Description

• Inflammation of the gastric mucosa
• Can be classified by time course
  • Acute: neutrophilic infiltration on histology
  • Chronic: mixture of mononuclear cells, lymphocytes, macrophages on histology
• Subtypes of gastritis include:
  • 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
    • A reaction to protracted reflux exposure to biliary and pancreatic fluid
  • Hemorrhagic gastritis (stress ulceration)
    • A reaction to hemodynamic disorder (e.g., hypovolemia or hypoxia [shock]). Common in intensive care unit (ICU) patients, particularly after severe burns and trauma
  • Infectious gastritis
    • Acute and/or chronic: Helicobacter pylori infection (most common cause of gastritis)
    • Viral infection (reaction to systemic infection) caused by cytomegalovirus or Epstein-Barr virus
    • Phlegmonous gastritis: a rapidly progressive and frequently fatal bacterial infection of the gastric wall
  • Atrophic gastritis
    • Metaplastic atrophic gastritis: autoimmune primary (pernicious) anemia
    • Frequent in elderly
    • Primarily from long-standing H. pylori infections
    • Prolonged proton pump inhibitor (PPI) use
    • Major risk factor for gastric cancer
  • Others
    • Granulomatous disease: sarcoidosis or Crohn disease

Geriatric Considerations
Persons age >60 years often harbor H. pylori infection.

Pediatric Considerations
Gastritis rarely occurs in infants or children; increases in prevalence with age. Most common etiology for pediatric gastritis is H. pylori infection.

Epidemiology

• Predominant age: all adult ages (more common in elderly)
• Predominant sex: male = female, although autoimmune gastritis is female > male

Incidence
1.8 to 2.1 million annual visits in the United States

Prevalence

• Gastritis is more prevalent in those born before 1950.
  • Roughly 50% of people >60 years are infected with H. pylori vs. 20% of people <40 years.
• In 2018, ~27% of U.S. adults were found to be infected with H. pylori.
  • Rates of infection are higher in minority groups and immigrants.
  • Prevalence higher in lower socioeconomic status

Etiology and Pathophysiology

• Noxious agents cause a breakdown in the gastric mucosal barrier, exposing underlying epithelial tissue to injury.
• Infection: H. pylori (most common cause), Staphylococcus aureus exotoxins, and viral infections (Epstein-Barr virus, human cytomegalovirus)
• Alcohol via cell DNA damage and subsequent pyroptosis
• Aspirin and other NSAIDs through inhibition of protective prostaglandin synthesis
• Bile reflux, pancreatic enzyme reflux
• Portal hypertensive gastropathy, causing erosion
• Emotional stress due to cortisol production
• Crohn-related gastritis, causing focally enhanced gastritis with 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
• Exposure to potentially noxious drugs or chemicals (e.g., alcohol or NSAIDs)
• Hypovolemia, hypoxia (shock), burns, head injury, complicated postoperative course
• Autoimmune diseases (thyroiditis and type 1 diabetes mellitus, Addison disease, vitiligo, erosive oral lichen planus)
• Family history of H. pylori and/or gastric cancer
• Tobacco use
• Radiation, chemotherapy, ischemia, 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 receptor antagonists, PPIs, prostaglandins, or sucralfate.
• Consider testing for H. pylori (and eradicating if present) in patients on long-term NSAID therapy, diagnosed with idiopathic thrombocytopenic purpura (ITP), or from endemic regions.

Commonly Associated Conditions

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