Atrophic gastritis
| Atrophic gastritis | |
|---|---|
| Other names | Type A gastritis[1] |
 | |
| Atrophic gastritis | |
| Specialty | Gastroenterology |
Atrophic gastritis is a process of chronic
Type A gastritis primarily affects the fundus (body) of the stomach and is more common with
Signs and symptoms
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% 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]
Associated conditions
People with atrophic gastritis are also at increased risk for the development of gastric adenocarcinoma.[5]
Causes
Recent research has shown that autoimmune metaplastic atrophic gastritis (AMAG) is a result of the immune system attacking the parietal cells.[6]
Environmental metaplastic atrophic gastritis (EMAG) 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.[7]
Pathophysiology
.jpg)
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] 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 (and elevated gastrin levels). 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.[citation needed]
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.[8]
Diagnosis
Detection of APCA(Antiparietal cell antibody), anti-intrinsic factor antibody (AIFA) and Helicobacter pylori (HP) antibodies in conjunction with serum gastrin are effective for diagnostic purposes.[9]
-
Histopathology of antral mucosa with atrophy. H&E 10x. Antral gastric mucosa with accentuated atrophy because replacement by extensive intestinal metaplasia. -
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.
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,[10] but no universally accepted classification exists as of 2017.[9]
Treatment
Supplementation of
See also
- Chronic gastritis
References
- ^ PMID 3365072.
- PMID 12631657.
- ^ PMID 27671008.
- S2CID 58551484.
- PMID 18332421.
- ^ a b Nimish Vakil, MD, Clinical Adjunct Professor, University of Madison School of Medicine and Public Health. "Autoimmune Metaplastic Atrophic Gastritis: Gastritis and Peptic Ulcer Disease: Merck Manual Professional". MSD Manual Professional Version. Merck & Co.
- ^ "Atrophic Gastritis - Cleveland Clinic".
- PMID 33266504.
- ^ PMID 28223833.
- S2CID 70488969.
- S2CID 4240988.