• Clinical science

Atrophic gastritis

Abstract

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]

Classification

The Sydney system for the classification of chronic gastritis is the more general and comprehensive classification and takes into account localization, endoscopic imaging, etiology, inflammatory activity, and histological grading. The ABC classification is part of the Sydney system.

  • Localization
    • Pangastritis
    • Corpus gastritis
    • Antral gastritis
  • Endoscopy
  • Etiology
    • Autoimmune gastritis (type A)
      • Autoimmune gastritis is a rare condition overall
      • In the US, people of Northern European descent and African Americans show a higher incidence compared to people of Asian or Hispanic origin.
    • Bacterial gastritis (type B)
      • Although bacterial infections (specifically H. pylori) represent the vast majority of cases, viruses, parasites and fungi may cause type B gastritis as well.
      • In the US, approx. 30–35% of adults are infected with H. pylori (incidence declining) compared to approx. 50% globally.
    • Chemical gastritis (type C)
      • Type C gastritis is less frequently distinguished than types A and B and usually refers to chronic gastritis caused by chemical agents.
      • Typical exogenous substances include drugs (particularly NSAIDs) and alcohol, bile reflux is an important endogenous factor.
    • Special varieties
  • Histopathological level of inflammation: acute, chronic, or chronic active
  • Grading

Pathophysiology

AMAG

EMAG

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
  • Number and localization of necessary biopsy samples depend on the issue
    • For detection of H. pylori: 2× antrum, 2× corpus; if the urease test is applied: 1× antrum and corpus each
    • In case of vitamin B12 deficiency and suspected type A gastritis: 2× dome of fundus, 2× corpus
    • In case of unspecific complaints in the epigastric region, visually inconspicuous endoscopy results and protracted course: diagnosis by exclusion via biopsy samples from distal duodenum (2×), antrum (2×), corpus (2×) and fundus (2×)

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 : culture of H. pylori requires a special nutrient broth and takes about 14 days. It may be conducted to test resistances (in exceptional cases!)
    • Detection of H. pylori DNA by PCR: very sensitive and specific, but almost never used in daily clinical practice
    • Interfering factors in H. pylori diagnostics (especially in the rapid urease test)
      • Preexisting medication with PPIs: PPIs should preferably be discontinued two weeks prior to the test.
      • Upper gastrointestinal bleeding: Verification methods are prone to interference if biopsies are taken in the context of bleeding or in the immediate vicinity of ulcerations
      • Pre- and peripyloric biopsies: especially prone to interference in the case of bile reflux
      • Preceding partial gastrectomy
      • Gastric cancer and MALToma
      • Mucosal atrophy and intestinal metaplasia revealed by histology
  • Non-invasive methods
    • H. pylori antigen detection in stool specimens
      • On the basis of ELISA testing, involving monoclonal antibodies
      • Suitable option as initial test (cost-effective)
    • 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)
  • Diagnostic confidence:
    • Diagnosis is generally confirmed if two tests are positive.
    • Exceptions:
      • Duodenal ulcer: one positive result is sufficient
      • Chronic active gastritis: if H. pylori is detected and signs of chronic active gastritis are observed simultaneously (infiltration of neutrophil granulocytes is characteristic), diagnosis is considered confirmed without further positive results.
      • Positive culture: Detection by culture is sufficient for diagnosis in itself.

Additional tests

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

Pathology

Microscopy findings

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

  • Chronic inflammation (→ granulocytic infiltrations in the mucosa, lymphocytic infiltrations in the submucosa)
  • Mucosal thinning
  • Loss of glands
  • Epithelial metaplasia
    • (Pseudo‑)pyloric: replacement of parietal and chief cells in oxyntic glands by mucus-secreting cells that are usually present in the pyloric region
    • Intestinal: replacement of epithelial cells in the oxyntic or antral mucosa by intestinal epithelium cells (e.g., goblet cells)
  • Possibly detection of H. pylori (gram-negative, rod-shaped bacteria)
  • G-cell hyperplasia (common in AMAG)

Patterns of affliction

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.