Atrophic gastritis refers to the process of chronic inflammation of the gastric mucosa of the stomach.
The chronic inflammation leads to a loss of gastric glandular cells and their
replacement by intestinal and fibrous tissues.
The stomach’s secretion of essential substances such as hydrochloric acid, pepsin, and intrinsic factor is impaired by the chronic inflammation, leading to digestive problems.
Vitamin B12 deficiency may result with megaloblastic anemia and malabsorption of iron, that leads to iron deficiency anemia can also occur.
AG can be cause d by persistent infection with Helicobacter pylori, or can be autoimmune in origin.
Autoimmune associated atrophic gastritis is statistically more likely to develop gastric carcinoma, Hashimoto’s thyroiditis, and achlorhydria, than AG induced by Helicobacter pylori.
Type A atrophic gastritis primarily affects the body/fundus of the stomach and is more common with pernicious anemia.
Type B atrophic gastritis primarily affects the antrum, and is more common with H. pylori infection.
AG may be asymptomatic process.
Symptomatic patients are mostly females.
Signs of atrophic gastritis are those associated with iron deficiency.
Such signs include: fatigue, restless legs syndrome, brittle nails, hair loss, impaired immune function, and impaired wound healing.
Symptoms, of delayed gastric emptying occurs in 80% of cases, reflux symptoms in 25%, peripheral neuropathy in 25% cases, and autonomic abnormalities, and memory loss, are less common and occur in 1%–2% of cases.
AG may be associated with psychiatric disorders: as mania, depression, obsessive compulsive disorder, psychosis and cognitive impairment.
AG patients are at increased risk for the development of gastric adenocarcinoma.
Autoimmune atrophic gastritis is a result of the immune system attacking the parietal cells: it is an inherited form of atrophic gastritis characterized by an immune response directed toward parietal cells and intrinsic factor.
Autoimmune atrophic gastritis manifests with serum antibodies to parietal cells and to intrinsic factor, leading to the destruction of parietal cells, which leads to achlorhydria and elevated gastrin levels.
The reduced production of intrinsic factor also leads to vitamin B12 malabsorption and pernicious anemia.
Atrophic gastritis, affects 10%–30% of older adults, decreases secretion of hydrochloric acid in the stomach, resulting in decreased absorption of vitamin B12.
Decreased hydrochloric acid levels potentially increase the growth of normal intestinal bacteria that use vitamin B12, reducing the amount of vitamin B12 available to the body.
Autoimmune atrophic gastritis is usually confined to the gastric body and fundus.
Environmental atrophic gastritis is due to environmental factors: diet and H. pylori infection.
Environmental atrophic gastritis is typically confined to the body of the stomach, and is also associated with an increased risk of gastric carcinoma.
Achlorhydria induces G cell hyperplasia, which leads to hypergastrinemia.
Gastrin exerts an effect on enterochromaffin-like cells for histamine secretion.
Hypergastrinemia is hypothesized to be one mechanism to explain the malignant transformation of enterochromaffin-like cells into carcinoid tumors.
Diagnosis: Antiparietal cell antibody, anti-intrinsic factor antibody, and Helicobacter pylori (HP) antibodies in conjunction with serum gastrin are effective for diagnostic purposes.
Folic acid supplementation in deficient patients can improve the histopathological findings of chronic atrophic gastritis and reduce the incidence of gastric cancer.