Gastritis

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Basics

Description

  • Inflammation of the gastric mucosa
  • Can be classified by time course (acute vs. chronic)
    • Acute: neutrophilic infiltration on histology
    • Chronic: mixture of mononuclear cells, lymphocytes, macrophages on histology
  • Multiple types of gastritis have been described. There is no universally accepted classification for gastritis.
  • Subtypes of gastritis include the following:
    • Erosive gastritis or reactive gastropathy
      • Mucosal injury by a noxious agent (especially NSAIDs or alcohol) or vascular congestion and/or mucosal ischemia
      • Damage to the surface epithelium caused by mucosal hypoxia or the direct action of NSAIDs with no associated inflammation
    • Reflux gastritis
      • A reaction to protracted reflux exposure to biliary and pancreatic fluid
      • Typically limited to the prepyloric antrum
    • Hemorrhagic gastritis (stress ulceration)
      • A reaction to hemodynamic disorder (e.g., hypovolemia or hypoxia [shock])
      • ICU patients, particularly after severe burns and trauma
      • Certain medications (e.g., dabigatran)
    • Infectious gastritis
      • Acute and/or chronic Helicobacter pylori infection (most common cause of gastritis)
      • Viral infection (reaction to systemic infection)
      • Phlegmonous gastritis
    • Atrophic gastritis
      • Autoimmune versus environmental
      • Frequent in the elderly
      • Primarily from long-standing H. pylori infections
      • Prolonged proton pump inhibitor (PPI) use
      • Major risk factor for gastric cancer
      • Associated with primary (pernicious) anemia

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 U.S.

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 (1)[A].
    • Rates of infection are higher in minority groups and immigrants.
    • Prevalence also 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 (particularly, 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 erosive gastritis
  • Emotional stress due to cortisol production
  • Crohn-related gastritis, causing focally enhanced gastritis with histiocytes, lymphocytes, and granulomatous inflammation
  • Hemodynamic instability (hypoxemia)

Genetics
Although some genome-wide studies reveal that genetic variations in toll-like receptor 1 (TLR1) are well correlated with severity of inflammation in H. pylori–infected gastric mucosa, other studies demonstrated no significant association between TLR1 genotypes and H. pylori gastric disease. Further research is warranted to determine the role of TLR1, and other polymorphisms play in H. pylori susceptibility and gastric pathogenesis.

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
  • Stress (hypovolemia or hypoxia)
  • Tobacco use
  • Radiation, ischemia, pernicious anemia, gastric mucosal atrophy

General Prevention

  • Avoid injurious drugs or chemical agents including but not limited to 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 or from endemic regions.

Commonly Associated Conditions

  • Gastric or duodenal peptic ulcer
  • Primary (pernicious) anemia—atrophic gastritis
  • Portal hypertension (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 vs. chronic)
    • Acute: neutrophilic infiltration on histology
    • Chronic: mixture of mononuclear cells, lymphocytes, macrophages on histology
  • Multiple types of gastritis have been described. There is no universally accepted classification for gastritis.
  • Subtypes of gastritis include the following:
    • Erosive gastritis or reactive gastropathy
      • Mucosal injury by a noxious agent (especially NSAIDs or alcohol) or vascular congestion and/or mucosal ischemia
      • Damage to the surface epithelium caused by mucosal hypoxia or the direct action of NSAIDs with no associated inflammation
    • Reflux gastritis
      • A reaction to protracted reflux exposure to biliary and pancreatic fluid
      • Typically limited to the prepyloric antrum
    • Hemorrhagic gastritis (stress ulceration)
      • A reaction to hemodynamic disorder (e.g., hypovolemia or hypoxia [shock])
      • ICU patients, particularly after severe burns and trauma
      • Certain medications (e.g., dabigatran)
    • Infectious gastritis
      • Acute and/or chronic Helicobacter pylori infection (most common cause of gastritis)
      • Viral infection (reaction to systemic infection)
      • Phlegmonous gastritis
    • Atrophic gastritis
      • Autoimmune versus environmental
      • Frequent in the elderly
      • Primarily from long-standing H. pylori infections
      • Prolonged proton pump inhibitor (PPI) use
      • Major risk factor for gastric cancer
      • Associated with primary (pernicious) anemia

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 U.S.

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 (1)[A].
    • Rates of infection are higher in minority groups and immigrants.
    • Prevalence also 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 (particularly, 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 erosive gastritis
  • Emotional stress due to cortisol production
  • Crohn-related gastritis, causing focally enhanced gastritis with histiocytes, lymphocytes, and granulomatous inflammation
  • Hemodynamic instability (hypoxemia)

Genetics
Although some genome-wide studies reveal that genetic variations in toll-like receptor 1 (TLR1) are well correlated with severity of inflammation in H. pylori–infected gastric mucosa, other studies demonstrated no significant association between TLR1 genotypes and H. pylori gastric disease. Further research is warranted to determine the role of TLR1, and other polymorphisms play in H. pylori susceptibility and gastric pathogenesis.

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
  • Stress (hypovolemia or hypoxia)
  • Tobacco use
  • Radiation, ischemia, pernicious anemia, gastric mucosal atrophy

General Prevention

  • Avoid injurious drugs or chemical agents including but not limited to 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 or from endemic regions.

Commonly Associated Conditions

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

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