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Helicobacter pylori gastritis

  • Lesion

A spiral bacterium caught in childhood lives in the stomach mucus for life, inflaming it and raising the risk of ulcers and stomach cancer.

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What it is

H. pylori is the commonest cause of chronic gastritis. It is acquired in childhood, mainly by the faecal-oral route in crowded, poorer settings, and persists without treatment. Its distribution in the stomach decides the outcome: antrum-predominant gastritis raises acid output and leads to duodenal ulcers, whereas spread to the body causes atrophy, intestinal metaplasia and gastric adenocarcinoma. Induced lymphoid tissue can give rise to MALT lymphoma. In Colombia and the Andean region infection is very common and gastric cancer is a leading cause of cancer death.

Structure

  • Endoscopy: red, coarse or nodular antral mucosa; thick folds can mimic early cancer.
  • Curved bacilli in surface mucus; visible on H&E, easier with silver (Warthin–Starry), Giemsa or immunostains.
  • Sheets of plasma cells in the superficial lamina propria, with lymphocytes and macrophages.
  • Neutrophils in the epithelium and pits (pit abscesses).
  • Lymphoid aggregates with germinal centres: acquired MALT.
  • Late: atrophy and intestinal metaplasia.

Step by step

  1. The bacterium enters the mucus, sensing pH and swimming toward the epithelium.
  2. Urease converts urea to ammonia, raising the local pH.
  3. Adhesins bind foveolar cells; CagA and VacA disturb epithelial signalling.
  4. Cytokines (IL-1, TNF, IL-8) recruit neutrophils and lymphocytes; antral gastrin rises and acid increases.
  5. Years later the infection may spread to the body: atrophy, metaplasia, dysplasia, cancer; or chronic B-cell stimulation leads to MALT lymphoma.

Clinical notes

  • Eradication with antibiotics and acid suppression heals most ulcers, can make early MALT lymphoma regress, and may reverse some metaplasia.
  • Reinfection is common where infection rates are high.

In the lab

  • Non-invasive: urea breath test, stool antigen, serology (shows past exposure).
  • On biopsy: histology, rapid urease test, culture or PCR.

Test yourself

Think of the answer, then tap the question to see it.

How does H. pylori survive gastric acid?

Its urease turns urea into ammonia, which buffers the acid around it, and flagella keep it in the less acidic mucus near the epithelium.

Why does antral H. pylori gastritis favour duodenal ulcer?

Antral inflammation increases gastrin and acid secretion, while duodenal bicarbonate falls.

What lymphoid change in H. pylori gastritis can become lymphoma?

Acquired mucosa-associated lymphoid tissue (lymphoid follicles), which can give rise to MALT lymphoma.

Which biopsy site is preferred to detect H. pylori?

The antrum, where the organism is most often found.

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: Helicobacter Pylori (StatPearls (NCBI Bookshelf), 2025); Gastric Cancer (StatPearls (NCBI Bookshelf), 2025).

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Representative model, for educational purposes only.