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 postburn/trauma
    • Infectious 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)
      • Phlegmonous gastritis: rapidly progressive and frequently fatal bacterial infection of the gastric wall
    • 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
    • Others—Granulomatous disease

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

EPIDEMIOLOGY

  • Prevalence increases with age (more common in elderly)

Incidence

~2 million annual visits in the United States

Prevalence

  • Roughly 50% of people aged >60 years are infected with H. pylori vs. 20% of people aged <40 years.
  • 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 to injury.
  • 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
  • Bile reflux, pancreatic enzyme reflux
  • Portal HTN gastropathy, causing erosion
  • Emotional stress due to cortisol production
  • Crohn disease–related gastritis; focally enhanced histiocytes, lymphocytes, and granulomatous inflammation
  • Hemodynamic instability (hypoxemia)

Genetics

There is difference in opinion regarding genome studies between the association of toll-like receptor 1 (TLR1) causing inflammation in H. pylori-infected gastric mucosa. Further research is warranted.

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)
  • Family history of H. pylori and/or gastric cancer
  • Radiation, chemotherapy, pernicious anemia, gastric mucosal atrophy

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, diagnosed with idiopathic thrombocytopenic purpura (ITP), or unexplained iron deficiency anemia.

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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