Causes of Duodenitis
Duodenitis is primarily caused by Helicobacter pylori infection and NSAID use, with H. pylori being the dominant etiological factor in most cases.
Primary Etiological Factors
Helicobacter pylori Infection
- H. pylori is the major causative agent of chronic duodenitis, establishing infection through gastric metaplasia in the duodenal bulb 1
- The organism colonizes areas of gastric metaplasia in the duodenum, which correlates with increased acid load and leads to chronic inflammation 1
- H. pylori-related duodenitis is strongly associated with duodenal ulcer development, with active duodenitis found in 80% of patients with duodenal ulcers 2
- The pathogenic mechanism involves bacterial attachment to gastric epithelial cells via surface lectins, followed by release of harmful toxins and enzymes that cause cellular damage and immune response 1
NSAID-Induced Duodenitis
- NSAIDs are the second major cause of duodenitis, though active duodenitis is paradoxically less common in NSAID users (27%) compared to non-users (57%) 2
- NSAIDs cause duodenal injury through mechanisms including decreased mucosal pH, imbalance between apoptosis and proliferation, reduced mucosal blood flow, and polymorphonuclear cell recruitment 3
- The hemorrhagic erosive form of duodenitis is a potentially serious complication in patients taking aspirin-alcohol combinations 4
- NSAID-induced duodenal ulcers occur more frequently in patients without H. pylori infection 3
Secondary and Contributing Factors
Acid Hypersecretion
- Excessive gastric acid production, particularly in the setting of H. pylori antral gastritis, contributes to duodenal injury 1
- Increased acid load promotes gastric metaplasia in the duodenum, creating sites vulnerable to H. pylori colonization 1
Corticosteroid Use
- Corticosteroid therapy is a recognized risk factor for duodenal perforation and complications 5
- Immunosuppressed patients may present with milder symptoms despite significant duodenal pathology 5
Stress-Related Mucosal Disease
- Severe physiologic stress in critically ill patients can cause stress ulcers with duodenal involvement 5
- This occurs particularly in intensive care settings where diagnosis may be obscured in sedated patients 5
Host and Environmental Factors
- Genetic predisposition, blood group, smoking, and dietary factors (particularly high salt intake) all modulate susceptibility to duodenitis 5, 1
- These factors affect acid secretion in the gastric mucosa and interact with primary etiological agents 5
Clinical Patterns
Endoscopic Manifestations
- Duodenitis presents in two general forms: (1) nodularity and erythema, or (2) erosions and friability 4
- Active duodenitis is characterized by neutrophilic infiltration, with severity dependent on the degree of neutrophil presence 2
- Gastric metaplasia in the duodenum is present in 27-39% of cases and serves as the substrate for H. pylori colonization 2
Association with Duodenal Ulceration
- H. pylori-positive gastritis combined with active duodenitis and gastric metaplasia are independent predictors of duodenal ulcer formation 2
- Duodenal ulcers are more closely related to H. pylori infection than gastric ulcers in NSAID users 3
Management Implications
H. pylori Eradication
- For H. pylori-associated duodenitis, triple therapy with amoxicillin, clarithromycin, and a proton pump inhibitor for 10-14 days is indicated 6
- H. pylori eradication is recommended for primary prevention of duodenal ulcers in patients requiring NSAID therapy 3
- Eradication markedly alters disease natural history, with studies showing no recurrence at 1 year compared to >70% natural recurrence 7
Acid Suppression
- Proton pump inhibitors such as omeprazole 20-40 mg daily are the most effective treatment for healing duodenal lesions 8, 9
- PPI therapy is mandatory for secondary prevention in NSAID users and appears to further reduce ulcer relapse risk in H. pylori-positive patients 3
- Treatment duration is typically 4-8 weeks for healing duodenal ulcers 9