Chronic Gastritis

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1- Introduction

2- Clinical Features & Examination Tips

3- Investigations & Interpretation

4- Pathophysiology

5- Symptoms

6- Treatment

Introduction

Chronic gastritis refers to persistent inflammation of the stomach lining, diagnosed histologically. It is often discovered during investigation of dyspepsia, anaemia, or incidentally during endoscopy. The two major types are:

  • H. pylori–associated gastritis (most common)

  • Autoimmune (atrophic) gastritis

 

These forms are distinct in cause, pathology, and clinical outcomes.

© image from Wikimedia Commons

Clinical Features & Examination Tips

Most patients with chronic gastritis are asymptomatic.

When symptomatic, possible features include:

  • Epigastric discomfort

  • Bloating, nausea

  • Anorexia

  • Iron-deficiency anaemia or pernicious anaemia

 

Tip: If a patient has unexplained macrocytic anaemia, check for autoimmune gastritis (B12 deficiency). Also consider H. pylori in chronic dyspepsia.

Investigations & Interpretation

-Blood tests:

  • Full blood count (look for anaemia)

  • Vitamin B₁₂ levels (for autoimmune gastritis)

  • Parietal cell/intrinsic factor antibodies

-Endoscopy + biopsy:

  • Required for histological confirmation

  • In H. pylori: shows chronic active gastritis

  • In autoimmune gastritis: shows glandular atrophy and intestinal metaplasia

H. pylori testing:

  • Urea breath test or stool antigen test (preferred for active infection)

Pathophysiology

H. pylori–associated gastritis:

The bacteria colonise gastric mucosa, release toxins (VacA, CagA), and trigger chronic inflammation. Depending on location:

  • Antral-predominant gastritis → ↑ acid → duodenal ulcer

  • Corpus-predominant gastritis → ↓ acid → atrophy/metaplasia → gastric cancer risk

Autoimmune gastritis:

Immune-mediated destruction of parietal cells (in stomach body/fundus), leading to:

  • ↓ acid production (hypochlorhydria)

  • ↓ intrinsic factor → B₁₂ deficiency → pernicious anaemia

  • Risk of gastric carcinoma increases 2–3x over time.

Symptoms

 
    • Often asymptomatic

    • Dyspepsia (indigestion)

    • Early satiety, bloating

    • Nausea

 

  • Anaemia symptoms (if bleeding or B₁₂ deficiency present)

Treatment

H. pylori–associated:

  • Triple therapy: PPI + two antibiotics (amoxicillin, clarithromycin/metronidazole) for 7–14 days

  • Confirm eradication if high-risk

  • Quadruple therapy is a key treatment strategy for H. pylori infection, especially in cases of treatment failure, clarithromycin resistance, or penicillin allergy.

    The standard bismuth-based regimen consists of four drugs:

    • A proton pump inhibitor (PPI) taken twice daily,

    • Bismuth subsalicylate or subcitrate (120 mg, four times daily),

    • Metronidazole (500 mg, three times daily), and

    • Tetracycline (500 mg, four times daily)

    This combination is given for 10–14 days.

    An alternative (non-bismuth) quadruple therapy, also called concomitant therapy, includes:

     

    • PPI,

    • Amoxicillin,

    • Clarithromycin, and

    • Metronidazole,
      all taken together for 10–14 days. This is useful when bismuth is unavailable or not tolerated.

 

Autoimmune gastritis:

  • No specific therapy for the gastritis

  • Treat vitamin B₁₂ deficiency with intramuscular B₁₂ injections

  • Monitor for gastric cancer with periodic surveillance if high-risk

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