| Atrophic gastritis | |
|---|---|
| Other names | Type A gastritis[1] |
 | |
| Atrophic gastritis | |
| Specialty | Gastroenterology |
Atrophic gastritis is a process of chronicinflammation of thegastric mucosa of thestomach, leading to a loss ofgastric glandular cells and their eventual replacement byintestinal andfibrous tissues. As a result, the stomach's secretion of essential substances such ashydrochloric acid,pepsin, andintrinsic factor is impaired, leading todigestive problems. The most common arepernicious anemia possibly leading tovitamin B12 deficiency; andmalabsorption of iron, leading toiron deficiency anaemia.[2] It can be caused by persistent infection withHelicobacter pylori, or can beautoimmune in origin. Those withautoimmune atrophic gastritis (Type A gastritis) are statistically more likely to developgastric carcinoma (a form ofstomach cancer),Hashimoto's thyroiditis, andachlorhydria.
Type A gastritis primarily affects the fundus (body) of the stomach and is more common withpernicious anemia.[1] Type B gastritis primarily affects theantrum, and is more common withH. pylori infection.[1]
Some people with atrophic gastritis may be asymptomatic. 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.[3] And other symptoms, such as delayed gastric emptying (80%), reflux symptoms (25%),peripheral neuropathy (25% of cases),autonomic abnormalities, and memory loss, are less common and occur in 1%–2% of cases. Psychiatric disorders are also reported, such as mania, depression,obsessive-compulsive disorder,psychosis, and cognitive impairment.[4]
Although autoimmune atrophic gastritis impairs iron and vitamin B12 absorption, iron deficiency is detected at a younger age than pernicious anemia.[3]
People with atrophic gastritis are also at increased risk for the development of gastric adenocarcinoma.[5]
Recent research has shown that autoimmune metaplastic atrophic gastritis (AMAG) is a result of the immune system attacking theparietal cells.[6]
Environmental metaplastic atrophic gastritis (EMAG) is due to environmental factors, such as diet andH. pylori infection. EMAG is typically confined to the body of the stomach. Patients with EMAG are also at increased risk of gastric carcinoma.[7]
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Autoimmune metaplastic atrophic gastritis (AMAG) is an inherited form of atrophic gastritis characterized by an immune response directed toward parietal cells and intrinsic factor.[6]
Achlorhydria inducesG cell (gastrin-producing) hyperplasia, which leads to hypergastrinemia. Gastrin exerts a trophic effect on enterochromaffin-like cells (ECL cells are responsible forhistamine secretion) and is hypothesized to be one mechanism to explain the malignant transformation of ECL cells intocarcinoid tumors in AMAG.[8]
Detection ofAPCA (anti-parietal cell antibodies), anti-intrinsic factor antibodies (AIFA), andHelicobacter pylori (HP) antibodies in conjunction withserum gastrin are effective for diagnostic purposes.[9]
The notion that atrophic gastritis could be classified depending on the level of progress as "closed type" or "open type" was suggested in early studies,[10] but no universally accepted classification exists as of 2017.[9]
Supplementation offolic acid in deficient patients can improve the histopathological findings of chronic atrophic gastritis and reduce the incidence of gastric cancer.[11]