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 pernicious anemia possibly leading to vitamin B<sub>12</sub> deficiency; 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 autoimmune atrophic gastritis (Type A gastritis) are statistically more likely to develop gastric carcinoma (a form of stomach cancer), Hashimoto's thyroiditis, and achlorhydria.
Type A gastritis primarily affects the fundus (body) of the stomach and is more common with pernicious anemia. 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.
Although autoimmune atrophic gastritis impairs iron and vitamin B<sub>12</sub> absorption, iron deficiency is detected at a younger age than pernicious anemia.
Causes
Recent research has shown that autoimmune metaplastic atrophic gastritis (AMAG) is a result of the immune system attacking the parietal cells.
Pathophysiology
thumb|Atrophic gastritis under low power. H&E stain.
Autoimmune metaplastic atrophic gastritis (AMAG) is an inherited form of atrophic gastritis characterized by an immune response directed toward parietal cells and intrinsic factor.
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.
Diagnosis
Detection of APCA (anti-parietal cell antibodies), anti-intrinsic factor antibodies (AIFA), and Helicobacter pylori (HP) antibodies in conjunction with serum gastrin are effective for diagnostic purposes.
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File:Histopathology of antral mucosa with atrophy.png|Histopathology of antral mucosa with atrophy. H&E 10x. Antral gastric mucosa with accentuated atrophy because of replacement by extensive intestinal metaplasia.
File:Histopathology of fundic mucosa with atrophy.png|Histopathology of fundic mucosa with atrophy. H&E 10x; square 20x. Fundic-corporal gastric mucosa with extensive loss of gastric glands, partially replaced by pseudo-pyloric metaplasia.
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Classification
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, but no universally accepted classification exists as of 2017.
See also
- Chronic gastritis