- 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); 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 (long-standing H. pylori infections)
- Major risk factor for gastric cancer
- Granulomatous disease: sarcoidosis or Crohn disease
- Erosive gastritis
Persons aged >60 years often harbor H. pylori infection.
Gastritis rarely occurs in infants or children. Most common etiology for pediatric gastritis is H. pylori infection.
- Predominant age: all adult ages, prevalence increases with age (more common in elderly)
- Predominant sex: male = female; autoimmune gastritis is female > male
1.8 to 2.1 million annual visits in the United States
- Roughly 50% of people aged >60 years are infected with H. pylori versus 20% of people aged <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, immigrants, and 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), 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)
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.
- Age >60 years
- Exposure to potentially noxious drugs or chemicals (e.g., alcohol or NSAIDs, tobacco use)
- 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
- 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 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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