Atrophic gastritis is a process of chronic inflammation of the gastric mucosa of the stomach, leading to a 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. The most common are vitamin B12 deficiency which results in a megaloblastic anemia and malabsorption 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.
|Other names||Type A or type B gastritis|
Type B gastritis primarily affects the antrum, and is more common with H. pylori infection.
Signs and symptoms
Some people with atrophic gastritis may be asymptomatic. That said, symptomatic patients are mostly females and signs of atrophic gastritis are those associated with iron deficiency: fatigue, restless legs syndrome, brittle nails, hair loss, impaired immune function, and impaired wound healing. And other symptoms such as: delayed gastric emptying (80%), reflux symptoms (25%), peripheral neuropathy (25% cases), autonomic abnormalities and memory loss are less common and occur in 1%–2% of cases. Other psychiatric disorders are also reported such as: mania, depression, obsessive compulsive disorder, psychosis and cognitive impairment.
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.
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 Achlorhydria (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.
Achlorhydria 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.
Immunosupressive drugs and chemotherapy with antineoplastic drugs are potential treatment options for AMAG. In the case of confirmed stomach cancer, stomach resection may be required.
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