Peptic Ulcer Disease
Summary
Peptic ulcer disease (PUD) refers to ulceration of the gastric or duodenal mucosa. The two main causes are Helicobacter pylori infection (~60-70%) and NSAID use (~20-30%). Classic symptoms include epigastric pain, often with a relationship to meals (duodenal ulcers: relieved by eating; gastric ulcers: worsened by eating). Diagnosis is confirmed by endoscopy. Management involves proton pump inhibitor (PPI) therapy and H. pylori eradication if test-positive. Complications include bleeding, perforation, and gastric outlet obstruction. Patients with alarm features (weight loss, dysphagia, anaemia, age >55 with new dyspepsia) require urgent endoscopy.
Key Facts
- Definition: Ulceration of gastric or duodenal mucosa
- Prevalence: Lifetime risk ~10%
- Main Causes: H. pylori (~60-70%), NSAIDs (~20-30%)
- Diagnosis: Endoscopy (OGD); H. pylori testing
- Treatment: PPI + H. pylori eradication (if positive)
- Complications: Bleeding, perforation, obstruction
Clinical Pearls
"Test and Treat vs Endoscope": In patients <55 without alarm features, NICE recommends H. pylori test-and-treat or empirical PPI before endoscopy. Alarm features or age >55 with new symptoms warrant urgent OGD.
Gastric vs Duodenal Ulcer Pain: Classic distinction — DU pain is relieved by food (buffer acid), GU pain is worsened by food (stimulates acid). However, overlap is common.
Verify Eradication: Always confirm H. pylori eradication after treatment (retest ≥4 weeks after completing therapy, off PPI for 2 weeks).
Why This Matters Clinically
PUD is common and treatable. Missed diagnosis or failure to eradicate H. pylori leads to recurrence and complications. GI bleeding from PUD is a significant cause of morbidity and mortality. NSAID-related ulcers are preventable with appropriate gastroprotection.
Incidence & Prevalence
- Lifetime Prevalence: ~10% of Western populations
- Annual Incidence: 0.1-0.3%
- Trend: Declining due to H. pylori eradication and reduced NSAID use
- Hospitalisation for Complications: Declining but still significant
Demographics
| Factor | Details |
|---|---|
| Age | Peak 50-70 years |
| Sex | Historically Male > Female; now equalising |
| Socioeconomic | H. pylori more common in lower SES |
Causes
| Cause | Proportion | Notes |
|---|---|---|
| H. pylori | 60-70% | Declining in developed countries |
| NSAIDs/Aspirin | 20-30% | Dose-dependent; risk increased with age, steroids, anticoagulants |
| Idiopathic | 5-10% | H. pylori-negative, NSAID-negative |
| Rare | <5% | Zollinger-Ellison syndrome, Crohn's, malignancy |
Mechanism
Normal Protective Mechanisms:
- Mucus-bicarbonate barrier
- Prostaglandin-mediated blood flow
- Rapid epithelial cell turnover
- Tight junctions
Imbalance → Ulceration:
H. pylori:
- Gram-negative spiral bacterium; resides in mucus layer
- Produces urease (neutralises gastric acid locally)
- Causes chronic gastritis
- Leads to increased gastrin and acid secretion (duodenal ulcers)
- Can cause atrophic gastritis and hypochlorhydria (gastric ulcers, cancer risk)
NSAIDs:
- Inhibit COX-1 → reduced prostaglandin synthesis
- Reduced mucus and bicarbonate secretion
- Reduced mucosal blood flow
- Impaired epithelial repair
Gastric vs Duodenal Ulcer
| Feature | Gastric Ulcer | Duodenal Ulcer |
|---|---|---|
| Location | Lesser curve, antrum | Duodenal bulb (D1) |
| Pain and food | Worsened by eating | Relieved by eating, returns 2-3h later |
| Acid | Normal or low | Often high |
| H. pylori | ~70% | ~90% (historically) |
| Malignancy risk | Biopsy required | Rare (no routine biopsy) |
| Repeat OGD | Yes (confirm healing) | Not routinely |
Symptoms
Signs
Red Flags / Alarm Features
[!CAUTION] Alarm Features Requiring Urgent OGD:
- Unintended weight loss
- Dysphagia
- GI bleeding (haematemesis, melaena)
- Iron deficiency anaemia
- Persistent vomiting
- Palpable abdominal mass
- Age >55 with new-onset dyspepsia
Structured Approach
General:
- Nutritional status (weight loss)
- Pallor (anaemia from chronic blood loss)
Abdominal:
- Inspect: Scars (previous surgery)
- Palpate: Epigastric tenderness; mass (rare); peritonism (perforation)
- Auscultate: Succussion splash (gastric outlet obstruction)
Signs of Complications
| Complication | Signs |
|---|---|
| Bleeding | Pallor, tachycardia, hypotension, melaena on PR |
| Perforation | Acute severe pain, rigidity, absent bowel sounds, peritonism |
| Gastric outlet obstruction | Distension, visible peristalsis, succussion splash |
First-Line
| Test | Purpose | Notes |
|---|---|---|
| H. pylori test | Identify infection | UBT or stool antigen (stop PPI 2 weeks before) |
| FBC | Anaemia | Iron deficiency suggests chronic blood loss |
Endoscopy (OGD)
Indications:
- Alarm features
- Age >55 with new-onset dyspepsia
- Persistent symptoms despite treatment
- Suspected complications
- Gastric ulcer (to exclude malignancy; repeat to confirm healing)
At OGD:
- Biopsy ALL gastric ulcers (multiple biopsies from ulcer edge and base)
- CLO test (rapid urease test) for H. pylori
- Assess for complications (bleeding, obstruction)
Other Investigations
| Test | When |
|---|---|
| Serum gastrin | If Zollinger-Ellison syndrome suspected (multiple/atypical ulcers) |
| CT Abdomen | If perforation suspected |
| Erect CXR | Free air under diaphragm (perforation) |
H. pylori Eradication
First-Line Triple Therapy (7-14 days):
- PPI (e.g., omeprazole 20mg BD) +
- Clarithromycin 500mg BD +
- Amoxicillin 1g BD (or metronidazole 400mg BD if penicillin-allergic)
Second-Line / Rescue (Quadruple Therapy):
- PPI +
- Bismuth subsalicylate +
- Metronidazole 400mg QDS +
- Tetracycline 500mg QDS
- Duration: 14 days
Verify Eradication:
- Test ≥4 weeks after completing treatment
- Off PPI for 2 weeks before testing
- UBT or stool antigen
PPI Therapy
- Ulcer healing: PPI for 4-8 weeks
- Gastric ulcer: Repeat OGD to confirm healing
- NSAID-related ulcer: PPI for 8 weeks
NSAID Management
- Stop NSAIDs if possible
- If NSAID essential: Use lowest dose, shortest duration + PPI
- Consider COX-2 selective inhibitor (celecoxib) if high GI risk + low CV risk
Maintenance/Prevention
| Indication | Strategy |
|---|---|
| Recurrent ulcers | Long-term PPI |
| Ongoing NSAID/aspirin | Co-prescribe PPI |
| H. pylori-negative, NSAID-negative | PPI; consider motility disorder |
Major Complications
| Complication | Presentation | Management |
|---|---|---|
| GI Bleeding | Haematemesis, melaena, shock | Resuscitation, urgent OGD, IV PPI, endoscopic haemostasis |
| Perforation | Sudden severe pain, peritonism, free air on imaging | Surgical repair (omental patch); antibiotics |
| Gastric Outlet Obstruction | Projectile vomiting, weight loss, succussion splash | NG decompression, IV PPI, endoscopic balloon dilatation or surgery |
| Malignant Transformation | Gastric ulcers (not DU) | Biopsy all gastric ulcers; repeat OGD |
Bleeding Ulcer Management (Rockall/Glasgow-Blatchford)
- Resuscitation (IV fluids, blood if needed)
- IV PPI infusion (omeprazole 80mg bolus then 8mg/h)
- Urgent OGD (within 24h)
- Endoscopic therapy (injection, clips, thermal)
- Surgery if endoscopic failure
Natural History
Untreated PUD is chronic and relapsing. With H. pylori eradication, recurrence drops from ~60-80% to <5% per year. NSAID-related ulcers recur if NSAIDs continued without gastroprotection.
Outcomes
| Variable | Outcome |
|---|---|
| Ulcer healing | >90% heal with PPI |
| H. pylori eradication | ~80-95% with triple therapy |
| Recurrence after eradication | <5% per year |
| Bleeding mortality | 5-10% (higher in elderly, comorbidities) |
Key Guidelines
-
NICE CG184: Dyspepsia and GORD (2014, updated 2019) — Test-and-treat strategy.
-
Maastricht VI/Florence Consensus (2022) — H. pylori management.
Landmark Studies
Meta-analyses of H. pylori Eradication:
- Key finding: Eradication reduces ulcer recurrence from 60-80% to <5%
- Clinical Impact: H. pylori eradication now standard of care
HALT-IT Trial (2020) — Tranexamic acid in GI bleeding
- Key finding: No benefit of tranexamic acid for GI bleeding
- Clinical Impact: Tranexamic acid not recommended for GI bleeding
Evidence Strength
| Intervention | Level | Key Evidence |
|---|---|---|
| H. pylori eradication | 1a | Cochrane reviews |
| PPI for ulcer healing | 1a | Multiple RCTs |
| Endoscopy for bleeding | 1a | RCTs, guidelines |
| PPI gastroprotection with NSAIDs | 1a | RCTs |
What is a Peptic Ulcer?
A peptic ulcer is a sore that develops on the lining of your stomach (gastric ulcer) or the first part of your small intestine (duodenal ulcer). It happens when the protective lining is damaged, allowing acid to erode the tissue.
What causes it?
The two most common causes are:
- A bacterial infection (H. pylori): This bug lives in the stomach lining and causes inflammation
- Painkillers (NSAIDs): Medications like ibuprofen and aspirin can damage the stomach lining
What are the symptoms?
- Burning or gnawing pain in the upper abdomen
- Pain may be worse or better after eating
- Nausea, bloating, feeling full quickly
- Wake-up at night with stomach pain
How is it treated?
- Testing for H. pylori: Usually a breath test or stool test
- Antibiotics: If H. pylori is found, a course of antibiotics (usually two) with a stomach-acid reducing tablet
- Acid-reducing tablets (PPI): To allow the ulcer to heal
- Stop NSAIDs: If these caused the problem, they need to be stopped or taken with protection
What to expect
- Most ulcers heal within 4-8 weeks with treatment
- You'll need a follow-up test to confirm the infection is gone
- Gastric ulcers may need a repeat camera test to check they've healed
When to seek urgent help
Go to A&E immediately if:
- You vomit blood or have black, tarry stools
- You have sudden severe abdominal pain
- You feel faint, dizzy, or have a rapid heartbeat
- You have persistent vomiting
Primary Guidelines
- National Institute for Health and Care Excellence. Gastro-oesophageal reflux disease and dyspepsia in adults: investigation and management (CG184). 2014 (updated 2019). nice.org.uk/guidance/cg184
Key Consensus
- Malfertheiner P, Megraud F, Rokkas T, et al. Management of Helicobacter pylori infection: the Maastricht VI/Florence consensus report. Gut. 2022;71(9):1724-1762. PMID: 35944925
Key Trials
- HALT-IT Trial Collaborators. Effects of a high-dose 24-h infusion of tranexamic acid on death and thromboembolic events in patients with acute gastrointestinal bleeding (HALT-IT). Lancet. 2020;395(10241):1927-1936. PMID: 32563378
Further Resources
- Guts UK Charity: gutscharity.org.uk
- British Society of Gastroenterology: bsg.org.uk
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate guidelines and specialists for patient care.