What are the levels of gastritis and their corresponding treatments?

Levels of Gastritis and Their Corresponding Treatments

Gastritis should be classified based on its etiology, anatomic distribution, and histological severity, with treatment tailored to the specific type and underlying cause. 1, 2

Classification of Gastritis

By Etiology:

• H. pylori-associated gastritis: The most common form, responsible for 71-95% of all gastric cancers 1, 3
• Autoimmune gastritis: Associated with parietal cell and intrinsic factor antibodies, leading to vitamin B12 deficiency and pernicious anemia 2, 4
• Chemical/reactive gastritis: Caused by bile reflux, NSAIDs, alcohol, or other chemical irritants 4

By Anatomic Distribution:

• Antral-predominant gastritis: Primarily affects the distal stomach (antrum), associated with increased acid production 3, 4
• Corpus-predominant gastritis: Affects the gastric body, associated with decreased acid production (hypochlorhydria) and substantially increased risk for gastric cancer 1, 3
• Pangastritis: Involves both antrum and corpus 2

By Histological Severity:

• Superficial gastritis: Inflammation limited to the lamina propria without atrophy 5
• Chronic active gastritis: Ongoing inflammation with neutrophilic activity 6
• Atrophic gastritis: Loss of appropriate glands with or without intestinal metaplasia 1, 7
• Advanced atrophic gastritis: Extensive atrophy with intestinal metaplasia, considered a premalignant condition 1, 2

Diagnostic Approach

• Endoscopy with biopsy: Gold standard for diagnosis, with samples taken from both antrum and corpus 1, 2
• H. pylori testing: Should be performed in all patients with gastritis using non-serological methods (urea breath test, stool antigen, or histology) 3, 2
• Autoimmune markers: Check anti-parietal cell and anti-intrinsic factor antibodies in suspected autoimmune gastritis 2

Treatment Algorithm by Gastritis Type

H. pylori-Associated Gastritis:

• First-line treatment: Bismuth quadruple therapy due to increasing clarithromycin resistance 2
• Alternative: Concomitant 4-drug therapy when bismuth is unavailable 2
• Post-treatment: Confirm eradication using non-serological testing 2
• Rationale: Eradication halts progression of gastritis and reduces gastric cancer risk 1, 3

Autoimmune Gastritis:

• Micronutrient replacement: Supplement vitamin B12 and iron as needed 1, 2
• Surveillance: Regular endoscopic monitoring for development of neuroendocrine tumors 2
• Screening: Evaluate for other autoimmune conditions, particularly thyroid disease 1

Chemical/Reactive Gastritis:

• Remove offending agent: Discontinue NSAIDs, alcohol, or other irritants 4
• Acid suppression: Proton pump inhibitors or H2 blockers to reduce symptoms 4
• Surgical intervention: Consider biliary diversion (Roux-Y-gastrojejunostomy) for severe bile reflux gastritis 4

Surveillance Based on Severity

• Mild to moderate gastritis without atrophy: No specific surveillance needed after appropriate treatment 2
• Advanced atrophic gastritis: Endoscopic surveillance every 3 years 1, 2
• Intestinal metaplasia: Regular surveillance as this is considered irreversible and increases cancer risk 1, 8

Important Clinical Considerations

• The risk of gastric cancer increases with the extent and severity of gastritis, especially with atrophy and intestinal metaplasia 1
• H. pylori eradication is most effective in reducing cancer risk when performed before the development of preneoplastic conditions 1, 2
• The intensity of H. pylori colonization correlates with the severity of gastritis and its complications 6
• Food-related symptoms may coexist with gastritis but are not diagnostic of gastritis on their own 9

Common Pitfalls to Avoid

• Failing to test for H. pylori in all patients with gastritis 3, 2
• Not confirming successful H. pylori eradication after treatment 2
• Overlooking micronutrient deficiencies, especially in corpus-predominant or autoimmune gastritis 1, 2
• Attributing non-specific dyspeptic symptoms to gastritis without histological confirmation 9, 4
• Neglecting surveillance in patients with advanced atrophic gastritis or intestinal metaplasia 1, 2