What is the appropriate treatment for gastritis?

Treatment of Gastritis

All patients with gastritis must be tested for Helicobacter pylori infection using non-serological methods, and if positive, eradication therapy is mandatory as this addresses the dominant cause of gastritis and prevents progression to atrophic gastritis, peptic ulcer disease, and gastric cancer. 1

Initial Diagnostic Approach

Confirm Gastritis and Identify Etiology

• Obtain endoscopy with biopsies from both the gastric body and antrum/incisura, placing specimens in separate jars to distinguish between H. pylori-associated gastritis (typically antral-predominant) and autoimmune gastritis (corpus-predominant). 1, 2

• Test all patients for H. pylori using non-serological methods such as urea breath test, stool antigen test, or biopsy-based testing (rapid urease test, histology, or culture), as serology remains positive after eradication and cannot distinguish active from past infection. 1, 2

• Look for endoscopic features of atrophic gastritis including pale mucosa, prominent submucosal vessels, loss of gastric folds, and when intestinal metaplasia is present, light-blue crests and white opaque fields on narrow-band imaging. 2

Treatment Algorithm Based on Etiology

H. pylori-Positive Gastritis

Eradication therapy is the cornerstone of treatment and must be administered promptly. 1, 2

• Use bismuth quadruple therapy as first-line treatment due to increasing clarithromycin resistance globally (bismuth subsalicylate + metronidazole + tetracycline + proton pump inhibitor for 10-14 days). 2

• Concomitant 4-drug therapy (PPI + amoxicillin + clarithromycin + metronidazole) is an alternative when bismuth is unavailable, but only in regions where clarithromycin resistance is <15%. 1, 2

• Confirm successful eradication 4-6 weeks after completing therapy using a non-serological test (urea breath test or stool antigen), as treatment failure occurs in 15-30% of cases with current regimens. 1

• Eradication heals gastritis and prevents progression to atrophic gastritis, though it has less effect on reversing established intestinal metaplasia. 1, 2

Autoimmune Gastritis

When histology shows corpus-predominant atrophy with antral sparing, pursue the following:

• Check antiparietal cell antibodies and anti-intrinsic factor antibodies to confirm the autoimmune etiology. 1, 2, 3

• Screen for autoimmune thyroid disease, as up to one-third of patients with autoimmune gastritis have concomitant thyroid autoimmunity. 1, 3

• Evaluate for iron and vitamin B-12 deficiencies in all patients, as iron deficiency occurs in up to 50% of those with corpus-predominant atrophy and often presents before B-12 deficiency. 1, 2

• Recognize that pernicious anemia (vitamin B-12 deficiency with macrocytic anemia) is a late-stage manifestation requiring lifelong B-12 replacement. 1

• Even in autoimmune gastritis, test for H. pylori and eradicate if present, as co-infection occurs and accelerates atrophic changes. 1, 2

Surveillance and Cancer Prevention

For Atrophic Gastritis (Any Etiology)

• Perform surveillance endoscopy every 3 years in patients with advanced atrophic gastritis, defined by extensive anatomic distribution (involving both antrum and corpus) and high histologic grade. 1, 2

• The risk of gastric adenocarcinoma is elevated in atrophic gastritis, with the highest risk in the first year after diagnosis of pernicious anemia, warranting prompt endoscopic evaluation. 1, 2

For Autoimmune Gastritis Specifically

• Screen for type 1 gastric neuroendocrine tumors (NETs) with upper endoscopy, as these develop in 5-10% of patients with autoimmune gastritis due to chronic hypergastrinemia. 1, 2

• Remove small NETs (<1-2 cm) endoscopically and perform surveillance endoscopy every 1-2 years depending on NET burden. 1, 2

• For NETs >2 cm, with invasion beyond the submucosa, or with lymph node metastasis, refer for surgical resection. 2

Management of Micronutrient Deficiencies

• Replace iron when deficiency is documented, using oral or intravenous formulations depending on severity and tolerance. 2, 3

• Provide vitamin B-12 replacement (typically intramuscular or high-dose oral) when deficiency is confirmed, with lifelong therapy required in pernicious anemia. 1, 2

• Monitor complete blood count and micronutrient levels periodically, as deficiencies may develop or worsen over time with progressive atrophy. 1, 2

Common Pitfalls and Caveats

• Do not use serological H. pylori testing in patients with atrophic gastritis, as advanced atrophy reduces antibody titers (seroreversion) leading to false-negative results. 1, 2

• Atrophic gastritis is frequently underdiagnosed due to subtle endoscopic features and inconsistent histopathological reporting; ensure proper biopsy sampling with separate jars for body and antrum. 1, 2

• Long-term proton pump inhibitor use in H. pylori-positive patients accelerates progression to corpus-predominant atrophic gastritis; eradicate H. pylori before initiating chronic PPI therapy when possible. 1

• Do not diagnose autoimmune gastritis based solely on positive antiparietal cell antibodies, as false positives occur with H. pylori infection and other autoimmune diseases; histologic confirmation is mandatory. 2, 3

• NSAIDs and aspirin cause acute gastric injury and ulcers but are not primary causes of chronic gastritis; H. pylori remains the dominant etiology even in NSAID users with peptic ulcers. 4, 5