Gastritis

Gastritis is an inflammatory process of the gastric mucosa that can be caused by a variety of conditions, commonly H. pylori infection or the use of drugs such as NSAIDs. Patients typically present with dyspepsia and can often be managed with a test-and-treat strategy for H. pylori if there are no indications for an upper endoscopy. Depending on the results, patients receive eradication therapy or a trial of pharmacological acid suppression. Upper endoscopy and biopsy, which can identify histopathological signs of inflammation, are required for definitive diagnosis. Upper endoscopy is indicated in patients over 60 years of age and considered on a case-by-case basis when red flags for dyspepsia are present. Often, gastritis is diagnosed incidentally, when upper endoscopy is performed for other reasons. The underlying cause of gastritis may be obvious (e.g., direct injury from medication intake), but further testing may be required in order to identify the etiology and provide the optimal treatment.

• Gastritis: inflammation of the gastric mucosa, typically in response to H. pylori infection (H. pylori gastritis), direct injury (e.g., substance-induced gastritis), or as part of a systemic inflammatory disease ^[1]
• Gastropathy: injury to the gastric mucosa, usually involving a disruption in the protective mucous barrier. In contrast to gastritis, gastropathy is accompanied by little to no inflammation.

Helicobacter pylori infection is the most common cause of gastritis.

There are multiple classification systems for gastritis. There is significant overlap between different types, e.g., in the histopathological findings of acute and chronic gastritis. The most common types are described here. ^[1][2]

• Acute gastritis
  • Inflammation of the gastric mucosa, predominantly by a neutrophilic infiltrate
  • Often used to describe self-limiting symptoms of suspected gastritis
• Chronic gastritis
  • Inflammation of the gastric mucosa characterized by a predominantly mononuclear infiltrate and loss of the normal architecture of the tissue (e.g., loss of normal mucosal glands)
  • Often used to describe long-term or recurring symptoms of suspected gastritis
• Atrophic gastritis
  • Chronic inflammation of the gastric mucosa, which results in loss of the native glands
  • Inflammatory changes are replaced over time by fibrosis or metaplastic changes (see “Atrophic gastritis”)
• Nonatrophic gastritis
  • Chronic inflammation of the gastric mucosa without atrophic changes
  • The mucosa may recover with minimal sequelae or begin to atrophy.
• Erosive gastritis
  • Multiple superficial erosions that do not extend beyond the muscularis mucosae and may occasionally cause bleeding
  • Subtypes
    • Stress-induced gastritis: acute erosions and/or superficial hemorrhages of the stomach caused by critical conditions (e.g., sepsis, shock)
    • Reactive gastropathy: injury to the gastric mucosa caused by chronic exposure to irritant endogenous (e.g., bile reflux) or exogenous substances (e.g., alcohol, NSAIDs, aspirin)
  • May progress to an ulcer ^[3]

• Typical symptoms ^[4]
  • Dyspepsia
  • Postprandial fullness, early satiety
  • Bloating
• Typical signs: Epigastric tenderness without peritoneal signs
• Atypical symptoms: concerning for underlying GI malignancy (see “Approach to dyspepsia” for more details)
  • Unintentional weight loss
  • Progressive dysphagia
  • Other red flag features of gastritis

Acute hemorrhagic erosive gastropathy ^[1][5]

• Definition: injury of the gastric mucosa caused by acute exposure to drugs or other exogenous or endogenous substances.
• Etiology
  • NSAIDs, aspirin ,
  • Alcohol, caffeine, corrosive substances (e.g., accidental or intentional ingestion of acid or disinfectant)
  • Certain supplements (e.g., iron, potassium)
  • Ischemic injury (e.g., hypovolemia, sepsis, severe burns).
• Pathophysiology: direct mucosal injury → edema → hyperemia → erosion → ulceration
• Clinical features: Patients often present with typical symptoms of gastritis, nausea/vomiting, and occult or massive bleeding (e.g., hematemesis).
• Treatment
  • Discontinue causative drugs (e.g., NSAIDs).
  • Abstain from tobacco and alcohol.
  • Avoid other substances that may worsen symptoms (e.g., caffeine, iron supplements).
  • Proton pump inhibitor (PPI) therapy (see ”Antacids and acid suppression medications”)

Reactive gastropathy ^[6]

• Definition: injury of the gastric mucosa caused by chronic exposure to drugs or other exogenous or endogenous substances.
• Etiology
  • Chronic NSAID use
  • Chronic high alcohol use
  • Bile reflux
• Clinical features: Patients may be asymptomatic or present with abdominal pain, nausea/vomiting, and weight loss.
• Treatment
  • Discontinue causative agents (e.g., NSAIDs)
  • Surgery (e.g., Roux-en-Y revision) for bile acid reflux gastropathy
• Complications: obstruction, bleeding, or perforation of the stomach or duodenum

Ménétrier disease ^[7][8]

• Definition: gastritis featuring massive enlargement of the mucosal folds
• Pathophysiology
  • Foveolar hyperplasia leads to:
    • Increased mucus production → loss of protein
    • Atrophy of parietal cells → decreased gastric acid production
    • Hyperplasia of gastric rugae
• Clinical features
  • Dyspeptic symptoms (i.e., abdominal pain, nausea, vomiting, diarrhea, weight loss)
  • Protein-loss gastropathy → hypoalbuminemia and peripheral edema
• Diagnostics: based on endoscopic and histopathological findings
  • Endoscopic findings: prominent rugae in the gastric fundus
  • Histopathological findings: foveolar hyperplasia and parietal cell atrophy
  • When performed, imaging (e.g., CT scan; ) shows thick, convoluted rugae (resembling cerebral gyri).
• Management
  • Most patients
    • Supportive care: high-protein diet and possibly IV albumin infusions
    • Test-and-treat strategy for H. pylori, if present
  • Severe cases with persistent protein loss
    • First line: cetuximab
    • Second line: total gastrectomy
• Complications
  • Peripheral edema
  • Malignant degeneration

Specific infiltrates

• Granulomatous gastritis: the presence of multiple granulomas in the gastric mucosa due to infectious or noninfectious causes ^[1][9]
  • Infectious granulomatous gastritis: e.g., tuberculosis , syphilis, Whipple disease, histoplasmosis, anisakiasis
  • Noninfectious granulomatous gastritis : e.g., Crohn disease , sarcoidosis, granulomatosis with polyangiitis, foreign body
• Eosinophilic gastritis: eosinophilic infiltration of the gastric mucosa with unknown etiology that is frequently associated with allergic diseases , blood eosinophilia, and ↑ IgE
  • Clinical and endoscopic features are nonspecific. The diagnosis is confirmed with histopathology.
  • Management
    • Antacids and acid suppression medications
    • Swallowed aerosolized steroids
      • An off-label treatment for eosinophilic GI disease in which aerosolized steroids originally intended for inhalation are swallowed.
      • These steroids can have a local antiinflammatory effect in the upper GI tract.
    • Elimination diet
      • A dietary regimen that may be part of the management of eosinophilic GI disease suspected to be caused by food allergies or intolerance
      • Consists of excluding certain protein groups (e.g., milk, soy, eggs, gluten, or nuts) from the diet until symptoms improve, followed by gradual reintroduction of the restricted proteins and monitoring for reappearing symptoms
• Lymphocytic gastritis: lymphocytic infiltration of the gastric mucosa, not specific to any particular disease, that is likely due to autoimmune or allergic inflammation

• See “Differential diagnoses of dyspepsia.”

The differential diagnoses listed here are not exhaustive.

Approach ^[4]

Although gastritis is diagnosed based on the results of gastric mucosal biopsy, not all patients require invasive diagnostic testing. For more detailed recommendations, see “Approach to dyspepsia.”

• Initial step: for most patients with upper GI symptoms, follow the test-and-treat strategy for H. pylori.
• Upper endoscopy and biopsies
  • Indicated in patients > 60 years old
  • Consider on a case-by-case basis if red flags for dyspepsia are present , or insufficient or no response to initial medical management
• Additional studies: indicated based on individual evaluation and clinical suspicion
  • Detecting complications: e.g., ↓ Hb and ↑ BUN/Cr ratio suggest GI bleeding
  • Evaluating differential diagnoses: e.g., liver chemistries, lipase, amylase to screen for hepatic or pancreatic disease
  • Identifying the underlying etiology: e.g., inflammatory markers or antibody testing if there is suspicion of systemic inflammatory disease or autoimmune disease

Esophagogastroduodenoscopy (EGD) with biopsies ^[1][4]

• Endoscopic findings
  • Common findings include:
    • Macroscopically normal mucosa
    • Mucosal hyperemia and edema
    • Erosion with or without bleeding
    • Atrophy (focal or multifocal), metaplasia
  • Other endoscopic findings may be present in some types of gastritis (e.g., significant enlargement of mucosal folds in hypertrophic gastritis).
• Histopathologic findings: dependent on etiology

Patients with upper GI symptoms are often treated empirically (see “Approach to dyspepsia”). If gastritis is confirmed by upper endoscopy, treatment should be tailored to the underlying etiology. ^[4]

• Pharmacological therapy
  • H. pylori eradication therapy
  • Antacids and acid suppression medications
• Nonpharmacological therapy ^[10][11][12]
  • Dietary and lifestyle modification
  • Trigger avoidance: e.g., NSAIDs, tobacco, caffeine, alcohol
• Specific treatment depending on etiology: see “Subtypes and variants.”