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Autoimmune gastritis (AIG) is a chronic, immune-mediated gastritis characterized by autoantibodies against parietal cells and intrinsic factor, leading to:

• Loss of parietal cells (achlorhydria, ↓ intrinsic factor).
• Vitamin B12 deficiency → Pernicious anemia
• ECL cell hyperplasia due to hypergastrinemia (risk of type I gastric carcinoids). </aside>

It is also called Type A atrophic gastritis.

Etiopathogenesis

Immune mechanism:

• Autoantibodies target H+/K+ ATPase of parietal cells and intrinsic factor.
• Chronic inflammation → glandular destruction → mucosal atrophy.
• Genetic predisposition: HLA-DR, HLA-DQ associations.

Associated autoimmune diseases:

• Thyroiditis (Hashimoto), type 1 diabetes, vitiligo, Addison’s disease.

Site: Primarily affects the fundus and body (sparing antrum).

![Anatomical localization of AIG: The gastric mucosa includes two phenotypic and functional compartments, namely, the cranial oxyntic and the distal mucosecreting. The different biological profiles of the oxyntic and mucosecreting gastric mucosa result in different susceptibilities to environmental or host-related noxious agents. In the native stomach, the oxyntic mucosa covers the cranial two-thirds of the mucosal surface (that is, the fundus and the corpus mucosa) and is gradually replaced distally by the antral mucosecreting glands. The boundary between these two functional areas follows a rounded line, cranially centred at the incisura angularis. Autoimmune gastritis (AIG) affects the corpus and fundus, causing mucosal atrophy that spares the antrum. Parietal cells, which are the main target cells in AIG, are located only in the oxyntic mucosa and produce hydrochloric acid and intrinsic factor. Parietal cells reside along with other cells including chief cells (also known as zymogenic cells, which mainly produce pepsinogen), mucous neck cells (which produce mucins), enterochromaffin-like (ECL) cells, ghrelin cells and somatostatin cells.

Lenti, M.V., Rugge, M., Lahner, E. et al. Autoimmune gastritis. Nat Rev Dis Primers 6, 56 (2020). https://doi.org/10.1038/s41572-020-0187-8](attachment:b910fe15-d44f-4152-95d1-e4ee68babe09:image.png)

Anatomical localization of AIG: The gastric mucosa includes two phenotypic and functional compartments, namely, the cranial oxyntic and the distal mucosecreting. The different biological profiles of the oxyntic and mucosecreting gastric mucosa result in different susceptibilities to environmental or host-related noxious agents. In the native stomach, the oxyntic mucosa covers the cranial two-thirds of the mucosal surface (that is, the fundus and the corpus mucosa) and is gradually replaced distally by the antral mucosecreting glands. The boundary between these two functional areas follows a rounded line, cranially centred at the incisura angularis. Autoimmune gastritis (AIG) affects the corpus and fundus, causing mucosal atrophy that spares the antrum. Parietal cells, which are the main target cells in AIG, are located only in the oxyntic mucosa and produce hydrochloric acid and intrinsic factor. Parietal cells reside along with other cells including chief cells (also known as zymogenic cells, which mainly produce pepsinogen), mucous neck cells (which produce mucins), enterochromaffin-like (ECL) cells, ghrelin cells and somatostatin cells.

Lenti, M.V., Rugge, M., Lahner, E. et al. Autoimmune gastritis. Nat Rev Dis Primers 6, 56 (2020). https://doi.org/10.1038/s41572-020-0187-8

Pathology

Histology:

• Loss of parietal and chief cells.
• Lymphoplasmacytic infiltrates.
• Intestinal metaplasia (goblet cells).
• Pseudopyloric metaplasia.

Laboratory: