H. pylori Infection

Overview.

Helicobacter pylori colonises the stomach of approximately 50% of the world's population. While most carriers remain asymptomatic, H. pylori is the primary cause of peptic ulcer disease and the strongest identified risk factor for gastric adenocarcinoma. Testing and eradication is recommended for all symptomatic patients and certain at-risk groups. Importantly, serology alone cannot distinguish active from past infection — stool antigen or urea breath test is preferred.

H. pylori is a gram-negative, spiral-shaped bacterium that colonises the gastric mucosa. It survives the acidic stomach environment by producing urease, which converts urea to ammonia, creating a local alkaline microenvironment. Chronic infection triggers a cascade from chronic gastritis to atrophic gastritis to intestinal metaplasia, and in a subset, to dysplasia and gastric cancer. This progression takes decades in most cases.

Prevalence: Approximately 50% of the global population is infected. Prevalence varies by region: >70% in developing countries, 20-40% in Western countries. Acquisition typically occurs in childhood. Prevalence is declining in developed countries due to improved sanitation.

Medical name: Helicobacter pylori Infection

Symptoms.

Early warnings

• Recurrent epigastric pain or burning (dyspepsia)
• Nausea and reduced appetite
• Early satiety
• Unexplained iron deficiency anaemia
• Bloating and belching

Classic symptoms

• Epigastric pain (burning, gnawing) — worse with fasting, improved with meals (duodenal ulcer pattern)
• Nausea and vomiting
• Bloating and early satiety
• Most H. pylori carriers are asymptomatic
• Peptic ulcer: epigastric pain, haematemesis (coffee-ground vomiting), melena (black stools)
• Gastric cancer symptoms (late): weight loss, anorexia, early satiety, dysphagia

Progression

Most infected individuals remain asymptomatic. Approximately 10-20% develop peptic ulcers over their lifetime. Gastric cancer develops in 1-3% of infected individuals, typically after decades of chronic infection through the Correa cascade: chronic gastritis → atrophic gastritis → intestinal metaplasia → dysplasia → carcinoma. Eradication therapy eliminates the ulcer recurrence risk and reduces (but does not eliminate) gastric cancer risk.

Risk factors.

• Childhood acquisition in areas of poor sanitation
• Household crowding
• Lower socioeconomic status
• First-generation immigrants from high-prevalence regions
• Family member with gastric cancer
• Personal history of peptic ulcer disease

Lab interpretation.

Key biomarkers

• H. pylori Stool Antigen — Positive = active infection; preferred non-invasive test alongside urea breath test (primary)
• hs-CRP — May be mildly elevated with active gastritis (supportive)
• Ferritin — May be low — H. pylori is an underrecognised cause of iron deficiency anaemia (supportive)

Diagnostic criteria

• Stool antigen test (monoclonal): sensitivity >95%, specificity >95% — preferred first-line non-invasive test
• Urea breath test (UBT): sensitivity >95%, specificity >95% — equivalent to stool antigen
• Serology (IgG): confirms exposure but CANNOT distinguish active from past/eradicated infection — not recommended for diagnosis or test of cure
• Rapid urease test (CLOtest): performed on endoscopic biopsy — gold standard during gastroscopy
• Must stop PPIs for 2 weeks and antibiotics for 4 weeks before stool antigen or UBT to avoid false negatives

When & next steps.

When to test

• Persistent dyspepsia or epigastric pain
• Active or history of peptic ulcer disease
• Before starting long-term NSAID or aspirin therapy
• Unexplained iron deficiency anaemia after other causes excluded
• First-degree relative with gastric cancer
• Idiopathic thrombocytopenic purpura (ITP)
• MALT lymphoma (eradication is first-line treatment)
• Immigration from high-prevalence region with GI symptoms

If suspected

• Order H. pylori stool antigen test (preferred) or urea breath test
• Ensure patient has stopped PPIs for ≥2 weeks and antibiotics for ≥4 weeks before testing
• Do NOT use serology alone for diagnosis — it cannot distinguish active from past infection
• If gastroscopy planned: rapid urease test (CLOtest) on biopsy

If confirmed

• Eradication therapy: bismuth quadruple therapy (PPI + bismuth + metronidazole + tetracycline) x 14 days — ACG recommended first-line in most regions
• Alternative: concomitant therapy (PPI + clarithromycin + amoxicillin + metronidazole) x 14 days
• Test of cure: stool antigen or UBT ≥4 weeks after completing therapy (NOT serology)
• If eradication fails: second-line therapy with different antibiotic class; consider culture with susceptibility testing
• Verify eradication in ALL treated patients — do not assume success

FAQs.

Important note.