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  • Clinician

Atrophic gastritis


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.


Epidemiological data refers to the US, unless otherwise specified.


Autoimmune metaplastic atrophic gastritis (AMAG)

  • Associated with major histocompatibility haplotypes HLA-B8 and HLA-DR3
  • Associated with other autoimmune diseases (e.g., autoimmune thyroiditis)

Environmental metaplastic atrophic gastritis (EMAG)

  • Helicobacter pylori infection
  • Dietary factors
    • N-nitroso compounds
    • Alcohol intake
    • High salt intake





Clinical features

General symptoms

Specific symptoms in AMAG

Specific symptoms in EMAG

Helicobacter-associated atrophic gastritis frequently manifests with ulcerations. Atrophic gastritis of autoimmune origin does not.


Esophagogastroduodenoscopy and biopsy

  • 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

Indications [6]

PPIs should be discontinued at least 2 weeks prior to testing for H. pylori to minimize false-negative rates. [8]


As a rule, at least two methods should be employed. The diagnosis is generally confirmed if two tests are positive.

  • Invasive methods
    • 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
  • Non-invasive methods
    • 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)

Additional tests


Microscopy findings

The following microscopic findings may be seen in both types of atrophic gastritis.

Patterns of affliction

  • AMAG: Lesions are confined to the gastric body and fundus.
  • EMAG: Lesions first manifest in the gastric antrum (predominant), then spread to body and fundus.

Differential diagnoses

Chemical gastritis [9]

  • Definition: a chemical injury of the gastric mucosa that may be caused by several drugs or other substances
  • Common etiologies: NSAIDs, aspirin , alcohol, caffeine, corrosive substances , certain supplements , bile reflux
  • Pathophysiology: direct mucosal injury → edema hyperemia erosion ulceration
  • Clinical features
  • Therapy
  • Complications: gastric ulcers bleeding, perforation

Granulomatous gastritis [9][10]

Lymphocytic gastritis [9][11][12]

  • Definition: a lymphocytic infiltration (predominantly CD8) of the gastric mucosa, unspecific to any particular disease, likely explained by autoimmune or allergic inflammation.
  • Clinical features: Symptoms are unspecific, ranging from dyspepsia to GI bleeding.
  • Diagnostics: infiltration of lymphocytes in biopsies of the gastric mucosa [12]
  • Treatment: varies according to suspected underlying etiology
  • Subtype: varioliform gastritis [11][9]
    • Description: a severe form of lymphocytic gastritis with thickened folds noted on endoscopy, capped by small nodules with a central depression or erosion
    • Clinical features: anorexia, rapid weight loss, and features of a protein-losing gastropathy (e.g., hypoproteinemia, hypoalbuminemia, edema).

Eosinophilic gastritis [9][13]

Ménétrier disease [11]

  • Definition: gastritis featuring massive enlargement of the mucosal folds
  • Pathophysiology
  • Clinical features
  • Diagnostics
  • Complications
    • Peripheral edema
    • Malignant degeneration
  • Management
    • All patients should follow a high-protein diet
    • Pharmacological therapy is not well established
    • Consider surgical therapy (total gastrectomy) for severe cases with persistent protein loss
    • If H. pylori is detected, eradication

A horse with a WAVEEy MANE: Weight loss, Anorexia, Vomiting, Edema, and Epigastric pain are the most important clinical features of MÉNétriere disease.

The differential diagnoses listed here are not exhaustive.



Sucralfate should not be given simultaneously with PPIs and/or H2 antagonists because it is activated by an acidic environment.


  • 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.

Helicobacter-associated atrophic gastritis

Helicobacter pylori eradication therapy

Consider treatment in any patient testing positive for H. pylori infection.

First-line treatment options [6][14]

PPIs twice daily PLUS 2 antibiotics with/without bismuth for 10–14 days [6]

“Three days of C(AM)Ping:” the triple therapy consists of Clarithromycin, Amoxicillin OR Metronidazole, and PPI.

Second-line management for treatment failure


  • Confirm eradication after each therapy regimen [15][8]
    • Urea breath test, stool antigen test, or biopsy 4–6 weeks after completion of therapy.
    • Serology is not preferred to confirm eradication, as it remains positive for weeks/months after eradication.
  • Antisecretory therapy can be discontinued once eradication is confirmed. [15]




We list the most important complications. The selection is not exhaustive.

  • 1. Coati I, Fassan M, Farinati F, Graham DY, Genta RM, Rugge M. Autoimmune gastritis: Pathologist's viewpoint. World J Gastroenterol. 2015; 21(42): pp. 12179–12189. doi: 10.3748/wjg.v21.i42.12179.
  • 2. Hilzenrat N, Lamoureux E, Weintrub I, Alpert E, Lichter M, Alpert L. Helicobacter heilmannii-like spiral bacteria in gastric mucosal biopsies. Prevalence and clinical significance. Arch Pathol Lab Med. 1995; 119(12): pp. 1149–53. pmid: 7503664.
  • 3. Kaneko H, Nakada K, Mitsuma T, et al. Helicobacter pylori infection induces a decrease in immunoreactive-somatostatin concentrations of human stomach. Dig Dis Sci. 1992; 37(3): pp. 409–16. doi: 10.1007/BF01307736.
  • 4. Sumii M, Sumii K, Tari A, et al. Expression of antral gastrin and somatostatin mRNA in Helicobacter pylori-infected subjects. Am J Gastroenterol. 1994; 89(9): pp. 1515–9. pmid: 7915874.
  • 5. Smoot DT, Mobley HL, Chippendale GR, Lewison JF, Resau JH. Helicobacter pylori urease activity is toxic to human gastric epithelial cells. Infect Immun. 1990; 58(6): pp. 1992–4. doi: 10.1128/IAI.58.6.1992-1994.1990.
  • 6. Chey WD, Leontiadis GI, Howden CW, Moss SF. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol. 2017; 112: pp. 212–238. doi: 10.1038/ajg.2016.563.
  • 7. Moayyedi PM, Lacy BE, Andrews CN, Enns RA, Howden CW, Vakil N. ACG and CAG Clinical Guideline: Management of Dyspepsia. Am J Gastroenterol. 2017; 112(7): pp. 988–1013. doi: 10.1038/ajg.2017.154.
  • 8. Fashner J, Gitu AC. Diagnosis and Treatment of Peptic Ulcer Disease and H. pylori Infection. Am Fam Physician. 2015; 91(4): pp. 236–242. pmid: 25955624.
  • 9. Odze RD, Goldblum JR. Surgical Pathology of the GI Tract, Liver, Biliary Tract, and Pancreas. Elsevier Health Sciences; 2009.
  • 10. Hauser SC, Pardi DS, Poterucha JJ. Mayo Clinic Gastroenterology and Hepatology Board Review. CRC Press; 2005.
  • 11. Longo D, Fauci A, Kasper D, Hauser S, Jameson J, Loscalzo J. Harrisons's Principles of Internal Medicine, 18th Edition, 2011. McGraw-Hill Medical; 2011.
  • 12. Morrow, Gonzales. Lymphocytic gastritis. http://www.pathologyoutlines.com/topic/stomachlymphocyticgastritis.html. Updated December 11, 2019. Accessed March 19, 2020.
  • 13. Prussin C. Eosinophilic Gastroenteritis and Related Eosinophilic Disorders. Gastroenterol Clin North Am. 2014; 43(2): pp. 317–327. doi: 10.1016/j.gtc.2014.02.013.
  • 14. Malfertheiner P, Megraud F, O’Morain CA, et al. Management of Helicobacter pylori infection—the Maastricht V/Florence Consensus Report. Gut. 2016; 66(1): pp. 6–30. doi: 10.1136/gutjnl-2016-312288.
  • 15. Ables AZ, Simon I, Melton ER. Update on Helicobacter pylori treatment. Am Fam Physician. 2007; 75(3): pp. 351–8. pmid: 17304866.
  • 16. Wong F, Rayner-hartley E, Byrne MF. Extraintestinal manifestations of Helicobacter pylori: a concise review. World J Gastroenterol. 2014; 20(34): pp. 11950–11961. doi: 10.3748/wjg.v20.i34.11950.
  • Hershko C, Ronson A, Souroujon M, Maschler I, Heyd J, Patz J. Variable hematologic presentation of autoimmune gastritis: age-related progression from iron deficiency to cobalamin depletion. Blood. 2006; 107(4): pp. 1673–1679. doi: 10.1182/blood-2005-09-3534.
  • Herold G. Internal Medicine. Cologne, Germany: Herold G; 2014.
last updated 11/13/2020
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