Peptic Ulcer Disease | H. pylori | Management

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Introduction

Peptic ulcers are defined by a break in the mucosal lining of the stomach or duodenum of more than 5 mm in diameter and extending into the submucosa.¹

Peptic ulcer disease (PUD) is a common condition, with duodenal ulcers four times more common than gastric ulcers.² The incidence of gastric ulcers peaks between the ages of 50 and 70 years old, whereas duodenal ulcers tend to occur earlier, between the ages of 30 and 50 years old.

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Aetiology

Peptic ulcers form due to a breakdown in the submucosa, which lines the stomach and duodenum. The stomach lining secretes bicarbonate-rich mucus, which protects the underlying mucosa from the acidic contents of the stomach and digestive enzymes.

The breakdown of the submucosa leaves the surfaces vulnerable to acid produced by the stomach, leading to ulcers.

Causes of PUD include:

• Helicobacter pylori (H. pylori) infection: a gram-negative bacterium responsible for increasing gastric acid secretion, causing mucosal damage
• NSAIDs: impair mucosal defences by inhibiting cyclooxygenase 1 (COX-1), reducing prostaglandin production
• Cigarette smoking: increases gastric acid production and decreases prostaglandin production. Prostaglandins are gastroprotective by promoting mucus production and inhibiting acid secretion.
• Delayed gastric emptying: seen in gastroparesis, a complication of type 1 diabetes mellitus
• Critically ill patients: prone to developing stress ulcers, known as Curling’s ulcers. These may lead to significant upper gastrointestinal bleeding.
• Zollinger-Ellison syndrome: caused by a gastrin-secreting tumour (usually in the duodenum or pancreas), leading to excessive acid secretion and multiple ulcers. Consider if ulcers persist despite PPI therapy.
• Illicit drug abuse: particularly cocaine, may cause perforation and peritonitis needing surgical intervention ³

Clinical anatomy

Gastric ulcers

The stomach starts at the inferior oesophageal sphincter, which marks the transition between the oesophagus and the stomach. Most gastric ulcers are found in the pyloric antrum and the lesser curvature of the stomach.

The lesser curvature is supplied by the left and right gastric arteries, which branch off the coeliac trunk. Therefore, ulcers on the lesser curvature can lead to massive gastrointestinal bleeding.

Duodenal ulcers

The pyloric sphincter controls the exit of chyme (food and gastric acid mixture). It is located at the end of the stomach and marks the boundary between the stomach and the duodenum.⁴

The duodenum is the first part of the small intestine and receives chyme from the pyloric sphincter.

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Risk factors

Risk factors for peptic ulcer disease vary based on location.

Table 1. Risk factors specific to gastric and duodenal ulcers.

Gastric ulcers	Duodenal ulcers
Non-steroidal anti-inflammatory drugs H. pylori infection Cigarette smoking Zollinger-Ellison syndrome Delayed gastric emptying Extreme stress and alcohol consumption	H. pylori infection Non-steroidal anti-inflammatory drugs Selective serotonin reuptake inhibitors Cigarette smoking

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Clinical features

History

Typical symptoms of PUD include:

• Dyspepsia: symptoms lasting for four or more weeks, including upper abdominal pain, heartburn and acid reflux
• Early satiety: sensation of fullness after eating less than usual
• Nausea and vomiting
• Loss of appetite
• Fatigue, pica, and koilonychia: in anaemia ⁵

Clinical examination

A complete abdominal examination is required in all cases of suspected PUD.

Typical clinical findings in PUD include:

• Epigastric tenderness: most common finding
• Percussion tenderness
• Melaena: if bleeding is present
• Systemic features: pallor, weight loss

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Differential diagnoses

Differential diagnoses to consider in suspected PUD include:

• Gastric cancer: symptoms include early satiety, nausea, haematemesis and melena. Systemic symptoms may also be present, such as weight loss and night sweats.
• Gastritis: symptoms include upper abdominal pain and vomiting. History may include recent infections, medications such as NSAIDs, or irritants such as alcohol and smoking.
• Gastro-oesophageal reflux disease: symptoms include chronic cough, sour taste, globus sensation, hoarseness, chest pain, and dysphagia.

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Investigations

Laboratory investigations

Relevant laboratory investigations include:

• Full blood count: may show anaemia from gastrointestinal bleeding
• Urea and electrolytes: may show dehydration and reduced renal function
• Liver function tests: to exclude alternative causes of epigastric pain (e.g. pancreatic or hepatobiliary causes)
• Fasting gastrin level: elevated in Zollinger-Ellison syndrome
• Group & save and crossmatch: in an upper gastrointestinal bleed

Imaging

Relevant imaging includes:

• Upper gastrointestinal endoscopy: gold standard with biopsies taken for rapid urease test to detect H. pylori and histology to exclude malignant changes
• Contrast CT abdomen and pelvis: if concerns of abscess formation or perforation

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Management

This focuses on the management of a non-bleeding ulcer. Actively bleeding PUD should be managed as an upper gastrointestinal bleed.

Conservative management

Lifestyle advice recommended to reduce recurrence includes:

• Smoking cessation
• Reducing alcohol to within recommended limits (14 units/week)
• Weight loss
• Avoiding foods that irritate the gastric mucosa (e.g. coffee, chocolate, spicy foods, tomatoes)
• Eating smaller, more frequent meals, with the last meal at least three hours before bed
• Medication review: NSAIDs, aspirin, bisphosphonates, potassium supplements and SSRIs all irritate the gastric mucosa

Medical management

H. pylori negative

Treatment is an 8 week course of a proton pump inhibitor (PPI), such as omeprazole.

This reduces the amount of stomach acid secreted, thereby reducing mucosal irritation and allowing the ulcer to heal.

H. pylori positive

Eradication therapy should be initiated with a PPI and two antibiotics for 7 days.

Triple therapy typically consists of:

• Twice daily PPI
• Amoxicillin
• Clarithromycin

In a penicillin allergy, metronidazole is an alternative to amoxicillin.

Retesting for H. pylori is not routinely recommended and is only indicated in certain circumstances, including:

• Poor compliance with eradication therapy
• Use of aspirin without a PPI
• Failure to stop PPI or antibacterial treatment before the initial test
• Severe or recurrent symptoms ⁸

The urea breath test is preferred for retesting, as it is most accurate.

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Complications

Complications of peptic ulcer disease include:

• Upper GI haemorrhage: haematemesis (may be called ‘coffee ground vomit’ due to blood clots), melena (black, tarry stool) and iron deficiency anaemia. This is the most common complication of peptic ulcer disease.
• Perforation: peritonitis, shock and sudden severe abdominal pain. The abdomen may be rigid on examination. This is a life-threatening complication with a 25% fatality rate, requiring urgent surgical repair.
• Gastric outlet obstruction: persistent vomiting, early satiety and weight loss, caused by scarring from ulceration
• Malignancy: chronic peptic ulcers can undergo dysplasia and become malignant ⁷

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Reviewer

Professor Bhaskar Kumar

Consultant Oesophagogastric Surgeon

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Editor

Dr Jamie Scriven

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References

1. BMJ Best Practice. Peptic ulcer disease. 2025. Available from: [LINK].
2. NICE CKS. Dyspepsia – proven peptic ulcer: Prevalence. 2024. Available from: [LINK].
3. NICE CKS. Dyspepsia – unidentified cause: Definition. 2024. Available from: [LINK].
4. NICE CKS. Dyspepsia – proven peptic ulcer: Risk factors. 2024. Available from: [LINK].
5. Eastwood GL. The Role of Smoking in Peptic Ulcer Disease. Journal of Clinical Gastroenterology. 1988. Available from: [LINK].
6. NICE. Suspected cancer: recognition and referral. 2025. Available from: [LINK].
7. NICE CKS. Dyspepsia – proven peptic ulcer: Prognosis. 2024. Available from: [LINK].
8. Public Health England. Helicobacter pylori in dyspepsia: test and treat. 2019. Available from: [LINK].

Image references

• Figure 1. Betts JG, Young KA, Wise JA, et al. Figure 23.15 Stomach. Anatomy and Physiology. OpenStax. 2013. Licence: [CC BY 4.0]. Available from: [LINK].
• Figure 2. Jiao B. Uncomplicated gastric ulcer. Radiopaedia. 2023. Licence: [CC BY-NC-SA 3.0]. Available from: [LINK].
• Figure 3. Knipe H. Acute peptic duodenal ulcer (gross pathology). Radiopaedia. 2014. Licence: [CC BY-NC-SA 3.0]. Available from: [LINK].

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