Gastritis

Descriptive text is not available for this image Basics

Description

  • Inflammation of the gastric mucosa
  • Classified as:
    • Acute: neutrophilic infiltration on histology
    • Chronic: mixture of mononuclear cells lymphocytes, macrophages on histology
  • Subtypes:
    • Erosive gastritis
      • Mucosal injury by a noxious agent (especially nonsteroidal anti-inflammatory drugs [NSAIDs] or alcohol)
      • Vascular congestion due to portal hypertension (HTN) or gastric antral vascular ectasia (GAVE)
    • Reflux gastritis—reaction to prolonged biliary/pancreatic fluid reflux
    • Hemorrhagic gastritis (stress ulceration)—a reaction to hemodynamic disorder (e.g., hypovolemia or hypoxia [shock]); common in intensive care unit (ICU) patients, especially post burn/trauma
    • Infectious/environmental gastritis
      • Helicobacter pylori infection (most common cause of gastritis); H. pylori has been linked with gastric cancer.
      • Viral systemic infection caused by cytomegalovirus (CMV) or Epstein-Barr virus (EBV)
    • Atrophic gastritis
      • Metaplastic atrophic gastritis: autoimmune primary (pernicious) anemia
      • Frequent in elderly and prolonged proton pump inhibitor (PPI) use (chronic H. pylori)
      • Major risk factor for gastric cancer

Geriatric Considerations
Persons aged >60 years often harbor H. pylori infection.Pediatric Considerations
Gastritis is rare in infants or children. Most common etiology for pediatric gastritis is H. pylori infection.

Epidemiology

  • Prevalence increases with age (more common in elderly).
  • Affects both sexes; autoimmune gastritis is more common in women.
  • H. pylori is common.

Incidence

~2 million annual visits in the United States

Prevalence

  • ~50% of people >60 years of age are infected with H. pylori versus 20% of people <40 years of age.
  • 1/4 to 1/3 of U.S. adults are infected with H. pylori. The prevalence increases with age.
  • Rates of infection are higher in minority groups, immigrants, and lower socioeconomic status.

Etiology and Pathophysiology

  • Noxious agents damage the gastric mucosal barrier, exposing underlying epithelial tissue.
  • Infection: H. pylori, Staphylococcus aureus exotoxins, and viral infections (EBV, CMV)
  • Alcohol via cell DNA damage and subsequent pyroptosis
  • Aspirin and other NSAIDs through inhibition of protective prostaglandin synthesis
  • Emotional stress due to cortisol production

Genetics

Potential role of toll-like receptor 1 (TLR1) in H. pylori-associated gastritis

Risk Factors

  • Age >60 years and exposure to noxious drugs/chemicals (e.g., alcohol, NSAIDs, tobacco)
  • Hypovolemia, hypoxia (shock), burns, head injury, complicated postoperative course
  • Autoimmune diseases (thyroiditis, type 1 diabetes mellitus, Addison disease, vitiligo, erosive oral lichen planus)

General Prevention

  • Avoid injurious drugs or chemical agents, alcohol, and tobacco.
  • Patients with hypovolemia or hypoxia (especially ICU patients) should receive prophylaxis with H2 antagonists, PPIs, prostaglandins, or sucralfate.
  • Consider testing for H. pylori in patients on long-term NSAID therapy, with idiopathic thrombocytopenic purpura (ITP), or unexplained iron deficiency anemia.
  • Test and treat H. pylori in individuals at increased risk of gastric cancer, those with atrophic gastritis or gastric intestinal metaplasia, and adult household contacts of H. pylori-positive patients (1).

Commonly Associated Conditions

  • Gastric or duodenal peptic ulcer
  • Primary (pernicious) anemia—atrophic gastritis
  • Portal HTN, hepatic failure
  • Mucosa-associated lymphoid tissue (MALT) lymphoma

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