation, apoptosis
├─ VacA (vacuolating cytotoxin A): Induces epithelial vacuolation, apoptosis
└─ Flagella: Motility through mucus layer
        ↓
Inflammatory Response:
├─ Acute phase: Neutrophil infiltration → acute gastritis
├─ Chronic phase: Lymphocytes, plasma cells → chronic active gastritis
└─ Cytokine release: IL-1β, IL-8, TNF-α → amplify inflammation
        ↓
DIVERGENT OUTCOMES (determined by bacterial strain, host genetics, environmental factors):

PATH 1: Antral-Predominant Gastritis
        ↓
Preserved/↑ Acid Secretion
        ↓
DUODENAL ULCER (10-15% of infected individuals)

PATH 2: Pangastritis/Corpus-Predominant
        ↓
Multifocal Atrophic Gastritis
        ↓
↓ Acid Secretion + Achlorhydria
        ↓
GASTRIC ULCER (5-10% of infected individuals)
        ↓
Intestinal Metaplasia (incomplete > complete type)
        ↓
Dysplasia (low-grade → high-grade)
        ↓
GASTRIC ADENOCARCINOMA (1-3% lifetime risk)
(Correa Cascade - typically 20-30 years progression)

PATH 3: MALToma Development
        ↓
Chronic Antigenic Stimulation
        ↓
B-cell Clonal Proliferation
        ↓
MALT LYMPHOMA (less than 0.1% of infected individuals)

Genetic Host Factors Influencing Outcome: [12]

• IL-1β polymorphisms: Enhanced IL-1β production → profound acid suppression → atrophic progression
• TNF-α polymorphisms: Associated with increased gastric cancer risk
• HLA class II: Certain haplotypes predispose to more severe inflammation

Bacterial Strain Factors: [13]

• CagA-positive strains: 2-3× higher risk of peptic ulcer and gastric cancer
• VacA s1/m1 genotypes: More virulent than s2/m2
• Geographic strain variation: East Asian CagA strains more oncogenic than Western strains

Type C (Chemical/Reactive) Gastropathy

Injurious Agent (NSAIDs or Bile Reflux)
        ↓
NSAID Pathway:
├─ COX-1 Inhibition
│   └─ ↓ Prostaglandin synthesis (PGE2, PGI2)
│       └─ ↓ Mucus/bicarbonate secretion
│       └─ ↓ Mucosal blood flow
│       └─ ↓ Epithelial proliferation
├─ Topical mucosal damage (weak acid properties)
└─ Mitochondrial uncoupling → epithelial injury
        ↓
BILE REFLUX Pathway (post-surgical, pyloric dysfunction):
├─ Bile acids + lysolecithin
│   └─ Detergent effect on mucus layer
└─ Direct epithelial cytotoxicity
        ↓
Common Final Pathway:
        ↓
Mucosal Barrier Disruption
        ↓
H+ Back-Diffusion + Epithelial Necrosis
        ↓
Reactive Gastropathy (Histological features):
├─ Foveolar hyperplasia (elongated, tortuous pits)
├─ Smooth muscle proliferation in lamina propria
├─ Vascular congestion and ectasia
└─ Minimal inflammatory infiltrate (key distinction from other types)
        ↓
Clinical Manifestations:
├─ Erosions/Ulceration (severe cases)
└─ Often asymptomatic or mild dyspepsia

NSAIDs and H. pylori Synergy: [14]

• Independent but additive/multiplicative risk factors for peptic ulceration
• H. pylori eradication moderately reduces NSAID ulcer risk
• Combined presence increases ulcer risk 60-fold compared to neither factor

Stress-Related Mucosal Disease (SRMD)

Critical Illness (shock, sepsis, burns, trauma, mechanical ventilation)
        ↓
Systemic Stress Response:
├─ Splanchnic hypoperfusion → mucosal ischemia
├─ ↑ Cortisol, catecholamines → ↑ acid secretion
└─ Coagulopathy (disseminated intravascular coagulation)
        ↓
Mucosal Ischemia + Reperfusion Injury
        ↓
Free Radical Formation + Lipid Peroxidation
        ↓
Epithelial Cell Death + Barrier Breakdown
        ↓
Acute Erosive Gastritis (diffuse, typically fundal/body)
        ↓
Progression (if untreated):
        ↓
Stress Ulceration (Curling ulcers - burns; Cushing ulcers - CNS injury)
        ↓
GI Bleeding (5-25% of ICU patients without prophylaxis)

The Correa Cascade (Gastric Carcinogenesis)

Normal Gastric Mucosa
        ↓
Chronic Active Gastritis (H. pylori)
        ↓ (10-20 years)
Multifocal Atrophic Gastritis
├─ Loss of specialized glands (parietal, chief cells)
└─ Glandular atrophy
        ↓ (5-10 years)
Intestinal Metaplasia
├─ Complete type (small intestinal phenotype) - lower risk
└─ Incomplete type (colonic phenotype) - higher risk
        ↓ (variable, 2-5 years)
Dysplasia
├─ Low-grade intraepithelial neoplasia
└─ High-grade intraepithelial neoplasia
        ↓ (months to years)
Invasive Adenocarcinoma
└─ Intestinal-type gastric cancer (Lauren classification)

Risk Stratification by OLGA/OLGIM Staging: [7]

• Stage 0: No atrophy/metaplasia → Very low risk
• Stage I-II: Mild atrophy/metaplasia, antrum or corpus only → Low risk
• Stage III-IV: Extensive atrophy/metaplasia, both antrum and corpus → High risk (annual cancer incidence 0.5-1%)

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4. Clinical Presentation

Symptomatology

Acute Gastritis

Chronic Gastritis

• Asymptomatic presentation: 50-80% of chronic gastritis cases, particularly H. pylori-associated, are entirely asymptomatic [15]
• Vague dyspepsia: Non-specific epigastric discomfort, bloating, early satiety
• Symptoms of anaemia (Type A):
  • Fatigue, exertional dyspnoea (iron and/or B12 deficiency)
  • "Neurological symptoms (B12 deficiency): paraesthesiae, ataxia, cognitive impairment, subacute combined degeneration"
  • Glossitis, angular stomatitis (iron/B12 deficiency)

Symptom-Aetiology Correlation

• NSAID-induced: Often asymptomatic until complication (ulcer, bleeding) - "silent ulcers"
• Alcohol-induced: Associated with binge drinking episodes, acute epigastric pain, vomiting
• Stress-related (ICU): Typically silent until catastrophic bleeding in 5-25% of critically ill without prophylaxis
• Autoimmune: Insidious onset, symptoms of megaloblastic anaemia may precede gastric symptoms by years

Physical Examination

General Inspection

Abdominal Examination

• Epigastric tenderness: Present in acute gastritis, non-specific
• No peritonism: Unless complicated by perforation (rare)
• Often entirely normal: Chronic gastritis frequently has no abnormal findings
• Hepatosplenomegaly: Not a feature (consider alternative diagnoses if present)
• Succussion splash: Suggests gastric outlet obstruction (complication of peptic ulcer disease)

Neurological Examination (Type A Gastritis)

• Peripheral neuropathy: Distal symmetrical sensory loss (B12 deficiency)
• Posterior column signs: Loss of vibration/proprioception, sensory ataxia
• Pyramidal tract signs: Spastic paraparesis, extensor plantars
• Cognitive impairment: "Megaloblastic madness"
• reversible dementia
• Optic neuropathy: Rare, severe B12 deficiency

Lymphadenopathy

• Left supraclavicular node (Virchow's node): Red flag for gastric malignancy (Troisier's sign)
• Generalized lymphadenopathy: Consider MALT lymphoma, systemic disease

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5. Differential Diagnosis

Upper Abdominal Pain/Dyspepsia Differentials

Anaemia Differentials (Autoimmune Gastritis)

• Other causes of megaloblastic anaemia: Folate deficiency, drugs (methotrexate, hydroxycarbamide), myelodysplasia
• Combined B12 and iron deficiency: Malabsorption (coeliac disease), chronic bleeding (GI malignancy)
• Other causes of iron deficiency: Menorrhagia, colorectal malignancy, coeliac disease
• Autoimmune haemolytic anaemia: May coexist with autoimmune gastritis

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6. Investigations

Non-Invasive Testing

Haematological Tests

Biochemical Tests

Serological Tests (Autoimmune Gastritis)

Helicobacter pylori Testing (Non-Invasive)

Important: False negatives with UBT/stool antigen if recent PPI (within 2 weeks) or antibiotic use (within 4 weeks). Serology remains positive for years after eradication (not useful for test-of-cure).

Invasive Testing (Endoscopy)

Indications for OGD (NICE Guidelines)

1. Age ≥55 years with persistent dyspepsia (new onset or persistent despite treatment)
2. Red flag symptoms at any age:
   • Dysphagia (progressive)
   • Unintentional weight loss
   • Persistent vomiting
   • GI bleeding (haematemesis, melaena)
   • Palpable abdominal mass
   • Iron deficiency anaemia (unexplained)
3. Failed empirical treatment (PPI trial and H. pylori eradication if applicable)
4. Surveillance for known atrophic gastritis/intestinal metaplasia
5. Family history of gastric cancer in first-degree relative

Endoscopic Findings

Gastric Biopsy Protocol (Updated Sydney System) [6]

Standard 5-site biopsy mapping:

1. Antrum (lesser curve): 2 biopsies 2-3 cm from pylorus
2. Antrum (greater curve): 1 biopsy
3. Body (lesser curve): 1 biopsy 8 cm from cardia
4. Body (greater curve): 1 biopsy
5. (Incisura angularis): 1 biopsy (optional but recommended)

Additional biopsies:

• Any visible lesion (ulcer, mass, polyp)
• Atrophic/metaplastic areas

Histopathological Assessment

Rapid Urease Test (CLO Test)

• Principle: Biopsy placed in urea-containing gel; H. pylori urease converts urea → ammonia → pH change → colour change (yellow to pink/red)
• Sensitivity/Specificity: 90-95% each
• Time to result: 1-24 hours (often positive within 1-2 hours if heavy colonization)
• Limitation: False negatives if PPI use, recent antibiotics, or low bacterial density

OLGA/OLGIM Staging (From Biopsies) [7]

• OLGA: Operative Link on Gastritis Assessment - grades atrophy
• OLGIM: Operative Link on Gastric Intestinal Metaplasia - grades metaplasia
• Stages 0-IV: Based on extent and distribution (antrum vs corpus)
• High-risk (III-IV): Warrants surveillance endoscopy

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7. Management

General Measures (All Types)

Lifestyle and Risk Modification

• Cease NSAID use: If possible, switch to alternative analgesia (paracetamol, topical NSAIDs for MSK pain)
  • "If NSAIDs unavoidable: co-prescribe PPI (standard dose), use lowest effective NSAID dose"
• Reduce/eliminate alcohol consumption: Particularly in acute gastritis
• Smoking cessation: Impairs mucosal healing, increases ulcer and cancer risk
• Dietary modification:
  • Avoid trigger foods if identified (spicy foods, coffee, citrus - patient-specific)
  • Reduce high-salt intake (associated with atrophic gastritis progression)
• Review medications: Identify and modify gastropathic drugs (bisphosphonates, potassium supplements, iron)

Helicobacter pylori Eradication Therapy

First-Line Regimens (UK/Europe) [17]

PPI options (standard dose): Omeprazole 20mg, Lansoprazole 30mg, Pantoprazole 40mg, Esomeprazole 20mg, Rabeprazole 20mg

Important Notes:

• High-dose PPI: Some guidelines recommend double-dose PPI to improve eradication rates
• Extended duration: 14 days superior to 7 days (5-10% improvement in eradication)
• Resistance patterns: Clarithromycin resistance rising globally (>15% in many regions) → bismuth quadruple increasingly preferred first-line
• Compliance: Critical; poor adherence drastically reduces eradication success

Second-Line Therapy (After First-Line Failure)

• If initial regimen was clarithromycin-based: Bismuth quadruple therapy (as above)
• If initial regimen was bismuth quadruple:
  • "Levofloxacin triple therapy: PPI (double dose BD) + Amoxicillin 1g BD + Levofloxacin 500mg OD × 10-14 days"
  • Consider culture and sensitivity testing via repeat OGD

Third-Line and Beyond

• Repeat OGD with biopsy for culture and antibiotic susceptibility testing
• Rifabutin-based therapy: PPI + Amoxicillin + Rifabutin (specialist use, TB considerations)
• Salvage therapy: Guided by antibiotic susceptibility

Confirmation of Eradication

• Test-of-cure MANDATORY: Urea breath test or stool antigen test ≥4 weeks after completion of eradication therapy
• Stop PPI: Withhold PPI for 2 weeks before test-of-cure (false negatives)
• Persistence: If eradication fails, consider second-/third-line therapy
• Re-infection: less than 1-2% per year in developed countries; higher in endemic areas

Acid Suppression Therapy

Proton Pump Inhibitors (PPIs)

PPI Risks with Long-Term Use (>1 year):

• Hypomagnesaemia (monitor if >1 year use, especially with diuretics)
• Hypocalcaemia and osteoporosis (consider calcium/vitamin D supplementation, DEXA scan if high risk)
• Clostridium difficile infection (relative risk 1.5-3×)
• Small bowel bacterial overgrowth (SIBO)
• Microscopic colitis (collagenous/lymphocytic colitis)
• Renal interstitial nephritis (rare, idiosyncratic)
• Fundic gland polyps (benign, no malignant potential)
• Potential drug interactions (clopidogrel-omeprazole interaction; reduced efficacy of clopidogrel)

PPI De-prescribing: If no ongoing indication, taper and discontinue (beware rebound acid hypersecretion for 2-8 weeks)

H2-Receptor Antagonists (H2RAs)

• Agents: Ranitidine (withdrawn in many countries due to NDMA contamination), Famotidine, Nizatidine
• Efficacy: Inferior to PPIs for gastritis and ulcer healing
• Use: Alternative if PPI intolerant/contraindicated; nocturnal acid suppression
• Tachyphylaxis: Develop tolerance after 2 weeks of continuous use (reduced efficacy)

Autoimmune Gastritis-Specific Management

Vitamin B12 Replacement

Loading Phase: Critical to replete body stores (liver contains 2-5 mg, daily requirement ~2.5 μg) and reverse neurological deficit before permanent damage

Iron Replacement (If Deficient)

• Oral iron: Ferrous sulfate 200mg (65mg elemental iron) OD-TDS, or alternative preparations (ferrous fumarate, ferrous gluconate)
• Absorption: Reduced in achlorhydria; consider taking with vitamin C to enhance absorption
• IV iron: Consider if oral intolerant, severe deficiency, or ongoing losses

Surveillance and Monitoring

• Annual FBC, B12, ferritin: Monitor for recurrent deficiency (check compliance with B12 replacement)
• Endoscopic surveillance:
  • Every 3-5 years if extensive atrophy (OLGA/OLGIM stage III-IV)
  • Annual if dysplasia detected
  • No surveillance needed for mild atrophy without intestinal metaplasia
• Gastrin monitoring: Very high gastrin (>1000 pg/mL) → consider screening for gastric carcinoid (Type I - associated with ECL hyperplasia)
• Thyroid function tests: Screen for associated autoimmune thyroid disease (annual TFTs)

Gastric Carcinoid (Type I) Management

• Prevalence: 2-5% of autoimmune gastritis patients develop Type I gastric carcinoids
• Characteristics: Typically less than 1 cm, multiple, fundus/body, indolent, rarely metastasise
• Management:
  • less than 1 cm, less than 3 lesions: Endoscopic resection + surveillance
  • "Multiple or recurrent: Endoscopic resection + consider somatostatin analogues (octreotide) to reduce hypergastrinaemia"
  • >2 cm or invasive: Surgical resection (rare to require)
• Surveillance: Annual endoscopy if history of carcinoid

NSAID/Chemical Gastropathy Management

• Discontinue offending agent: NSAIDs, aspirin (if possible)
• PPI therapy: Standard dose × 4-8 weeks for healing
• If NSAIDs essential:
  • Co-prescribe PPI (standard dose OD) for duration of NSAID therapy
  • Use lowest effective NSAID dose for shortest duration
  • Consider COX-2 selective inhibitor (celecoxib) + PPI in very high-risk patients (though cardiovascular risk considerations)
• Alternative analgesia: Paracetamol, topical NSAIDs, or opioids (MSK pain)

Acute Stress-Related Mucosal Disease (SRMD) Prophylaxis

ICU/Critical Illness

• High-risk patients (mechanically ventilated >48 hours, coagulopathy, severe sepsis, major burns, traumatic brain injury):
  • "PPI: Pantoprazole 40mg IV OD or Esomeprazole 40mg IV OD (preferred over H2RA)"
  • "H2RA: Famotidine 20mg IV BD (alternative, though PPIs superior)"
• Duration: Continue until enteral feeding established and risk factors resolved
• No prophylaxis needed: Low-risk ICU patients (increases C. difficile and pneumonia risk without benefit)

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8. Complications

Early/Acute Complications

Late/Chronic Complications

Gastric Cancer Risk Stratification [18]

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9. Prognosis & Outcomes

Acute Gastritis

• NSAID/Alcohol-induced: Excellent prognosis with cessation of offending agent; mucosal healing typically within 2-4 weeks with acid suppression
• Stress-related mucosal disease: Prognosis dependent on underlying critical illness; bleeding associated with increased ICU mortality
• Erosive gastritis with bleeding: Mortality 5-10% (higher in elderly, comorbidities, rebleeding)

Helicobacter pylori-Associated Gastritis

• With successful eradication:
  • Gastritis resolves/improves significantly within 1-2 years [19]
  • Peptic ulcer recurrence reduced from 60-70% to less than 5% per year
  • Gastric cancer risk reduced by 30-50% if eradicated before development of atrophic gastritis/metaplasia
  • Critical window: Eradication most beneficial before "point of no return" (extensive atrophy/metaplasia)
• Without eradication:
  • Chronic gastritis persists indefinitely
  • Progressive atrophy in subset (10-30% over decades)
  • 1-3% lifetime risk of gastric cancer
  • 10-20% risk of peptic ulcer disease

Autoimmune Gastritis

• Natural history: Chronic, progressive, irreversible
• B12 replacement: Prevents neurological sequelae if started before irreversible damage; lifelong therapy required
• Gastric cancer risk: 3-5% develop gastric adenocarcinoma (intestinal type); surveillance detects early lesions amenable to curative endoscopic resection
• Quality of life: Generally good if B12 adequately replaced and surveillance adhered to

Atrophic Gastritis and Intestinal Metaplasia

• Regression: Rare; atrophy/metaplasia generally considered irreversible even after H. pylori eradication (though some studies show histological improvement in minority)
• Progression to cancer: 0.5-1% per year in extensive atrophy (OLGA/OLGIM III-IV)
• Surveillance outcomes: Early detection via surveillance allows curative endoscopic or surgical resection (5-year survival >90% for early gastric cancer)

MALT Lymphoma

• Eradication therapy: 70-80% complete remission in localized (stage I-II) gastric MALT lymphoma after H. pylori eradication alone [20]
• Regression time: Median 12-18 months; requires prolonged endoscopic and imaging follow-up
• Advanced/resistant cases: May require chemotherapy, radiotherapy, or rituximab
• Prognosis: Excellent (>90% 5-year survival) for localized disease

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10. Evidence & Guidelines

International Consensus Statements

National Guidelines (UK)

Landmark Evidence

1. EUROGAST Study (1993): Demonstrated clear association between H. pylori prevalence and gastric cancer mortality across European populations (ecological study)
2. Correa Cascade (1988-present): Longitudinal studies confirming progression from chronic gastritis → atrophy → metaplasia → dysplasia → cancer over decades
3. Surveillance Trials: Meta-analyses show endoscopic surveillance in high-risk patients (extensive atrophy) detects early gastric cancer with curative potential (>90% 5-year survival if detected at early stage)
4. Wong et al. (2004): Randomized trial showing H. pylori eradication reduces gastric cancer incidence in asymptomatic infected individuals (though benefit limited once atrophy/metaplasia present)

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11. Special Populations

Pregnancy

• H. pylori testing/treatment: Generally deferred until post-partum unless severe ulcer disease
  • "Antibiotics in pregnancy: Amoxicillin safe; clarithromycin/metronidazole/tetracycline avoided"
• PPI use: Omeprazole/lansoprazole considered safe (Category B); use if benefit outweighs risk
• Iron/B12 deficiency: May worsen in pregnancy; supplement appropriately

Elderly

• Higher prevalence: Atrophic gastritis, H. pylori, NSAID use
• Presentation: Often atypical or asymptomatic until complication (bleeding, perforation)
• PPI use: Increased risk of osteoporosis, fractures, C. difficile; use lowest effective dose
• Polypharmacy: Review all gastropathic medications

Immunosuppressed (HIV, Transplant, Biologics)

• Opportunistic infections: CMV gastritis, cryptosporidium, candida (consider if refractory symptoms)
• MALT lymphoma risk: Possibly increased in immunosuppression
• H. pylori eradication: May be more challenging; higher failure rates

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12. Patient / Layperson Explanation

What is gastritis?

Gastritis is inflammation (swelling and irritation) of the stomach lining. It can be short-term (acute) or long-lasting (chronic), depending on the cause.

What causes it?

• Bacteria: A germ called Helicobacter pylori (H. pylori) is the most common cause of chronic gastritis. About half of the world's population has this infection, though many people never have symptoms.
• Painkillers: Anti-inflammatory drugs like ibuprofen, aspirin, and diclofenac can damage the stomach lining, especially with long-term use.
• Alcohol: Excessive drinking irritates the stomach lining and can cause acute gastritis.
• Autoimmune disease: Rarely, the body's immune system mistakenly attacks the stomach lining, leading to a specific type called autoimmune gastritis. This can cause vitamin B12 deficiency (pernicious anaemia).
• Stress: Severe illness, major surgery, or critical illness can cause stress-related stomach inflammation.

What are the symptoms?

Many people with chronic gastritis have no symptoms at all. When symptoms do occur, they may include:

• Burning or gnawing pain in the upper tummy (between your ribs)
• Feeling sick (nausea) or being sick (vomiting)
• Bloating and feeling full quickly when eating
• Loss of appetite
• Sometimes, if there is bleeding: vomiting blood (like coffee grounds) or black, tarry stools

How is it diagnosed?

• Blood tests: Check for anaemia (low blood count) and vitamin deficiencies
• Breath or stool test: Detects H. pylori infection
• Endoscopy (camera test): A thin, flexible camera is passed down your throat to look at your stomach lining and take small samples (biopsies) if needed. This is usually done if you are over 55, have worrying symptoms (like weight loss or bleeding), or treatment hasn't worked.

How is it treated?

Treatment depends on the cause:

• If H. pylori is found: A course of antibiotics (usually two types) plus a tablet to reduce stomach acid (proton pump inhibitor or PPI) for 1-2 weeks. This clears the infection in most cases.
• If caused by painkillers: Stop the painkillers if possible, or take a PPI to protect your stomach while you continue them.
• If caused by alcohol: Cut down or stop drinking alcohol.
• If autoimmune gastritis: Lifelong vitamin B12 injections every 2-3 months to prevent anaemia and nerve damage.
• Acid-reducing tablets (PPIs): Such as omeprazole or lansoprazole, help heal the stomach lining and reduce symptoms.

Can gastritis lead to serious problems?

Most cases of gastritis get better with treatment. However, if left untreated for many years, chronic gastritis (especially from H. pylori or autoimmune causes) can lead to:

• Stomach ulcers: Painful sores in the stomach lining
• Stomach cancer: Long-term inflammation can, rarely, lead to changes in the stomach lining that increase cancer risk over decades. This is why treating H. pylori is important.
• Vitamin deficiencies: Autoimmune gastritis can cause B12 and iron deficiency, leading to anaemia and nerve problems if not treated.

What can I do to help myself?

• Take prescribed medications as directed (complete antibiotic courses)
• Avoid or reduce NSAIDs/aspirin (speak to your doctor about alternatives)
• Cut down on alcohol
• Stop smoking (smoking slows healing)
• Eat a healthy, balanced diet
• Attend follow-up tests to confirm H. pylori has cleared

When should I seek urgent medical help?

Contact your doctor urgently or go to A&E if you have:

• Vomiting blood or material that looks like coffee grounds
• Black, tarry, or bloody stools
• Severe, sudden tummy pain
• Unexplained weight loss
• Difficulty swallowing

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13. References

1. Dixon MF, Genta RM, Yardley JH, et al. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol. 1996;20(10):1161-1181. PMID: 8827022

2. Rugge M, Savarino E, Sbaraglia M, et al. Gastritis: The clinico-pathological spectrum. Dig Liver Dis. 2021;53(9):1166-1172. PMID: 33785282

3. Lenti MV, Rugge M, Lahner E, et al. Autoimmune gastritis. Nat Rev Dis Primers. 2020;6(1):56. PMID: 32647173

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