• Clinical science

Atrophic gastritis

Summary

Atrophic gastritis is a condition characterized by chronic inflammation of the gastric mucosa with atrophy, gland loss, and metaplastic changes. It is classified into autoimmune metaplastic atrophic gastritis (AMAG) and environmental metaplastic atrophic gastritis (EMAG). Chronic infection with Helicobacter pylori (H. pylori) is the most common cause. Patients suffering from atrophic gastritis often do not display any symptoms or may only experience nonspecific discomfort in the epigastric region. Important diagnostic steps include gastroscopy with biopsy and laboratory studies (e.g., gastrin). Therapeutic emphasis depends on the underlying etiology: substitution of vitamin B12 (AMAG) or H. pylori eradication therapy (helicobacter-associated atrophic gastritis). If left untreated, atrophic gastritis may lead to peptic ulcer disease or result in the development of various cancers.

Epidemiology

Prevalence in the general population:

References:[1][2][3]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

  • AMAG
    • Associated with major histocompatibility haplotypes HLA-B8 and HLA-DR3
    • Associated with other autoimmune diseases (e.g., autoimmune thyroiditis)
  • EMAG
    • Helicobacter pylori infection (most important risk factor of atrophic gastritis overall)
    • Dietary factors (e.g., N-nitroso compounds , alcohol intake, high salt intake)

References:[1][3]

Pathophysiology

AMAG

EMAG

  • Helicobacter-associated: colonization by H. pylori → decreased production of mucins → increased production of gastric acids → inflammation primarily of the antrum→ ascending propagation; → shift of the corpus-antrum border → in case of chronification: atrophy of the gastric glands hypochlorhydria (not achlorhydria) and epithelial metaplasiaincreased risk of gastric cancers
  • Diet: bacteria in the stomach metabolize nitrates present in food → formation of N-nitroso compounds (carcinogenic) → epithelial metaplasia → increased risk of gastric cancers

References:[1][3]

Clinical features

References:[1][3][4]

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

  • Collection of biopsies
  • Applied methods: As a rule, there should always be a combination of two methods.
    • Histology (gold standard) including staining and direct microscopic identification
    • Rapid urease test: detection of ammonia production by the urease of H. pylori
    • Culture and resistogram
  • Non-invasive methods
    • H. pylori antigen detection in stool specimens
    • Positive 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

References:[1][3][5][6]

Differential diagnoses

References:[7][8]

The differential diagnoses listed here are not exhaustive.

Treatment

General

AMAG

Helicobacter-associated atrophic gastritis

Helicobacter pylori eradication therapy with proton pump inhibitors (PPIs) at twice the standard dose + 2 antibiotics (+ possibly bismuth) for a minimum of 7 (possibly 10) days , thereafter continue one PPI at standard dose

References:[4][9][6]

Complications

AMAG

EMAG

Helicobacter-associated atrophic gastritis frequently presents with ulcerations. Atrophic gastritis of autoimmune origin does not!
References:[1][3][10][11]

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