Chemical Reactive Gastropathy Without NSAID/Alcohol Use
For chemical reactive gastropathy without typical risk factors, proton pump inhibitor (PPI) therapy is the primary treatment, combined with investigation for other causative factors—particularly bile reflux and H. pylori infection. 1
Initial Management Approach
Start acid suppression therapy immediately with a standard-dose PPI, as this was the treatment used in all pediatric cases of chemical gastropathy and remains the cornerstone of management. 2
Key Diagnostic Considerations
Since you lack the typical NSAID/alcohol exposure, investigate these alternative causes:
Bile reflux is a major cause of chemical gastropathy in the absence of NSAIDs—look for evidence of bile in the stomach during endoscopy (this was found in 7 of 21 pediatric cases without clear NSAID exposure). 2
H. pylori testing is essential, as eradication reduces gastropathy risk and is recommended before any potential future NSAID use. 1
Review ALL medications, not just obvious NSAIDs—multiple medications were associated with chemical gastropathy in over half of pediatric cases, suggesting cumulative effects from various drugs. 2
Assess for gastroesophageal reflux disease (GERD), which was present in 12 of 21 children with chemical gastropathy and may contribute to the reactive changes. 2
Treatment Protocol
Primary Therapy
- PPI at standard doses (e.g., omeprazole 20-40 mg daily or equivalent) should be continued for at least 8-12 weeks based on symptom response. 1, 2
If H. pylori Positive
- Eradicate H. pylori infection as this is a modifiable risk factor that increases gastropathy risk 2-4 fold, even without NSAID use. 1, 3
Expected Outcomes
- In the pediatric study with mean 11-month follow-up, symptoms resolved completely in 65% and partially in 35% of patients treated with acid suppression. 2
Important Clinical Pitfalls
Chemical gastropathy is a histopathologic diagnosis—it shows foveolar hyperplasia, vascular congestion, lamina propria edema, and smooth muscle fibers WITHOUT significant inflammatory cell infiltration. 2, 4 This distinguishes it from true gastritis caused by H. pylori.
The absence of inflammation is key—NSAIDs do not cause diffuse inflammatory cell infiltration; any such gastritis is due to H. pylori and should be treated separately. 4
Bile reflux may require additional management beyond PPIs if it's the primary driver—this might include prokinetic agents or, in severe refractory cases, surgical consultation for bile diversion procedures. 2
Follow-Up Strategy
Reassess symptoms at 8-12 weeks on PPI therapy. 2
Consider repeat endoscopy if symptoms persist despite adequate PPI therapy, to evaluate for healing and rule out other pathology. 2
Long-term PPI use is safe with very low side effect rates, though recent data suggest monitoring for potential risks like pneumonia and hip fracture in prolonged use. 1