Gastritis

Gastritis refers to inflammation of the gastric mucosa. Gastritis may occur suddenly (acute gastritis) or slowly over time (chronic gastritis). Gastritis may be asymptomatic or with symptoms, including burning abdominal pain (which either worsens or improves with eating), dyspepsia, nausea, and vomiting. The most common etiologies for gastritis are Helicobacter pylori infection and autoimmune disease. Chronic gastritis is a risk factor for gastric cancer. Management involves the use of proton pump inhibitors with antibiotics (in case of H. pylori infection), avoidance of offending agents, and replacement of associated deficiencies.

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Overview

Definition

Gastritis is the inflammation of gastric mucosa associated with mucosal injury.

Epidemiology

  • Prevalence of 6.3 per 100,000 population
  • Helicobacter pylori: prevalence in the pediatric population (primary determinant of H. pylori gastritis):
    • 10% in Western countries
    • 50% in developing countries
    • Transmitted by feco-oral route
  • Autoimmune gastritis:
    • Prevalence: 2%–5% in Western countries
    • More common in women and increases with age
    • Associated with other autoimmune diseases (e.g., thyroid disease, diabetes)

Etiology

Gastritis is usually due to an infection or an immune-mediated process.

  • Infectious: 
    • H. pylori (most common)
    • Mycobacterium avium intracellulare
    • Enterococcus
    • Herpes simplex
    • Cytomegalovirus
    • Parasites
  • Autoimmune (associated with anti-parietal and anti-intrinsic factor antibodies)
  • Rare causes:
    • Crohn’s disease
    • Sarcoidosis
    • Vasculitis
    • Collagenous gastritis
    • Eosinophilic gastritis
    • Ischemic gastritis

Pathophysiology

H. pylori–associated gastritis

  • Can be acute or chronic
  • H. pylori resides in the gastric mucus adjacent to epithelial cells and invades the lamina propria.
  • Acute (early stage):
    • Antral-predominant inflammation or gastritis
    • gastrin + ↓ somatostatin = ↑ acid production
    • Increased acid exacerbates mucosal injury and inflammation.
    • Due to antral location, duodenal ulcer is a complication.
  • Chronic (late stage):
    • Environmental metaplastic atrophic gastritis (EMAG)
    • Ongoing inflammation of gastric mucosa results in loss of G cells (gastrin-producing) and parietal cells (acid-producing).
    • This change allows proximal migration of H. pylori → spread from the antrum to the gastric body
    • Effects:
      • Atrophic glands → intestinal metaplasia of gastric mucosa (increased risk of gastric cancer)
      • Loss of acid production → hypochlorhydria → reduced iron absorption
      • Loss of parietal cells → ↓ intrinsic factor → B12 deficiency  
    • Cancer risk: 
      • Gastric adenocarcinoma
      • Mucosa-associated lymphoid tissue (MALT) lymphoma

Chronic H. pylori gastritis:
A: Normal mucosa of the corpus
B: Non-atrophic gastritis: mild mononuclear inflammation seen in upper layer of the mucosa (superficial gastritis as indicated by arrows). Gland layer is still intact.
C: Moderate atrophic gastritis: intense chronic mononuclear inflammation occurs in the lower layers, accompanied by atrophy of the oxyntic glands (indicating stomach with hypochlorhydria). Acid secretion is impaired due to loss of parietal cells (in the oxyntic glands).
D: Severe atrophic gastritis, showing mild inflammation but there is loss of oxyntic glands.

Image: “Corpus mucosa” by Patolab Oy, Espoo, Finland and Tartu State University, Tartu, Estonia. License: CC BY 4.0

Autoimmune metaplastic atrophic gastritis (AMAG)

  • Corpus-predominant inflammation or gastritis
  • Associated with chronic T cell–mediated autoimmune disease:
    • T cells destroy oxyntic mucosa.
    • Antibodies against parietal cells and intrinsic factor 
    • Effects:
      • Loss of oxyntic glands, replaced by atrophic mucosa → intestinal metaplasia
      • Pathologic changes lead to reduced acid production → hypochlorhydria/achlorhydria → ↑ gastrin (loss of negative feedback)
      • Reduced acid → reduced iron absorption
      • Loss of parietal cells and intrinsic factor due to antibodies: pernicious anemia (B12 deficiency)
  • Cancer risk: 
    • Gastric neuroendocrine/carcinoid tumors: Elevated gastrin also stimulates enterochromaffin cells.
    • Gastric adenocarcinoma

Gastropathy

  • Damage to the epithelial lining with no or minimal associated inflammation
  • Technically a separate entity from gastritis 
  • Associated with mucosal injury from destruction of the normal protective barrier (mucins, bicarbonate, and epithelium)
  • May cause similar presentation as gastritis
  • Bleeding can occur (acute hemorrhagic gastropathy).
  • Common causes:
    • Drugs
    • Alcohol
    • Bile reflux
    • Nonsteroidal anti-inflammatory drugs (NSAIDs)
    • Stress (shock, trauma, central nervous system (CNS) injury)

Acute erosive gastritis changes (endoscopic view) in a patient who has had prolonged COX-2 NSAID therapy

Image: “Acute erosive gastritis” by Department of Medical Sciences II, Medical Rehabilitation, University of Medicine and Pharmacy of Craiova, Romania. License: CC BY 2.0

Clinical Presentation and Diagnosis

Clinical presentation

  • H. pylori gastritis (acute and chronic):
    • Asymptomatic or mild dyspepsia in acute onset
    • Abdominal pain, dyspepsia in EMAG
    • Iron deficiency anemia 
    • B12 deficiency 
  • AMAG:
    • May be asymptomatic, but often with dyspepsia
    • B12 deficiency: fatigue, glossitis, cognitive decline, and other neurologic manifestations
    • Iron deficiency anemia: occurs earlier than B12 deficiency 
  • Others: hematemesis (hemorrhagic gastropathy)

Diagnostic studies

  • Laboratory studies:
    • AMAG:
      • ↑ gastrin level (fasting) in acute/early stages
      • ↓ pepsinogen I/pepsinogen II ratio
      • Complete blood count (CBC): anemia (↓ iron, ↓ B12 level)
      • Serology: antibodies to parietal cells and intrinsic factor
    • EMAG:
      • Gastrin not as elevated
      • Low serum pepsinogen I levels or ↓ pepsinogen I/pepsinogen II ratio
      • Pernicious anemia absent
      • No autoantibodies against parietal cells and intrinsic factor
  • Esophagogastroduodenoscopy:
    • May not have obvious pathologic changes
    • Findings, often nonspecific, may include:
      • Mucosal erythema/friable mucosa
      • Antral nodularity
      • Flattening of rugal folds (advanced atrophic gastritis)
      • Mucosal erosions, petechial hemorrhages (erosive gastropathy)
  • Biopsy:
    • Multiple biopsies recommended (corpus and antrum)
    • All abnormal-looking areas are biopsied.
    • Adjacent normal tissue also included
    • Acute H. pylori gastritis findings: 
      • Spiral bacilli on specimen
      • Mucosal neutrophils 
    • Chronic H. pylori gastritis findings: 
      • Lymphocytes, plasma cells, eosinophils
      • Lymphoid follicles 
    • Early AMAG findings: 
      • Deep inflammation, eosinophils
      • Destruction of oxyntic glands
      • Intestinal or pseudopyloric metaplasia
    • Advanced AMAG findings: 
      • Metaplastic glands replace the oxyntic glands.
      • Megaloblastic epithelial cells

Chronic gastritis. A: mucosal inflammation with many mononuclear cells (arrows); B: normal mucosa.

Image: “Corpus mucosa” by Informa Healthcare. License: CC BY 4.0

Specific tests for H. pylori

  • Non-invasive:
    • Stool antigen assay: 
      • For initial diagnosis
      • To confirm eradication
    • Urea breath test: 
      • Patient is given radioactively labeled urea orally.
      • Urease produced by H. pylori splits it and liberates CO2.
      • Radioactive CO2 is detected in the breath.
    • Serology:
      • Detection of serum immunoglobulin G (IgG) against H. pylori
      • Low accuracy
      • IgG remains positive after eradication.
  • Invasive (require sampling of gastric mucosa):
    • Biopsy urease test: 
      • Urease produced by H. pylori liberates ammonia from urea.
      • Alkaline pH changes color of a pH reagent.
    • Histology: 
      • Hematoxylin and eosin (H&E), immunohistochemical, Giemsa stains
      • Curved, flagellated gram-negative rods are seen.
    • Bacterial culture and sensitivity

Immunohistochemical stain for H. pylori in the gastric antrum

Image: “Immunohistochemical H. pylori” by Department of Gastroenterology, Bakirkoy Dr Sadi Konuk Training and Research Hospital, Istanbul, Turkey. License: CC BY 2.0

Management and Complications

Management

  • General principles: 
    • Proton pump inhibitors (PPIs)
    • B12 replacement therapy
    • Iron deficiency treatment
    • For symptomatic patients: Avoid any gastric-irritating/precipitating agents.
  • H. pyloriassociated gastritis:
    • Treatment aimed to eradicate H. pylori
    • A combination of  antibiotic regimen and PPIs:
      • Triple therapy: PPI + clarithromycin + amoxicillin or metronidazole
      • Bismuth containing quadruple therapy: PPI + bismuth + tetracycline + metronidazole

Complications

  • Intestinal-type gastric cancer:
    • Associated with AMAG and EMAG
    • Progression of mucosal atrophy to intestinal metaplasia
    • Metaplasia progresses to dysplasia and eventually to invasive adenocarcinoma.
  • MALToma (mucosa-associated lymphoid tumor):
    • B-cell lymphoma of the stomach
    • Clear association with H. pylori infection
    • Often will regress with H. pylori eradication

Differential Diagnosis

  • Ménétrier’s disease (MD): protein-losing gastropathy characterized by giant hyperplastic mucosal folds of stomach body and fundus. The disease presents with abdominal pain, nausea, and vomiting, but associated weight loss and diarrhea can help differentiate MD from gastritis. Further evaluation via EGD and biopsy can help confirm MD.
  • Peptic ulcer disease (PUD): full-thickness ulcer involving gastric or duodenal wall. Peptic ulcer disease presents with abdominal pain, nausea/vomiting, and, sometimes, upper gastrointestinal bleed. The disease is also associated with H. pylori. Diagnosis is made by endoscopy.
  • Cholelithiasis/cholecystitis: gallstones obstructing cystic duct (cholelithiasis) that can be associated with inflammation of the gallbladder (cholecystitis). Cholecystitis commonly presents with right upper quadrant and epigastric pain, nausea, and vomiting. Unlike gastritis, the condition is frequently associated with right upper quadrant or subcostal tenderness.
  • Viral gastroenteritis: acute self-limited illness associated with diffuse abdominal pain, vomiting, and diarrhea. Watery diarrhea can help differentiate this condition from acute gastritis.
  • Pancreatitis: inflammation of the pancreas; can be acute or chronic. Pancreatitis usually presents with epigastric pain radiating to the back, nausea, vomiting, and bloating. Bloodwork will show elevated amylase and lipase.

References

  1. Azer S.A., Akhondi H. (2020). Gastritis. https://www.ncbi.nlm.nih.gov/books/NBK544250/
  2. Jensen P.J, Feldman M. (2020). Acute and chronic gastritis due to Helicobacter pylori. Retrieved 25 November 2020, from https://www.uptodate.com/contents/acute-and-chronic-gastritis-due-to-helicobacter-pylori?search=gastritis&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
  3. Jensen P.J, Feldman M. (2020). Metaplastic (chronic) atrophic gastritis. Retrieved 25 November 2020, from https://www.uptodate.com/contents/metaplastic-chronic-atrophic-gastritis?search=gastritis&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2
  4. Jensen P.J, Feldman M. (2020). Gastritis: Etiology and diagnosis. Retrieved 25 November 2020, from https://www.uptodate.com/contents/gastritis-etiology-and-diagnosis?search=gastritis&source=search_result&selectedTitle=4~150&usage_type=default&display_rank=4

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