Peptic Ulcer Disease: H. pylori Eradication & Ulcer Complications

Creator: Progress Note
Published: 2026-07-22
Keywords: peptic ulcer disease treatment H pylori, H pylori triple therapy, duodenal vs gastric ulcer, peptic ulcer NSAIDs, PUD complications, Zollinger-Ellison syndrome

The 60-second version

DU: food relieves pain; GU: food worsens pain — biopsy all GUs to rule out cancer; DU rarely malignant
H. pylori causes 95% of DU and 70% of GU — test with urea breath test or stool antigen; treat with PPI + clarithromycin + amoxicillin × 14 days
Confirm eradication with UBT or stool antigen 4 weeks after antibiotics — serology is useless for test-of-cure
Free air under diaphragm on CXR = perforated ulcer (usually anterior DU) → emergency surgery (Graham patch)
Zollinger-Ellison: multiple/refractory ulcers + diarrhea + gastrin >1000 → secretin stimulation test; 25% have MEN1

Duodenal vs Gastric Ulcers

**Duodenal ulcers**: most common (95% H. pylori), located in duodenal bulb (first part of duodenum). Pathophysiology: increased acid production (H. pylori damages antral D cells → decreased somatostatin → increased gastrin → increased HCl). Pain: epigastric, worse 2–3h after meals and at night ('hunger pain'), relieved by food (food buffers acid). Posterior DU → erodes gastroduodenal artery → massive upper GI bleed. **Gastric ulcers**: less common; H. pylori (70%) or NSAIDs (25%). Multiple subtypes by location. Pain: epigastric, worse with eating (food stimulates acid when mucosal defenses impaired), no relief with food. Malignancy risk: biopsy all gastric ulcers (DU rarely malignant, GU must be biopsied to rule out cancer). Must confirm GU healing after 8–12 weeks of treatment. **NSAID ulcers**: inhibit COX-1 → decreased prostaglandin → decreased mucus/bicarb/blood flow. Prefer COX-2 selective NSAIDs (celecoxib) or add PPI for NSAID users at risk. **Stress ulcers**: critically ill patients (Cushing's ulcers with head trauma — increased vagal tone → hypersecretion; Curling's ulcers with burns — decreased mucosal blood flow). Prophylax with PPI or H2 blocker in ICU.

H. pylori Diagnosis and Eradication

**Diagnosis**: Non-invasive: urea breath test (UBT — gold standard for test-and-treat; high sensitivity/specificity; false negative if recent PPI/antibiotic use — stop PPIs 2 weeks, antibiotics 4 weeks before test); stool antigen test (also excellent, cheaper). Serology (IgG anti-H. pylori) stays positive after eradication — poor for test-of-cure. Invasive (EGD): rapid urease test (CLO test — fast, cheap), histology (gold standard — shows organisms in gastric mucosa), culture/sensitivity. Biopsy both antrum and body — H. pylori is patchy. **First-line eradication (standard triple therapy × 14 days)**: Clarithromycin + amoxicillin + PPI. Test-and-treat strategy: if H. pylori confirmed → treat without EGD for uncomplicated PUD (age <55, no alarm features). **Bismuth quadruple therapy (preferred in areas with high clarithromycin resistance >15%)**: bismuth + metronidazole + tetracycline + PPI. **Confirm eradication** with UBT or stool antigen 4 weeks after completing antibiotics (serology useless for test-of-cure). If eradication fails → second-line (levofloxacin-based triple or bismuth quadruple if not used first).

Complications and Zollinger-Ellison Syndrome

**Hemorrhage** (most common PUD complication): posterior DU → gastroduodenal artery; lesser curve GU → left gastric artery. Hematemesis, melena, hemodynamic instability. Manage with endoscopic hemostasis (epinephrine injection + thermal therapy/clip); interventional radiology if endoscopy fails; surgery as last resort. **Perforation** (most dangerous complication): acute peritonitis — sudden severe epigastric pain radiating to shoulder, rigid abdomen, free air under diaphragm on upright CXR (classic finding) or CT. Emergency surgery (Omental patch — 'Graham patch' repair). Anterior DU perforation → peritonitis; posterior DU → bleeds. **Gastric outlet obstruction** (scarring from repeated ulcers): succussion splash, nausea/vomiting of undigested food, weight loss. Diagnose with barium swallow (dilated stomach, narrowed pylorus); treat with balloon dilation or surgery. **Zollinger-Ellison syndrome (ZES)**: gastrinoma (usually pancreatic/duodenal) → massive gastrin → acid hypersecretion → multiple severe/refractory ulcers. Suspect with: multiple ulcers, distal duodenal/jejunal ulcers (unusual location), diarrhea (excess acid inactivates pancreatic enzymes, damages small bowel), failed standard treatment. Diagnosis: fasting serum gastrin >1000 pg/mL + secretin stimulation test (paradoxical rise in gastrin with secretin injection). 25% MEN1 syndrome. Treat: high-dose PPI + surgical resection of gastrinoma.

Test yourself

Quick check — 3 questions

1. A 42-year-old man reports epigastric pain that wakes him at 2 AM and is relieved by antacids. UBT is positive. What is the appropriate treatment?

2. A 55-year-old woman has persistent PUD despite PPI therapy. EGD shows multiple ulcers in the second and third portions of the duodenum and jejunum. She also reports chronic watery diarrhea. What is the most likely diagnosis and best diagnostic test?

3. A 68-year-old man presents with sudden onset severe epigastric pain radiating to both shoulders and a rigid abdomen. His epigastric pain began after a large meal. CXR shows air under the right hemidiaphragm. What is the diagnosis and treatment?

Frequently asked questions

Why must gastric ulcers be biopsied but duodenal ulcers typically don't require biopsy?

Gastric ulcers carry a 1–3% malignancy risk — gastric adenocarcinoma and gastric lymphoma (MALToma) can present as ulcerating lesions indistinguishable endoscopically from benign ulcers. Multiple biopsies (at least 6 from the ulcer margins and base) are required at index EGD. Gastric ulcers must also be reassessed at 8–12 weeks to confirm healing — non-healing GU requires repeat biopsy and possible gastrectomy. Duodenal ulcers virtually never harbor malignancy and don't require biopsy (H. pylori testing is sufficient).

What is the secretin stimulation test and when is it used?

The secretin stimulation test is used to confirm Zollinger-Ellison syndrome when fasting gastrin is 200–1000 pg/mL (equivocal range). Normally, secretin inhibits gastrin release. In ZES (gastrinoma), secretin paradoxically stimulates gastrin release from the tumor — a positive test shows gastrin rise >200 pg/mL above baseline after IV secretin injection. Fasting gastrin >1000 pg/mL + compatible symptoms (multiple ulcers, diarrhea, acid hypersecretion) is essentially diagnostic without the stimulation test.

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