What is the management of gastritis?

Management of Gastritis

Confirm Diagnosis and Identify Etiology

The cornerstone of gastritis management is histopathological confirmation of the diagnosis and identification of the underlying cause—primarily Helicobacter pylori infection or autoimmunity—followed by targeted treatment and risk stratification. 1

Diagnostic Confirmation

• All suspected gastritis requires endoscopic biopsy for histopathological confirmation, as clinical symptoms alone are insufficient for diagnosis 1
• Obtain biopsies from both the gastric body and antrum/incisura at minimum, placing them in separately labeled containers to assess distribution and extent 1
• Target any additional mucosal abnormalities with separate biopsies 1
• Recognize that intestinal metaplasia on histology almost invariably indicates underlying atrophic gastritis, even when not explicitly stated in pathology reports 1

Identify Endoscopic Features

Look for characteristic findings of atrophic gastritis during endoscopy 1:

• Pale appearance of gastric mucosa
• Increased visibility of submucosal vasculature due to mucosal thinning
• Loss of gastric folds
• Light blue crests and white opaque fields (when intestinal metaplasia is present)

Test and Treat H. pylori

Every patient with confirmed gastritis must be tested for H. pylori infection, and if positive, receive eradication therapy with confirmation of successful treatment. 1

Testing Protocol

• Test all individuals with atrophic gastritis for H. pylori using non-serological methods 1
• Immunohistochemical stains for H. pylori are particularly useful when moderate-to-severe chronic or active gastritis is present but organisms are not identified on routine staining, when extensive intestinal metaplasia is present, or in follow-up biopsies after treatment 2

Eradication Therapy

• Administer appropriate antibiotic therapy (typically including clarithromycin or amoxicillin) for 10-14 days 1, 3
• For H. pylori-associated duodenal ulcers, an additional 14-18 days of proton pump inhibitor (PPI) therapy alone may be prescribed after antibiotics 3
• Confirm successful eradication using non-serological testing modalities 1

Manage Autoimmune Gastritis

When histology suggests autoimmune gastritis (corpus-predominant atrophy), implement the following 1:

Serological Testing

• Check anti-parietal cell antibodies and anti-intrinsic factor antibodies to support the diagnosis 1
• These autoantibodies target the gastric proton pump H+/K+ ATPase 4

Screen for Nutritional Deficiencies

• Evaluate for both vitamin B12 and iron deficiency anemia, as autoimmune gastritis causes loss of intrinsic factor and reduced acid output leading to malabsorption 1, 4
• Recognize that pernicious anemia represents a late-stage manifestation characterized by vitamin B12 deficiency and macrocytic anemia 1

Endoscopic Surveillance for Neoplasia

• Screen for type 1 gastric neuroendocrine tumors with upper endoscopy 1
• Remove small neuroendocrine tumors endoscopically 1
• Follow with surveillance endoscopy every 1-2 years depending on tumor burden 1

Acid Suppression Therapy

PPI Administration

For symptomatic relief and healing of erosive changes 3:

• Omeprazole 20-40 mg once daily before meals is the standard approach 3
• Duration varies by indication: up to 4 weeks for symptomatic GERD, up to 8 weeks for erosive esophagitis or gastric ulcers, up to 8 weeks for duodenal ulcers 3
• Use the lowest effective dose for the shortest duration necessary to minimize risks 3

Special Populations Requiring Dose Adjustment

• Reduce to 10 mg once daily for patients with hepatic impairment (Child-Pugh Class A, B, or C) 3
• Reduce to 10 mg once daily for Asian patients due to approximately four-fold higher drug exposure 3

Monitor for PPI-Related Adverse Effects

Long-term PPI use carries specific risks 3:

• Tubulointerstitial nephritis (monitor urine output and check for hematuria)
• Clostridium difficile infection (evaluate for watery diarrhea, abdominal pain, and fever)
• Increased fracture risk of hip, wrist, or spine with prolonged use (≥1 year)
• Drug-induced lupus erythematosus (watch for new joint pain or photosensitive rash)

Surveillance Strategy for Atrophic Gastritis

Implement endoscopic surveillance based on the extent and severity of atrophic changes, as atrophic gastritis represents a preneoplastic condition with progressive gastric cancer risk. 1, 5

Risk Stratification

• The extent and anatomic site of atrophic changes correlate significantly with cancer risk 5
• Advanced atrophic gastritis is defined by both anatomic extent and histologic grade 1

Surveillance Intervals

• Consider surveillance endoscopy every 3 years for patients with advanced atrophic gastritis 1
• For autoimmune gastritis specifically, determine surveillance intervals through individualized risk assessment 1
• Patients with new pernicious anemia who have not had recent endoscopy should undergo endoscopy with topographical biopsies to confirm corpus-predominant atrophy, stratify risk, and exclude prevalent gastric neoplasia including neuroendocrine tumors 1

Distinguish from Reactive Gastropathy

Recognize that reactive gastropathy differs fundamentally from gastritis 6:

• Reactive gastropathy lacks significant inflammatory cell infiltration (neutrophils, lymphocytes, plasma cells) that characterizes true gastritis 6
• Treatment requires identification and removal of the offending agent (NSAIDs, bile reflux) rather than antimicrobial or immunosuppressive therapy 6
• The cancer risk profile differs, with atrophic gastritis being clearly preneoplastic while reactive gastropathy's cancer risk remains poorly established 6