What is the treatment for chronic active gastritis?

Treatment of Chronic Active Gastritis

The primary treatment for chronic active gastritis is testing for and eradicating Helicobacter pylori infection when present, as this addresses the underlying cause in the vast majority of cases. 1

Immediate Management Algorithm

Step 1: Test for H. pylori Infection

• All individuals with chronic active gastritis must be assessed for H. pylori infection 1
• Use non-invasive testing (urea breath test or stool antigen test) or invasive methods (endoscopic biopsy with histology or rapid urease test) 1
• Avoid proton pump inhibitors, antibiotics, or bismuth products for 2 weeks prior to testing to prevent false negatives 1

Step 2: Eradicate H. pylori if Positive

• Administer H. pylori eradication therapy immediately when infection is confirmed 1
• Current effective regimens include:
  • Sequential therapy (5 days of PPI + amoxicillin, followed by 5 days of PPI + clarithromycin + metronidazole) 2
  • Concomitant therapy (PPI + amoxicillin + clarithromycin + metronidazole for 10-14 days) 2
  • Simpler regimens with omeprazole plus amoxicillin or clarithromycin may be better tolerated 3
• Confirm successful eradication using non-serological testing modalities (urea breath test or stool antigen test, NOT serology) at least 4 weeks after completing therapy 1

Step 3: Obtain Histopathological Confirmation

• The diagnosis of chronic active gastritis and any associated atrophic changes must be confirmed by histopathology 1
• Obtain topographical biopsies from both the gastric body and antrum/incisura in separately labeled jars 1
• This allows proper assessment of the extent and severity of gastritis and identifies atrophic gastritis, which has cancer risk implications 1, 4

Additional Management Based on Etiology

If Autoimmune Gastritis is Suspected

• Check antiparietal cell antibodies (PCA) and anti-intrinsic factor antibodies (IFA) when histology shows corpus-predominant atrophic gastritis 1
• Evaluate for vitamin B12 and iron deficiencies regardless of anemia status 1, 4
• Screen for autoimmune thyroid disease and maintain low threshold for evaluating other autoimmune conditions 1

Micronutrient Replacement

• Assess and replace iron and vitamin B12 deficiencies in all patients with atrophic gastritis, especially if corpus-predominant 1, 4
• This is critical even in the absence of anemia 1

Surveillance Strategy

For Advanced Atrophic Gastritis

• Perform surveillance endoscopy every 3 years in patients with advanced atrophic gastritis (defined by anatomic extent and histologic grade) 1, 4
• This reduces gastric cancer risk through early detection 1

For Autoimmune Gastritis

• Surveillance interval should be based on individualized risk assessment 1
• Screen for type 1 gastric neuroendocrine tumors with upper endoscopy 1
• Remove small neuroendocrine tumors endoscopically, followed by surveillance every 1-2 years depending on tumor burden 1

For Newly Diagnosed Pernicious Anemia

• Perform upper endoscopy with topographical biopsies to confirm corpus-predominant atrophic gastritis, stratify risk, and rule out prevalent gastric neoplasia including neuroendocrine tumors 1

Critical Evidence on Cancer Prevention

Eradicating H. pylori before the development of atrophic gastritis and intestinal metaplasia is most effective for reducing gastric cancer risk 1. Once atrophic changes develop, eradication halts progression but does not eliminate existing cancer risk 1. Gastric cancer is rare in the absence of chronic active gastritis, and the extent and severity of gastritis with atrophy is positively associated with cancer development 1.

Common Pitfalls to Avoid

• Do not rely on serology alone to confirm H. pylori eradication—it remains positive for years after successful treatment 1
• Do not assume false positive tests without confirmation—in patients with achlorhydria or atrophic gastritis, non-H. pylori urease-producing organisms can cause false positive urea breath tests; confirm with stool antigen or endoscopy before retreatment 1
• Do not overlook the distinction between reactive gastropathy and true gastritis—reactive gastropathy lacks significant inflammatory infiltration and requires removal of the offending agent rather than antimicrobial therapy 5
• Do not assume symptom resolution equals cure—chronic active gastritis requires objective confirmation of H. pylori eradication, not just symptomatic improvement 3