Pathophysiology
H. pylori (60-90% of duodenal, 50% of gastric ulcers) urease-driven inflammation disrupts mucosal defence. NSAIDs inhibit COX-1, reducing prostaglandin-mediated mucus/bicarbonate. Rare: Zollinger-Ellison (gastrin-secreting gastrinoma), Crohn, stress ulcers, cocaine.
Sources: ACG H. pylori Treatment Guideline (Am J Gastroenterol 2024;119:1730); ACG Peptic Ulcer Bleeding Guideline (Am J Gastroenterol 2021;116:899); NICE Dyspepsia and GORD (CG184, updated 2019)
Clinical presentation
Epigastric burning pain: duodenal ulcers relieved by food (pain returns 2-3 h later); gastric ulcers worsen with food and cause weight loss. Complications: haematemesis/melaena (posterior duodenal ulcer erodes gastroduodenal artery), perforation (free air, rigid abdomen), gastric outlet obstruction.
Diagnosis
Test all dyspeptic patients <60 y for H. pylori (urea breath test or stool antigen, off PPI 2 weeks and antibiotics 4 weeks). Endoscopy for alarm features (age >=60, bleeding, weight loss, dysphagia, anaemia); biopsy gastric ulcers to exclude malignancy.
Management
Optimised bismuth quadruple therapy (bismuth + PPI + tetracycline + metronidazole x 14 days) is first-line per ACG 2024; alternative rifabutin triple. Stop NSAIDs, add PPI 4-8 weeks. Confirm eradication with urea breath test 4 weeks post-therapy.
Bleeding & surgery
Endoscopic dual therapy (adrenaline injection + clips or thermal) for Forrest Ia-IIb ulcers, IV PPI infusion, and consider transarterial embolisation if rebleed. Emergency surgery (Graham patch) for perforation.
