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.
- Prevalence 
Epidemiological data refers to the US, unless otherwise specified.
- 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 (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
- Hematemesis; (coffee-ground appearance or bright red), possibly melena
- Epigastric pain is possible.
- Nausea, vomiting
- Abdominal paresthesia and dyspepsia
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 “ ”).
- Diagnostic test of choice
- To evaluate the gastric mucosa and collect biopsy samples from the gastric antrum and corpus, possibly also from the fundus
Helicobacter pylori diagnostics
- Dyspepsia (method depends on patient characteristics)
- Peptic ulcer disease (active or positive history without prior eradication)
- Endoscopically resected early gastric cancer
As a rule, at least two methods should be employed. The diagnosis is generally confirmed if two tests are positive.
- Collection of biopsy samples
- Histology (gold standard) including staining and direct microscopic identification shows curved, flagellated gram-negative rods
- Rapid urease test: detection of ammonia production by the urease of H. pylori
- Culture and resistogram: culture of H. pylori requires a special nutrient broth
- Detection of H. pylori DNA by PCR: very sensitive and specific, but almost never used in daily clinical practice
H. pylori stool antigen test: detects the presence of H. pylori antigens in a stool sample
- Can be used for diagnosis of H. pylori infection and proof of eradication after treatment
- Suitable option as initial test (cost-effective)
- Urea breath test: detection of a labeled carbon isotope in breath samples
- Serum IgG antibodies against H. pylori: H. pylori antibodies may be detected even after eradication → test indicates (past) exposure, not necessarily current infection (lower specificity)
- H. pylori stool antigen test: detects the presence of H. pylori antigens in a stool sample
- 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
- Chemical gastritis
- Granulomatous gastritis
- Eosinophilic gastritis
- Lymphocytic gastritis
- Ménétrier disease
The differential diagnoses listed here are not exhaustive.
- 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.
- See “H. pylori eradication therapy” below.
Consider treatment in any patient testing positive for H. pylori infection.
First-line treatment options 
- Clarithromycin triple therapy: in areas of low (< 15%) clarithromycin resistance
- Clarithromycin-based concomitant therapy
Bismuth quadruple therapy: in areas of high (> 15%) clarithromycin resistance
- PPIs at standard dose twice daily (e.g., omeprazole ) 
- PLUS bismuth (e.g., bismuth subcitrate OR bismuth subsalicylate 
- PLUS tetracycline 
- PLUS metronidazole 
- Duration: 10–14 days
“Three days of C(AM)Ping:” the triple therapy consists of Clarithromycin, Amoxicillin OR Metronidazole, and PPI.
Second-line management for treatment failure
- Choose antibiotics other than what the patient received as first-line therapy.
- Bismuth quadruple therapy (see above): if clarithromycin triple therapy fails
- Levofloxacin-containing therapy: e.g., levofloxacin triple therapy
- Confirm eradication after each therapy regimen 
- Antisecretory therapy can be discontinued once eradication is confirmed. 
- 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.