Gastritis

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Basics

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

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Basics

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

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