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Atrophic gastritis is a process of chronic inflammation of the stomach mucosa, leading to loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues. As a result, the stomach's secretion of essential substances such as hydrochloric acid, pepsin, and intrinsic factor is impaired, leading to digestive problems, vitamin B12 deficiency, and megaloblastic anemia. It can be caused by persistent infection with Helicobacter pylori, or can be autoimmune in origin.

Autoimmune Metaplastic Atrophic Gastritis (AMAG) is an inherited form of atrophic gastritis characterized by an immune response directed toward parietal cells and intrinsic factor. The presence of serum antibodies to parietal cells and to intrinsic factor are characteristic findings. The autoimmune response subsequently leads to the destruction of parietal cell mass which then results in profound hypochlorhydria (and elevated gastrin levels). The inadequate production of intrinsic factor also leads to vitamin B12 malabsorption and pernicious anemia. AMAG is typically confined to the gastric body and fundus

Hypochlorhydria induces G Cell (Gastrin producing) hyperplasia which leads to hypergastrinemia. Gastrin exerts a trophic effect on enterochromaffin-like cells (ECL cells are responsible for histamine secretion) and is hypothesized to be one mechanism to explain the malignant transformation of ECL cells into carcinoid tumors in AMAG.

Patients with AMAG and pernicious anemia are also at increased risk for the development of gastric adenocarcinoma. The optimal endoscopic surveillance strategy is not known but all nodules and polyps should be removed in these patients.

Environmental metaplastic atrophic gastritis (EMAG) is due to environmental factors, such as diet and H. pylori infection. EMAG is typically confined to the antrum. Patients with EMAG are also at increased risk of gastric carcinoma.

Recent research has shown that AMAG is a result of the immune system attacking the parietal cells,the attack is being triggered by h pylori through a mechanism called molecular mimicary.

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