Peptic Ulcer Disease

Characterized by a localized mucosal defect ≥5 mm in the stomach or proximal duodenum, penetrating through the muscularis mucosae, caused by acid–pepsin injury

Aetiology

  • H. pylori
    • 90% of duodenal ulcers
    • 60% of gastric ulcers
  • NSAIDs - most of the rest of cases
  • Zollinger Ellison syndrome - gastrinoma (tumour in the head of pancreas or duodenum) produces large amounts of gastrin which increases stomach acid → peptic ulcer disease
  • Occur in predominantly middle-aged men but anyone is susceptible

Pathophysiology

H. pylori

  • Gram negative microaerophilic flagellated bacillus which is acquired in infancy (oral-oral/faecal oral spread), although consequences don’t arise until later life
  • pylori inhabits a niche between the epithelial cell surface and the mucous barrier and excites an acute inflammatory response
  • If cleared - no pathology (majority of people)
  • In 20-40% of people, H. pylori is not cleared and there is chronic active inflammation, resulting in a breach in the GI mucosa - ulcer

NSAIDs

  • Small abrasions to the lining of the stomach happen all the time, would normally heal
  • NSAIDs inhibit prostaglandin formation which reduces the ability of the stomach to heal itself

Gastric ulcers

  • Typically manifests along the greater curvature and gastric antrum
  • Associated with gastric carcinoma

Duodenal ulcer

  • Typically first part of duodenum
  • 50% of patients with DU have increased acid secretion - causes further ulceration

Clinical presentation

Gastric ulcer

  • Dyspepsia
  • Epigastric pain worse after eating
  • Pain eased by antacids and lying flat
  • Rupture will present as haematemesis

Duodenal ulcer

  • Dyspepsia
  • Epigastric pain relieved by eating
  • Pain worse when lying flat - may wake patient during the night
  • Rupture will present as rectal bleeding/meleana

Investigations

Upper Gastrointestinal Endoscopy (Esophagogastroduodenoscopy, EGD)

Gold standard investigation
Indications
  • Suspected PUD with:
    • Alarm features (bleeding, anemia, weight loss, vomiting)
    • Age ≥50–60 years with new-onset dyspepsia
    • Refractory symptoms despite treatment
    • Suspected complications
  • All suspected gastric ulcers
Endoscopic Findings
  • Gastric ulcer: discrete mucosal crater with surrounding erythema
  • Duodenal ulcer: typically in the first part of the duodenum
  • Signs of complications:
    • Active bleeding
    • Visible vessel
    • Adherent clot
    • Pyloric narrowing

Helicobacter pylori Testing

Invasive Tests (During Endoscopy)
Test
Method
Advantage
Limitation
Rapid urease test (CLO test)
Biopsy-based
Fast, cheap
False negatives with PPIs
Histology
Biopsy staining
High sensitivity
Operator dependent
Culture
Biopsy
Antibiotic sensitivity
Limited availability
Non-Invasive Tests
Test
Indication
Notes
Urea breath test
Diagnosis & test-of-cure
Most accurate
Stool antigen test
Diagnosis & test-of-cure
Widely available
Serology
Past exposure
Not for active infection
⚠ False negatives occur with:
  • Recent PPI use (<2 weeks)
  • Antibiotics or bismuth (<4 weeks)

Management

Helicobacter pylori–Associated PUD

Eradication Therapy (First-Line)
  • 14-day therapy preferred
Regimen
Drugs
Dose
Duration
Triple therapy
PPI + Amoxicillin + Clarithromycin
PPI 2x1 + Amoxicillin 1 g 2x1 + Clarithromycin 500 mg 2x1
14 days
Quadruple therapy
PPI + Bismuth + Metronidazole + Tetracycline
PPI 2x1 + Bismuth 120 mg 4x1 + Metronidazole 500 mg 3x1 + Tetracycline 500 mg 4x1
10–14 days
Post-Treatment
  • Continue PPI:
    • Duodenal ulcer: 2–4 weeks
    • Gastric ulcer: 4–8 weeks
  • Confirm eradication after ≥4 weeks

NSAID-Induced PUD

  • Discontinue NSAID if possible
  • PPI for 8 weeks
  • If NSAID must continue:
    • PPI co-therapy
    • Switch to COX-2 inhibitor
    • Add misoprostol (if tolerated)

Idiopathic PUD

  • Long-term PPI therapy
  • Exclude rare causes (ZES, malignancy)

Complications

  • Bleeding
  • Perforation
  • Gastric outlet/duodenal obstruction - due to fibrotic scar
  • Malignancy - H. pylori implicated in almost all non-cardia gastric adenocarcinoma, gastric lymphoma (MALT) also associated