Autoimmune atrophic gastritis
- Lesion
The immune system attacks the acid-making cells of the stomach body, so acid and intrinsic factor are lost and vitamin B12 deficiency follows.
What it is
Autoimmune atrophic gastritis destroys parietal cells of the body and fundus while sparing the antrum. CD4 T cells and antibodies against the proton pump (H+/K+-ATPase) and intrinsic factor drive the injury. Without acid, antral G cells release gastrin in excess; without intrinsic factor, vitamin B12 is not absorbed in the ileum and pernicious anaemia develops. It is the second leading cause of chronic gastritis after H. pylori and NSAIDs, and the risk of adenocarcinoma and neuroendocrine tumours rises.
Structure
- Thin oxyntic mucosa with loss of rugal folds.
- Loss of parietal and chief cells; residual islands of oxyntic mucosa can look like polyps.
- Intestinal metaplasia (goblet cells, sometimes Paneth cells) and pseudopyloric metaplasia.
- Linear and nodular ECL-cell hyperplasia; megaloblastic nuclear change in epithelium if B12 is very low.
Step by step
- T cells and autoantibodies target the parietal-cell proton pump.
- Parietal cells are lost: acid and intrinsic factor fall.
- Low acid removes feedback on antral G cells: gastrin rises.
- Gastrin drives ECL-cell hyperplasia, sometimes to neuroendocrine tumour.
- No intrinsic factor: vitamin B12 malabsorption and pernicious anaemia years later.
The two main chronic gastritides compared
| Feature | H. pylori gastritis | Autoimmune atrophic gastritis |
|---|---|---|
| Main site | Antrum (later the body) | Body and fundus; antrum spared |
| Inflammation | Superficial plasma cells, neutrophils, lymphoid follicles | Deep, gland-centred lymphocytes and plasma cells; few neutrophils |
| Acid | Normal to increased (lower if atrophic) | Absent (achlorhydria) |
| Gastrin | Normal to mildly increased | Markedly increased; G-cell and ECL-cell hyperplasia |
| Antibodies | Against H. pylori | Against parietal cells and intrinsic factor |
| Complications | Peptic ulcer, adenocarcinoma, MALT lymphoma | Pernicious anaemia, adenocarcinoma, neuroendocrine tumour |
| Associations | Poverty, crowding, rural childhood | Other autoimmune disease |
Clinical notes
- Median age at diagnosis is about sixty; women slightly more often.
- Achlorhydria may allow bacterial overgrowth and nitrosamine production, one proposed reason for the cancer risk.
Test yourself
Think of the answer, then tap the question to see it.
Which region of the stomach does autoimmune gastritis spare?
The antrum (and cardia); damage is centred on the oxyntic mucosa of the body and fundus.
Why is serum gastrin very high in autoimmune gastritis?
Loss of acid removes the normal inhibition of antral G cells, which release gastrin and become hyperplastic.
Which tumour can arise from ECL-cell hyperplasia in autoimmune gastritis?
Small, often multiple, low-grade gastric neuroendocrine (carcinoid) tumours.
Elsewhere in DurgiPedia
- Absorption of iron, calcium and vitamin B12
- Cobalamin (vitamin B12)
- Autoantibodies: the table to know
- Type IV hypersensitivity (delayed, T cells)
Connections
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: Pernicious anemia: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025); Helicobacter Pylori (StatPearls (NCBI Bookshelf), 2025).
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Representative model, for educational purposes only.