What is peptic ulcer disease?

Peptic ulcer disease is the presence of one or more erosions (ulcers) penetrating through the mucosal lining of the stomach (gastric ulcer) or the first part of the duodenum (duodenal ulcer). It affects approximately 5-10% of the global population during their lifetime. Ulcers form when damaging factors (gastric acid, H. pylori, NSAIDs) overwhelm the mucosal protective mechanisms (mucus layer, bicarbonate secretion, prostaglandins). The hallmark symptom is epigastric pain — typically burning, occurring 2-3 hours after meals (duodenal) or immediately after eating (gastric).

What causes peptic ulcers?

H. pylori infection (approximately 70% of duodenal, 50% of gastric ulcers): the bacterium causes chronic gastritis, disrupts mucosal defences and triggers ulceration in approximately 5-10% of infected individuals. NSAIDs (ibuprofen, aspirin, diclofenac etc): inhibit prostaglandin synthesis → impaired mucus/bicarbonate production → mucosal vulnerability; the most important cause of H. pylori-negative PUD. Hypersecretory states: Zollinger-Ellison syndrome (gastrinoma causing massive acid hypersecretion — rare but important). Stress ulcers: in critically ill ICU patients. Idiopathic: approximately 5-10% of ulcers with no H. pylori or NSAID cause.

How is H. pylori diagnosed and treated?

Non-invasive testing: urea breath test (gold standard non-invasive — H. pylori metabolises urea, releasing CO2); stool antigen test (monoclonal — accurate, cheap); serology (IgG — only indicates prior exposure, not active infection). Invasive (endoscopy): biopsy for rapid urease test, histology, culture and sensitivity. Treatment: standard triple therapy (PPI + clarithromycin + amoxicillin, 7-14 days) — efficacy declining due to clarithromycin resistance; bismuth quadruple therapy (PPI + bismuth + metronidazole + tetracycline, 10-14 days) — increasingly preferred; concomitant therapy; rifabutin triple therapy for resistant strains. Eradication should be confirmed 4+ weeks after treatment.

When is endoscopy needed?

Upper GI endoscopy (gastroscopy) is recommended: for alarm symptoms (unexplained weight loss, dysphagia, GI bleeding, anaemia, persistent vomiting, palpable mass); age >45-55 with new dyspepsia (cancer risk); all patients with upper GI bleeding; suspected gastric ulcer (biopsy required to exclude malignancy); and follow-up of gastric ulcers to confirm healing and malignancy exclusion. Duodenal ulcers do not require follow-up endoscopy if healed symptomatically.

What are the complications of peptic ulcers?

Bleeding (most common — approximately 20% lifetime risk in PUD): upper GI haemorrhage presenting as haematemesis, melaena or haematochezia. Perforation (approximately 2-10% of PUD): gastric contents spill into the peritoneal cavity causing acute abdomen — surgical emergency. Gastric outlet obstruction (rare): fibrous stricture from repeated ulceration/healing causing vomiting and weight loss. Malignant transformation: gastric ulcers have a small malignancy risk (approximately 1-3%) — biopsies mandatory; duodenal ulcers virtually never malignant.

How is peptic ulcer bleeding managed?

Peptic ulcer bleeding is a medical emergency — mortality remains approximately 3-10% despite modern treatment. Management: risk stratification (Blatchford score in emergency; Rockford score after endoscopy); IV fluid resuscitation and blood transfusion targeting Hb >7-8 g/dL; urgent upper endoscopy (within 24 hours, within 12 hours for high-risk); endoscopic haemostasis (adrenaline injection + thermal therapy or clipping — for high-risk stigmata: active bleeding, visible vessel, adherent clot); high-dose PPI infusion (80mg IV bolus then 8mg/hour infusion × 72 hours reduces rebleeding); H. pylori testing and eradication; avoidance of NSAIDs.

How does GMJ News cover peptic ulcer disease?

GMJ News covers WHO PUD burden data, H. pylori eradication evidence, clarithromycin resistance, NSAID gastroprotection, upper GI bleeding management and PPI use in high-risk settings. PUD is a common gastrointestinal condition in Georgia — relevant to PHIG's primary care and gastroenterology coverage in the Georgian Medical Journal.

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Peptic Ulcer Disease

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

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Peptic ulcer disease (PUD) — erosions or ulcers of the gastric or duodenal mucosa — affects an estimated 5-10% of the population lifetime, causing pain, bleeding (the most common cause of upper GI haemorrhage) and — in complications — perforation and gastric outlet obstruction (WHO). Helicobacter pylori infection causes approximately 70% of duodenal and 50% of gastric ulcers; NSAID use (including low-dose aspirin) is the second most important cause. H. pylori eradication heals ulcers and prevents recurrence in approximately 90% of H. pylori-associated PUD — with 7-14 day triple therapy (PPI + two antibiotics) the standard approach, though rising antibiotic resistance is reducing standard regimen efficacy.

Key messages

5-10% lifetime prevalence — H. pylori causes 70%

Peptic ulcer disease affects approximately 5-10% of the global population during their lifetime, with H. pylori infection causing approximately 70% of duodenal ulcers and 50% of gastric ulcers — making it one of the most preventable gastrointestinal conditions (WHO).

H. pylori eradication cures ulcers

Successful H. pylori eradication heals ulcers and prevents recurrence in approximately 80-90% of H. pylori-associated PUD — vastly superior to antisecretory therapy alone. Triple therapy (PPI + two antibiotics, 7-14 days) has been standard, though resistance requires regional protocol adaptation.

NSAIDs are the second major cause

NSAID use (including low-dose aspirin) is the most important cause of H. pylori-negative PUD — by inhibiting prostaglandin synthesis, impairing mucosal defence, and causing direct mucosal injury. PPI co-prescription protects high-risk NSAID users.

Bleeding — a medical emergency

Upper GI bleeding from peptic ulcer is the most common cause of acute upper gastrointestinal haemorrhage and a major cause of emergency hospital admission globally. Endoscopic haemostasis, PPI infusion and H. pylori eradication are the key interventions.

Declining incidence in HICs

PUD incidence has declined dramatically in high-income countries over the past 30-40 years — driven by declining H. pylori prevalence (improved sanitation and hygiene) and effective antisecretory therapy. However, NSAID-related ulcers are increasing with ageing populations on long-term aspirin.

PPI — the cornerstone of treatment

Proton pump inhibitors (omeprazole, pantoprazole, esomeprazole) — by suppressing gastric acid production — are the cornerstone of PUD treatment and prophylaxis. On the WHO Essential Medicines List.

Key statistics

5-10%

lifetime prevalence globally

WHO/GBD

70%

of duodenal ulcers caused by H. pylori

WHO

5-10%

of H. pylori-infected people develop PUD (lifetime)

WHO/research

80-90%

ulcer healing with H. pylori eradication

WHO/Cochrane

2-14x

increased GI bleed risk with NSAID use

WHO/Cochrane

cause of upper GI bleeding (peptic ulcer bleeding)

WHO/BSG

Peptic ulcer bleeding outcomes with modern management — endoscopic haemostasis + PPI

Source: Published clinical data. Endoscopic haemostasis + high-dose PPI significantly reduces rebleeding and mortality.

Glossary of key terms

Peptic ulcer
WHO/BSGA break in the mucosal lining of the stomach (gastric ulcer — most commonly on the lesser curvature) or duodenum (duodenal ulcer — most commonly in the first part of the duodenum) extending through the muscularis mucosae. Caused by an imbalance between damaging factors (acid, pepsin, H. pylori, NSAIDs) and protective factors (mucus, bicarbonate, prostaglandins).

Helicobacter pylori (H. pylori)
IARC/WHO EMLA Gram-negative spiral bacterium colonising the gastric mucosa — IARC Group 1 carcinogen; the most common cause of PUD. Disrupts mucosal defences and triggers gastritis. Eradication with 7-14 day antibiotic combinations (triple therapy: PPI + clarithromycin + amoxicillin; quadruple therapy for resistant strains) heals ulcers and prevents recurrence.

NSAIDs (non-steroidal anti-inflammatory drugs)
WHOCyclooxygenase (COX) inhibitors — ibuprofen, naproxen, diclofenac, aspirin — that reduce prostaglandin synthesis, impairing gastric mucosal protection. Increase PUD risk 2-14 fold. COX-2 selective NSAIDs (celecoxib) have lower GI risk. PPI co-prescription reduces NSAID-related GI risk by approximately 50-66%.

PPI (proton pump inhibitor)
WHO EMLThe most effective acid-suppressing medications — omeprazole, pantoprazole, esomeprazole, lansoprazole. WHO Essential Medicines. Standard treatment for PUD; combined with antibiotics for H. pylori eradication; used for prophylaxis in NSAID users, ICU patients and post-upper GI bleeding.

Peptic ulcer bleeding
WHO/BSGThe most common and most serious complication of PUD — presenting as haematemesis (vomiting blood), melaena (black tarry stool) or haematochezia (bright red rectal blood). Managed with: urgent upper endoscopy for diagnosis and haemostasis (adrenaline injection, thermal coagulation, clipping); high-dose IV PPI infusion; H. pylori testing and eradication.

Clarithromycin resistance
WHO/ESGEIncreasing H. pylori resistance to clarithromycin (>15-20% in many European countries) is reducing efficacy of standard triple therapy. Bismuth-containing quadruple therapy or concomitant therapy (PPI + 3 antibiotics) is now recommended in high-resistance settings. Culture and susceptibility testing before H. pylori treatment is increasingly recommended.

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