|Classification and external resources|
Atrophic gastritis (also known as Type A or Type B Gastritis more specifically) 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, leading to megaloblastic anemia or malabsorbtion of iron, leading to iron deficiency anaemia. It can be caused by persistent infection with Helicobacter pylori, or can be autoimmune in origin. Those with the autoimmune version of atrophic gastritis are statistically more likely to develop gastric carcinoma, Hashimoto's thyroiditis, and achlorhydria.
Type A gastritis primarily affects the body/fundus of the stomach, and is more common with pernicious anemia.
Type B gastritis primarily affects the antrum, and is more common with H. pylori infection.
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 cells, which leads to 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 atrophic gastritis 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.
Atrophic gastritis is classified depending on the level of progress as "close type" or "open type". This classification was advocated by Takemoto and Kimura of Tokyo University at 1966.
Recent research has shown that AMAG is a result of the immune system attacking the parietal cells, the attack is being triggered by Helicobacter pylori through a mechanism called molecular mimicry.
Environmental Metaplastic Atrophic Gastritis (EMAG) is due to environmental factors, such as diet and H. pylori infection. EMAG is typically confined to the body of the stomach. Patients with EMAG are also at increased risk of gastric carcinoma.
- Gut 2003;52:496-501 doi:10.1136/gut.52.4.496
- "Autoimmune Metaplastic Atrophic Gastritis: Gastritis and Peptic Ulcer Disease: Merck Manual Professional".
- Giannakis M, Chen SL, Karam SM, Engstrand L, Gordon JI (March 2008). "Helicobacter pylori evolution during progression from chronic atrophic gastritis to gastric cancer and its impact on gastric stem cells". Proc. Natl. Acad. Sci. U.S.A. 105 (11): 4358–63. doi:10.1073/pnas.0800668105. PMC 2393758. PMID 18332421.