How should I initially treat a patient with epigastric burning, nausea, early satiety and risk factors (NSAIDs, alcohol, smoking, stress, prior Helicobacter pylori infection) suggestive of gastritis?

Initial Treatment of Gastritis

Start empiric proton pump inhibitor (PPI) therapy at standard dose once daily, taken 30-60 minutes before a meal, for 4-8 weeks, while simultaneously testing for H. pylori and eradicating if positive. 1, 2

Immediate Assessment and Risk Stratification

Rule Out Life-Threatening Conditions First

• Obtain ECG and troponins immediately – myocardial infarction can present as epigastric pain as the primary manifestation 3
• Assess for perforation signs: sudden severe epigastric pain with fever, abdominal rigidity, or board-like abdomen carries 30% mortality if treatment is delayed 3
• Check for occult blood in stool, vomiting, fever, and tachycardia indicating complications requiring immediate investigation 3

Identify Alarm Features Requiring Urgent Endoscopy

For patients ≥55 years, urgent endoscopy is indicated for: 4, 3

• Weight loss (≥9.1 kg over 6 months) with dyspepsia
• Treatment-resistant dyspepsia despite PPI therapy
• Progressive symptoms despite acid suppression
• Any signs of bleeding, perforation, or obstruction

Clinical Pearl: Most patients with dyspepsia (80%) will have functional dyspepsia after investigation, but alarm features have a ≥3% positive predictive value for gastro-oesophageal cancer in this age group. 4, 3

First-Line Pharmacologic Management

PPI Therapy Protocol

• All commercially available PPIs are functionally equivalent when dosed appropriately – absolute differences in efficacy are small 1
• Standard dosing: omeprazole 20 mg, lansoprazole 30 mg, or equivalent once daily 1, 2
• Timing is critical: Take 30-60 minutes before a meal for optimal effect 2
• Duration: 4-8 weeks initially 1, 2

PPIs are superior to H2-receptor antagonists, which are superior to placebo for treating dyspepsia. 1, 2 Note that H2-receptor antagonists develop tolerance within 6 weeks, limiting long-term effectiveness. 2

H. Pylori Testing and Eradication

• Test all patients with dyspepsia using urea breath test or stool antigen test 1, 2
• If positive, initiate eradication therapy with bismuth quadruple therapy or concomitant therapy as first-line regimens 2
• Eradication is particularly important in patients beginning NSAID therapy – it reduces ulcer occurrence and eliminates peptic ulcer mortality risk 2, 5

Important caveat: H. pylori eradication is estimated to improve only 5% of dyspepsia symptoms in the community, but it identifies most peptic ulcer disease cases. 1 The interaction between H. pylori and NSAIDs is complex: both are independent risk factors, and eradication before NSAID treatment decreases ulcer occurrence. 6, 5, 7

Symptom-Based Treatment Approach

For Ulcer-Like Dyspepsia (Epigastric Pain/Burning Predominant)

• Full-dose PPI therapy is first choice 2
• Symptom response confirms acid-related nature 1, 2

For Dysmotility-Like Dyspepsia (Bloating, Fullness, Early Satiety)

• Consider adding prokinetic agent to PPI therapy 1, 2
• PPI monotherapy remains reasonable as initial approach 1

Treatment Escalation Algorithm

If symptoms persist after 4-8 weeks of once-daily PPI: 1, 2

1. Increase to twice-daily PPI dosing (morning and evening before meals)
2. Continue twice-daily dosing for additional 4-8 weeks
3. For dysmotility symptoms, add prokinetic agent

If symptoms persist despite twice-daily PPI for 8 weeks: 1, 2

• Proceed to endoscopy to evaluate for structural disease or alternative diagnoses
• This is mandatory when optimized therapy fails

Critical Risk Factor Management

NSAID-Related Considerations

• Approximately 10-30% of regular NSAID users develop gastric ulcers, though clinically significant complications occur in only ~0.75% over 6 months 8
• NSAIDs cause subepithelial hemorrhages, erosions, and ulcers through mechanisms independent of H. pylori 8, 9
• There is no correlation between NSAID gastropathy and upper abdominal symptoms – endoscopic lesions are common but often asymptomatic 8
• If NSAIDs must be continued, consider misoprostol cotherapy to decrease ulcer incidence 8

Alcohol and Smoking

• These agents cause gross gastric injury but do not induce inflammatory cell infiltration (histologic gastritis) 9
• Any histologic gastritis present is due to underlying H. pylori infection, not alcohol or smoking 9
• Counsel cessation but recognize these factors don't clearly influence H. pylori-associated gastritis 9

Long-Term Management

If symptoms resolve with initial therapy: 1

• Taper PPI to lowest effective dose
• Consider on-demand therapy for maintenance (though data are limited in functional dyspepsia)
• Document appropriate indications and consider de-prescribing in absence of ongoing indication

For patients requiring long-term PPI: 1

• Most patients with dyspepsia have nonerosive disease and should be considered for trial of de-prescribing after symptom control
• Objective reflux testing should be considered to confirm diagnosis if long-term therapy needed

Common Pitfalls to Avoid

• Never assume benign disease without tissue diagnosis when gastric ulcers are found – all gastric ulcers require biopsy to exclude malignancy 3
• Don't dismiss cardiac causes in epigastric pain presentations 3
• Don't rely on physical examination alone to rule out perforation – up to one-third of patients with perforated peptic ulcer may have minimal or absent peritoneal signs 3
• Avoid unnecessary long-term PPI use without documented appropriate indication 1
• Remember that symptom severity doesn't correlate with endoscopic findings in NSAID gastropathy 8