Peptic Ulcer Disease — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Peptic ulcer disease (PUD) refers to open sores (ulcers) that develop in the inner lining of the stomach (gastric ulcers) or the proximal small intestine (duodenal ulcers — most commonly in the first part of the duodenum, the duodenal cap). Ulcers form when the mucosal protective mechanisms (mucus, bicarbonate, prostaglandins, mucosal blood flow) are overwhelmed by damaging factors (gastric acid, pepsin, H. pylori, NSAIDs). The lifetime prevalence of PUD is 5-10%, with an annual incidence of approximately 4 million new cases globally. Duodenal ulcers are 4 times more common than gastric ulcers and predominantly affect younger patients (30-55 years); gastric ulcers are more common in older patients (55-70 years) and carry a higher risk of malignancy. The two major causative factors — Helicobacter pylori infection and NSAID use — account for over 90% of cases. PUD incidence has declined significantly in high-income countries with widespread H. pylori treatment and safer analgesic use, but it remains a major global health burden, particularly in developing countries where H. pylori prevalence can reach 70-90%.

Helicobacter pylori (H. pylori) is a gram-negative bacterium that colonises the gastric mucosa, causing chronic active gastritis and disrupting mucosal defence mechanisms. H. pylori infection causes 70-90% of duodenal ulcers and 50-70% of gastric ulcers. Transmission is faecal-oral or oral-oral; prevalence is highest in low-income countries (60-90%) and in lower socioeconomic groups in high-income countries. Non-steroidal anti-inflammatory drugs (NSAIDs — including aspirin, ibuprofen, naproxen, diclofenac) are the second major cause, inhibiting cyclo-oxygenase (COX) enzymes and reducing prostaglandin synthesis, thereby impairing mucosal protection. Risk of NSAID-induced ulcer increases with: advanced age (over 65), high NSAID dose, concurrent corticosteroid or anticoagulant use, prior peptic ulcer, and H. pylori infection. Selective COX-2 inhibitors (celecoxib) are less ulcerogenic than traditional NSAIDs. Other causes: Zollinger-Ellison syndrome (gastrin-secreting pancreatic tumour — gastrinoma — causing massive hypersecretion of gastric acid; suspect if multiple, recurrent, or refractory ulcers); smoking (doubles ulcer risk and impairs healing); stress ulcers (in critically ill patients in ICU — related to ischaemia and reduced mucosal perfusion); and rarely, Crohn's disease affecting the duodenum. 'NSAID-negative, H. pylori-negative' ulcers occur in approximately 5-10% of cases.

The classic symptom of peptic ulcer disease is epigastric pain (burning, gnawing, or aching in the upper central abdomen). Duodenal ulcer pain: typically occurs 2-3 hours after meals, often wakes the patient at night (nocturnal pain is characteristic — 75% of cases), and is relieved by food or antacids (food buffers acid). Gastric ulcer pain: typically worsened by eating (food stimulates acid secretion), not relieved and may be aggravated by meals; patients may reduce food intake causing weight loss. Nausea and vomiting occur in approximately 30-40% of cases. Bloating and belching are common. Up to 70% of NSAID-induced ulcers are asymptomatic ('silent ulcers') — first presentation may be a complication (haemorrhage or perforation). Alarm (red flag) symptoms requiring urgent endoscopy: unexplained weight loss (possible malignancy); dysphagia (difficulty swallowing); persistent vomiting; haematemesis (vomiting blood); melaena (black tarry stools from digested upper GI blood — 60+ mL required to colour stools black); anaemia; and age over 55 years with new onset dyspepsia. Sudden severe generalised abdominal pain with rigidity ('peritonism' — board-like abdomen) indicates peptic ulcer perforation — a surgical emergency requiring immediate laparotomy.

Upper GI endoscopy (gastroscopy/OGD) is the gold standard investigation — it visualises the ulcer directly, allows biopsy of gastric ulcers to exclude malignancy (all gastric ulcers must be biopsied; duodenal ulcers are almost never malignant), and enables treatment of bleeding ulcers with haemostatic techniques (adrenaline injection, clips, thermal coagulation). Testing for H. pylori: urea breath test (UBT — non-invasive, 95% sensitivity and specificity — gold standard for confirmation of eradication; PPI must be stopped 2 weeks before testing); stool H. pylori antigen test (alternative to UBT; requires PPI cessation); rapid urease test (CLO test — on endoscopic biopsy — immediate result); serology (IgG antibody — cannot distinguish active from past infection — not recommended for diagnosis or eradication confirmation); H. pylori culture (from biopsy) used for antibiotic sensitivity testing in treatment failures. Barium meal swallow is an older investigation, now rarely used. Blood tests: FBC (anaemia), LFT, coagulation, and serum gastrin (fasting serum gastrin above 10x upper normal strongly suggests Zollinger-Ellison syndrome — gastrin levels above 1000 pg/mL with elevated acid secretion are diagnostic). CT scan for suspected perforation (free air under diaphragm on erect CXR is diagnostic).

H. pylori eradication is the cornerstone of treatment for H. pylori-positive ulcers and results in healing of the ulcer and prevention of recurrence (relapse rate drops from 50-80% without eradication to under 5% with eradication). First-line triple therapy (14 days): clarithromycin 500 mg twice daily + amoxicillin 1g twice daily + PPI (omeprazole 20-40 mg twice daily or equivalent) — eradication rates of 70-85%. Bismuth-based quadruple therapy is now preferred in areas with high clarithromycin resistance (over 15%) or in clarithromycin-allergic patients: bismuth subsalicylate + PPI + metronidazole + tetracycline for 10-14 days — eradication rates over 90%. Sequential therapy (PPI + amoxicillin for 5 days followed by PPI + clarithromycin + metronidazole for 5 days) or concomitant quadruple therapy (all four simultaneously) are alternatives. Confirm eradication by urea breath test or stool antigen 4-8 weeks after completing eradication therapy. Proton pump inhibitors (PPIs): continue for 4-8 weeks for duodenal ulcers and 8-12 weeks for gastric ulcers to ensure healing. NSAID management: stop the causative NSAID if possible; switch to COX-2 selective inhibitor (celecoxib); co-prescribe PPI (omeprazole or lansoprazole) for all patients requiring ongoing NSAID therapy at risk of PUD. Zollinger-Ellison syndrome: high-dose PPI, surgical resection of gastrinoma if localised; octreotide for metastatic disease. Complicated PUD: endoscopic haemostasis for bleeding ulcers (Forrest Ia — active arterial spurting — requires emergency endoscopy within 12-24 hours); emergency surgery for perforation (laparotomy/laparoscopic repair of perforated ulcer).

Peptic ulcer complications are serious and potentially life-threatening, requiring emergency management. Haemorrhage (bleeding peptic ulcer) is the most common and deadly complication — occurs in 15-20% of PUD patients; presents as haematemesis (vomiting blood), melaena (black tarry stools), or haemodynamic instability. Upper GI bleeding carries an overall 10% mortality. Forrest classification guides endoscopic treatment: Ia (active arterial spurting — 55% rebleeding risk without treatment) requires endoscopic haemostasis (combined adrenaline injection + thermal/clipping); high-risk stigmata (Ia, Ib, IIa, IIb) require PPI infusion post-endoscopy to reduce rebleeding. Perforation (3-5% of cases): sudden onset severe abdominal pain followed by board-like rigidity and peritonitis; erect chest X-ray shows free air under the diaphragm; requires emergency laparotomy or laparoscopic repair within hours — mortality 10-40% depending on contamination time, age, and comorbidities. Gastric outlet obstruction (pyloric stenosis): recurrent duodenal or pyloric channel ulcers cause fibrosis and narrowing, leading to persistent vomiting, dehydration, hypokalaemic hypochloraemic metabolic alkalosis ('gastric outlet obstruction metabolic alkalosis'); managed by endoscopic balloon dilatation or surgical pyloroplasty. Gastric cancer: H. pylori infection in the context of atrophic gastritis and intestinal metaplasia — the 'Correa cascade' — increases gastric adenocarcinoma risk 3-6 fold. H. pylori eradication reduces (but does not eliminate) this risk.

H. pylori eradication prevents ulcer recurrence and reduces gastric cancer risk (H. pylori is a WHO Group 1 carcinogen for non-cardia gastric cancer). Population-level H. pylori screening and treat programs in high-prevalence countries reduce gastric cancer incidence by 30-50%. For NSAID-related ulcer prevention: use the lowest effective NSAID dose for the shortest time; prefer paracetamol for analgesia when anti-inflammatory effect is not required; use COX-2 selective inhibitors (celecoxib) in patients at moderate ulcer risk; prescribe gastroprotective PPI co-therapy with all NSAIDs in patients at high ulcer risk (over 65, prior PUD history, concurrent steroids or anticoagulants). Test and treat for H. pylori before starting long-term NSAID therapy. Smoking cessation significantly reduces ulcer risk and improves healing. Avoid regular analgesic use with alcohol. Follow up with repeat endoscopy 6-12 weeks after initiating treatment for all gastric ulcers to confirm healing and exclude malignancy.

Seek emergency care immediately for: vomiting blood (haematemesis) or passing black tarry stools (melaena) — signs of upper gastrointestinal bleeding; sudden onset severe abdominal pain with board-like rigidity (possible ulcer perforation — a surgical emergency); or feeling faint, having cold sweats, or racing pulse associated with GI symptoms (shock from haemorrhage). Seek urgent medical review within days for: persistent unexplained weight loss with upper abdominal pain; difficulty swallowing; persistent vomiting; or new onset epigastric symptoms in anyone over 55 years. See your GP or gastroenterologist promptly for: burning upper abdominal pain waking you at night; symptoms that have not responded to 2-4 weeks of over-the-counter antacids; or recurrent dyspepsia occurring more than twice weekly. Do not self-medicate ongoing symptoms with antacids alone without investigation — gastric ulcers require endoscopic biopsy to exclude cancer.