Atrophic gastritis is a condition characterized by chronic inflammation of the gastric mucosa with atrophy, gland loss, and metaplastic changes. There are two types: autoimmune metaplastic atrophic gastritis (AMAG) and environmental metaplastic atrophic gastritis (EMAG), which is commonly caused by Helicobacter pylori (H. pylori). Patients with atrophic gastritis are often asymptomatic or may only experience nonspecific discomfort in the epigastric region. Important diagnostic steps include gastroscopy with biopsy and laboratory studies (e.g., gastrin). The therapeutic approach depends on the underlying etiology. AMAG is treated with vitamin B12 substitution, whereas individuals with EMAG will receive H. pylori eradication therapy. If left untreated, atrophic gastritis may lead to peptic ulcer disease or result in the development of various cancers.
- Associated with major histocompatibility haplotypes HLA-B8 and HLA-DR3
- Associated with other autoimmune diseases (e.g., autoimmune thyroiditis)
- Autoimmune destruction of the parietal cells in the gastric corpus and fundus (T-cell induced autoantibodies against H+/K+ ATPase); → achlorhydria → increased release of gastrin (due to loss of negative feedback); → G cell hyperplasia → hypergastrinemia → hyperplasia of enterochromaffin-like cells → ↑ risk of carcinoid tumors.
- Achlorhydria impairs the intestinal absorption of inorganic iron → iron deficiency anemia (early manifestation)
- Autoantibodies against intrinsic factor → vitamin B12 deficiency → pernicious anemia
Colonization by H. pylori
- Inflammation of the antrum → destruction of D cells → ↓ somatostatin → ↑ gastrin → ↑ production of gastric acids → duodenal ulcers 
- Inflammation of the gastric body → local destruction of mucosa (via cytotoxins such as ammonia) → ↓ production of mucins and atrophy of the gastric glands → hypochlorhydria → hypergastrinemia and epithelial dysplasia → epithelial metaplasia → ↑ risk of gastric cancers 
- Diet: bacteria in the stomach metabolize nitrates present in food → formation of carcinogenic N-nitroso compounds → epithelial metaplasia → ↑ risk of gastric cancers
Specific symptoms in AMAG
- Symptoms of other autoimmune diseases (e.g., goiter in Hashimoto thyroiditis)
Specific symptoms in EMAG
- Asymptomatic progression is common.
- Patients often have recurring ulcers (abdominal pain, dyspepsia)
- Symptoms often occur as a result of gastric or duodenal ulcer bleeding (see “ ”).
- Esophagogastroduodenoscopy and biopsy
- : The should be used when indicated 
- Additional tests
- Chronic inflammation → granulocytic infiltrations in the mucosa, lymphocytic infiltrations in the submucosa
- Mucosal thinning
- Loss of glands
- Epithelial metaplasia
- Possible detection of H. pylori (gram-negative, rod-shaped bacteria)
- G-cell hyperplasia (common in AMAG)
Patterns of affliction
- Avoid intake of substances that may exacerbate ongoing inflammation (e.g., alcohol, NSAIDs).
- Symptomatic treatment with proton pump inhibitors (PPIs), antacids, sucralfate, or H2-receptor blockers
- Vitamin B12 replacement therapy (parenteral)
- If H. pylori is detected: attempt to eradicate (may lead to healing)
- Because there is a risk of malignant degeneration, regular endoscopic check-ups are required.
- Vitamin B12 deficiency; (leading to pernicious anemia, which potentially causes funicular myelosis)
- Gastric adenocarcinoma
- Gastric : particularly carcinoid tumors (commonly featuring polypoid precursors)
- Esophageal squamous cell carcinoma
- Ulcerations in the stomach/duodenum (peptic ulcer disease) → upper gastrointestinal bleeding or perforation
- Gastric adenocarcinoma
- Extraintestinal manifestations (e.g., chronic urticaria, Parkinson disease, migraine, immune thrombocytopenic purpura, iron deficiency anemia, rosacea) 
We list the most important complications. The selection is not exhaustive.