Atrophic gastritis

Epidemiology

Feature	Helicobacter pylori–induced chronic gastritis	Autoimmune gastritis
Distribution	Multifocal; patchy (start from antrum)	Corpus; diffuse (spares antrum)
Inflammatory cells	Neutrophils, plasma cells, lymphocytes	Lymphocytes, macrophages
Gastrin level	Normal or ↑	↑
Acid production	Normal or ↓	↓
Sequelae	Gastric ulcer	Vitamin B12 deficiency/pernicious anemia
Associated malignancy	Adenocarcinoma, MALT lymphoma	Adenocarcinoma, carcinoid
Risk factors	Living in resource-limited area	Other autoimmune diseases

Autoimmune metaplastic atrophic gastritis (AMAG)
- Associated with major histocompatibility haplotypes HLA-B8 and HLA-DR3
Environmental metaplastic atrophic gastritis (EMAG)
- Helicobacter pylori infection
  - Most important risk factor for chronic gastritis, including atrophic gastritis
  - Colonizes mainly antrum of stomach

Autoimmune destruction of the parietal cells in the gastric corpus and fundus (T-cell induced autoantibodies against H⁺/K⁺ ATPase) → achlorhydria → increased release of gastrin (due to loss of negative feedback) → G cell hyperplasia → hypergastrinemia → hyperplasia of enterochromaffin-like cells → ↑ risk of carcinoid tumors.
Achlorhydria impairs the intestinal absorption of inorganic iron → iron deficiency anemia (early manifestation)
Autoantibodies against intrinsic factor → vitamin B12 deficiency → pernicious anemia

Colonization by H. pylori
- Inflammation of the antrum → destruction of D cells → ↓ somatostatin → ↑ gastrin → ↑ production of gastric acids → duodenal ulcers
- Inflammation of the gastric body → local destruction of mucosa (via cytotoxins such as ammonia) → ↓ production of mucins and atrophy of the gastric glands → hypochlorhydria → hypergastrinemia and epithelial dysplasia → epithelial metaplasia → ↑ risk of gastric cancers