What is the management approach for a patient with reactive gastropathy diagnosed by gastric mucosa biopsy?

Reactive Gastropathy: Diagnosis and Management

Reactive gastropathy is a histopathologic pattern of chemical injury to the gastric mucosa characterized by foveolar hyperplasia, interfoveolar smooth muscle fibers, edema, and minimal inflammation—most commonly caused by NSAIDs or bile reflux, but in your non-drinking patient, the priority is identifying and eliminating the causative agent (typically NSAIDs, aspirin, or bile reflux from prior surgery) and initiating PPI therapy if symptomatic. 1

What Reactive Gastropathy Means

Reactive gastropathy represents a constellation of histologic changes resulting from chemical injury to the stomach lining 1:

• Characteristic features include foveolar hyperplasia, interfoveolar smooth muscle proliferation, mucosal edema and hyperemia, with notably absent or minimal inflammation—this distinguishes it from H. pylori gastritis 1, 2
• The diagnosis exists on a spectrum of certainty because individual features can occur in other conditions, but the combination in the absence of significant inflammation is diagnostic 1
• Mucin expression is altered: loss of MUC1 (membrane mucin) occurs in 67% of cases, and aberrant MUC5AC expression in pyloric glands occurs in 81% of cases—these changes differ mechanistically from H. pylori gastritis 3

Common Causes to Investigate

Primary Etiologies (Even Without Alcohol)

• NSAIDs and aspirin are the most common causes—ask specifically about over-the-counter ibuprofen, naproxen, low-dose aspirin for cardiovascular prophylaxis, and any prescription NSAIDs 1, 3, 4
• Bile reflux occurs in patients with prior gastric surgery (Billroth procedures, gastrojejunostomy) or pyloric dysfunction allowing duodenal contents to reflux into the stomach 1, 3
• Indeterminate etiology accounts for a substantial proportion of cases when neither NSAIDs nor bile reflux are identified 3

Important Clinical Context

• Reactive gastropathy is the second most common diagnosis on gastric biopsies and shows age-dependent increase, rising from 2% in the first decade to over 20% in octogenarians 4
• It is associated with inflammatory conditions throughout the GI tract, including Barrett's esophagus (OR 1.21), duodenitis (OR 1.36), active ileitis (OR 1.88), and collagenous colitis (OR 1.50)—suggesting shared pathophysiologic mechanisms 4

Management Algorithm

Step 1: Identify and Eliminate the Causative Agent

• Conduct a detailed medication review focusing on NSAIDs (prescription and over-the-counter), aspirin (including low-dose cardioprotective therapy), and any other potentially gastrotoxic medications 1
• Assess for bile reflux risk factors: history of gastric surgery, pyloric dysfunction, or symptoms suggesting duodenogastric reflux (bilious vomiting, postprandial epigastric pain) 1, 3
• Discontinue or substitute NSAIDs if identified—consider switching to acetaminophen for pain control or, if NSAIDs are essential for cardiovascular protection, use the lowest effective dose with gastroprotection 1

Step 2: Initiate Acid Suppression Therapy

• Start standard-dose PPI once daily (taken 30 minutes before the first meal) for 4-8 weeks if the patient has symptoms such as epigastric pain, nausea, or dyspepsia 5, 6
• PPIs are first-line therapy and significantly more effective than H2-receptor antagonists for symptom control and mucosal healing 5
• Avoid adding H2RAs to PPI therapy—combination provides no additional benefit, and H2RAs develop tachyphylaxis within days 5

Step 3: Lifestyle and Adjunctive Measures

• Eliminate coffee completely—caffeine directly relaxes the lower esophageal sphincter and can exacerbate symptoms regardless of timing 5
• Avoid meals within 3 hours of bedtime, eliminate spicy foods, chocolate, peppermint, and elevate the head of bed by 6-8 inches 5
• Consider alginate antacids (Gaviscon) for breakthrough symptoms, particularly after meals and at bedtime, as they neutralize the post-prandial acid pocket 5

Step 4: Reassess and Escalate if Needed

• If symptoms persist after 4-8 weeks on once-daily PPI, escalate to twice-daily dosing (before breakfast and dinner) 5, 6
• If symptoms persist on twice-daily PPI, perform upper endoscopy to assess for erosive esophagitis, ulceration, or other structural causes 5, 7
• Consider prolonged pH monitoring (96-hour wireless pH study off PPI) if endoscopy is unrevealing, to determine if pathologic acid exposure is present or if symptoms represent functional disorder 8, 7

Critical Pitfalls to Avoid

• Do not assume correlation between histologic findings and bleeding risk—while reactive gastropathy can predispose to erosions, the clinical significance of histologic changes alone is not well-established 1
• Do not overlook "hidden" NSAID use—patients often forget about over-the-counter medications, topical NSAIDs, or combination products containing aspirin 1
• Do not continue empiric PPI therapy indefinitely without reassessment—if symptoms resolve, taper to the lowest effective dose or on-demand therapy with H2RAs/antacids 5, 6
• Recognize that up to 60% of PPI-refractory patients may have functional disorders (functional heartburn, reflux hypersensitivity) rather than acid-mediated disease, requiring neuromodulation or behavioral therapy instead of escalating acid suppression 5, 7
• Do not ignore associated GI conditions—reactive gastropathy is associated with duodenitis, microscopic colitis, and other inflammatory conditions that may require independent evaluation 4

When to Consider Alternative Diagnoses

• If significant inflammation is present, reconsider the diagnosis—reactive gastropathy is characterized by minimal inflammation, and prominent inflammatory infiltrate suggests H. pylori gastritis, autoimmune gastritis, or other etiologies 1, 2
• If H. pylori testing was not performed, consider testing—H. pylori gastritis can coexist but shows different mucin expression patterns (increased MUC6, reduced MUC5AC) compared to reactive gastropathy 3, 2