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Atrophic gastritis

Last updated: November 13, 2020

Summary

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.

Epidemiology

Epidemiological data refers to the US, unless otherwise specified.

Etiology

Autoimmune metaplastic atrophic gastritis (AMAG)

Environmental metaplastic atrophic gastritis (EMAG)

Pathophysiology

AMAG

EMAG

.

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.

Diagnostics

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]

Modalities

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

  • Invasive methods
  • 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

Pathology

Microscopy findings

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

Patterns of affliction

Differential diagnoses

Chemical gastritis [9]

Granulomatous gastritis [9][10]

Lymphocytic gastritis [9][11][12]

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.

Treatment

General

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

AMAG

  • 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

Follow-up

  • Confirm eradication after each therapy regimen [8][15]
    • 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]

Complications

AMAG

EMAG

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

References

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  4. Lymphocytic gastritis. http://www.pathologyoutlines.com/topic/stomachlymphocyticgastritis.html. Updated: December 11, 2019. Accessed: March 19, 2020.
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  8. 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): p.409-16. doi: 10.1007/BF01307736 . | Open in Read by QxMD
  9. 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): p.1515-9.
  10. 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): p.1992-4. doi: 10.1128/IAI.58.6.1992-1994.1990 . | Open in Read by QxMD
  11. Chey WD, Leontiadis GI, Howden CW, Moss SF. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol. 2017; 112 : p.212-238. doi: 10.1038/ajg.2016.563 . | Open in Read by QxMD
  12. 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): p.988-1013. doi: 10.1038/ajg.2017.154 . | Open in Read by QxMD
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  14. 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): p.1673-1679. doi: 10.1182/blood-2005-09-3534 . | Open in Read by QxMD
  15. Wong F, Rayner-hartley E, Byrne MF. Extraintestinal manifestations of Helicobacter pylori: a concise review. World J Gastroenterol. 2014; 20 (34): p.11950-11961. doi: 10.3748/wjg.v20.i34.11950 . | Open in Read by QxMD
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