Atrophic gastritis is characterized by chronic inflammation of the gastric mucosa
Associated with loss of gastric glandular cells and replacement by intestinal-type epithelium, pyloric-type glands, and fibrous tissue.
Atrophy of the gastric mucosa, such as chronic gastritis associated with Helicobacter pylori infection, other unidentified environmental factors, and autoimmunity directed against gastric glandular cells.
Helicobacter pylori chronic active gastritis.
A mononuclear lymphoplasmacytic and polymorphonuclear cell infiltrate is observed in the mucosal tissues.
There are 2 main causes of atrophic gastritis result in distinct topographic types of gastritis, which can be distinguished histologically.
Autoimmune gastritis essentially is restricted to the gastric corpus and fundus.
The corpus is the anatomical location where autoimmune type gastritis is dominant and the largest increase in gastric corpus tumors has occurred is in younger women.
Individuals with autoimmune gastritis may develop pernicious anemia due to loss of parietal cells and the presence of anti-intrinsic factor antibodies.
H pylori- associated atrophic gastritis is frequently asymptomatic.
H pylori- associated atrophic gastritis associated with an increased risk of developing gastric carcinoma.
Patients with chronic atrophic gastritis develop low gastric acid output and hypergastrinemia, which may lead to enterochromaffin-like cell hyperplasia and carcinoid tumors.
Autoimmune gastritis is a chronic progressive inflammatory disease that replaces gastric parietal cells by atrophic and metaplastic mucosa, leading to reduced or absent production of acid and intrinsic factor.
Thos results in malabsorption and B 12 deficiency resulting in pernicious anemia, which is associated with gastric carcinoma.
Dagnosis of autoimmune gastritis is supported by detection of gastric autoantibodies.