Causes of Multiple Duodenal Ulcers
Multiple duodenal ulcers are most commonly caused by Helicobacter pylori infection, followed by NSAID use, with rare cases attributable to Zollinger-Ellison syndrome or Crohn's disease. 1, 2
Primary Etiologies
Helicobacter pylori Infection
- H. pylori is found in the overwhelming majority of patients with duodenal ulcers and plays a pivotal role in ulcer pathogenesis, particularly in recurrent disease 3
- The bacterium causes chronic gastritis and colonization of antral mucosa with metaplasia extending to the proximal duodenum 4
- All patients with duodenal ulcers should undergo H. pylori testing 1, 2
- Eradication significantly reduces ulcer recurrence rates compared to acid suppression alone 5
NSAID-Induced Ulceration
- NSAIDs cause duodenal ulcers through inhibition of mucosal prostaglandin synthesis and disruption of mucosal defenses 3
- NSAID-induced ulcers typically respond well to H2-receptor antagonists or proton pump inhibitors once the offending agent is discontinued 6
- In pediatric studies, all NSAID-induced ulcers healed with acid suppression therapy alone, unlike unprovoked ulcers 6
Zollinger-Ellison Syndrome
- Consider in patients with multiple ulcers, particularly when located in unusual sites (post-bulbar duodenum) 5
- Characterized by pathological gastric acid hypersecretion from gastrinoma 5
- Requires long-term proton pump inhibitor therapy at higher doses 5
Crohn's Disease
- Primary Crohn's disease of the duodenum occurs in 0.5-5% of Crohn's patients based on clinical and radiographic findings, though endoscopic inflammation is found in 60-70% 1
- Multiple strictures occur in 10% of patients with gastroduodenal Crohn's disease 1
- Strictures are distributed: 50-60% in distal stomach/duodenal bulb, 25-30% in second/third portion, 10-15% in third/fourth portion 1
Pathophysiologic Mechanisms
Acid-Pepsin Imbalance
- Gastric acid hypersecretion occurs in approximately one-third of duodenal ulcer patients, though most secrete normal amounts 3
- Decreased mucosal bicarbonate secretion may contribute in some patients 3
- The mucosa becomes susceptible when aggressive factors overwhelm defensive mechanisms 3
Distribution Patterns
- In a study of 1320 patients with chronic duodenal ulcers, 31.4% had multiple ulcers 7
- Location distribution: 45.8% anterior wall, 26.4% posterior wall, 26.4% lesser curve, 3.7% greater curve 7
- Classification by site: Bulbar (most common), Apical, Post-bulbar, and Pyloric 7
Clinical Implications for Giant Ulcers
- Giant duodenal ulcers (≥2 cm diameter) represent a distinct subset with higher morbidity and mortality 8, 9
- These ulcers frequently harbor malignancy and require different management than standard peptic ulcers 9
- The 2 cm threshold represents a critical point where simple closure failure rates increase dramatically, with leak rates up to 12% 8
- Surgical evaluation should remain integral to patient care for giant ulcers despite medical advances 9
Diagnostic Approach
- CT scan is the recommended first-line imaging for suspected complicated ulcers 1, 2
- Chest/abdominal X-ray should be performed when CT is unavailable 1, 2
- Laboratory findings are non-specific but may show leukocytosis, metabolic acidosis, and elevated serum amylase in complicated cases 1, 2
- Up to 12% of perforations may have normal CT scans, requiring additional diagnostic measures 2
Treatment Principles
Medical Management
- Standard triple therapy (omeprazole, clarithromycin, amoxicillin) is first-line when H. pylori is present with low clarithromycin resistance 2, 5
- Sequential four-drug therapy is recommended with high clarithromycin resistance 2
- Full-dose PPI therapy (omeprazole 20 mg daily) is first choice for ulcer-like dyspepsia 2, 5
- Most duodenal ulcers heal within 4 weeks; some require an additional 4 weeks 5