Atrophic gastritis


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.
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.

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, reflux symptoms, peripheral neuropathy, 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.

Associated conditions

People 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.

Causes

Recent research has shown that autoimmune metaplastic atrophic gastritis is a result of the immune system attacking the parietal cells.
Environmental metaplastic atrophic gastritis 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.

Pathophysiology

Autoimmune metaplastic atrophic gastritis 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. 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 hyperplasia, which leads to hypergastrinemia. Gastrin exerts a trophic effect on enterochromaffin-like cells and is hypothesized to be one mechanism to explain the malignant transformation of ECL cells into carcinoid tumors in AMAG.

Diagnosis

Detection of APCA, anti-intrinsic factor antibody and Helicobacter pylori antibodies in conjunction with serum gastrin are effective for diagnostic purposes. Due to its high specificity for both AGA and AGC, GastroPanel® is a valid test for stomach health.

Classification

The notion that atrophic gastritis could be classified depending on the level of progress as "close type" or "open type" was suggested in early studies, but no universally accepted classification exists as of 2017.

Treatment

Supplementation of folic acid in deficient patients can improve the histopathological findings of chronic atrophic gastritis and reduce the incidence of gastric cancer.