Key Facts

Helicobacter pylori is one of the most common chronic bacterial infections worldwide, affecting approximately half the global population. In the UK, prevalence is ~30% and falling. It is the major aetiological factor in peptic ulcer disease and gastric cancer.

Epidemiology

Global prevalence is approximately 50% but varies enormously by country and socioeconomic status. UK prevalence is ~30% overall, higher in older adults (birth cohort effect — declining prevalence). Prevalence is higher in lower socioeconomic groups, crowded living conditions, and among immigrants from high-prevalence countries. Infection is usually acquired in childhood and persists unless treated.

Aetiology

Transmission is person-to-person via oral-oral, faecal-oral, or gastro-oral routes. Childhood acquisition is most common, associated with household crowding. The bacterium has evolved sophisticated mechanisms to colonise the hostile gastric environment.

Pathophysiology

H. pylori colonises the gastric antral mucosa beneath the mucus layer. Key virulence factors:

• Urease: converts urea to ammonia + CO₂, creating an alkaline microenvironment protecting the organism; ammonia itself damages epithelium
• CagA (cytotoxin-associated gene A): injected into epithelial cells via type IV secretion system; disrupts cell signalling, promotes inflammation and carcinogenesis
• VacA (vacuolating cytotoxin A): induces apoptosis and immune evasion
• Flagella: motility through mucus layer

Chronic infection causes:

1. Antral-predominant gastritis → increased gastrin → increased acid → duodenal ulcer
2. Pan-gastritis/corpus gastritis → gastric atrophy → intestinal metaplasia → dysplasia → adenocarcinoma (Correa cascade)
3. MALT lymphoma: chronic antigenic stimulation of gastric lymphoid tissue

Asymptomatic

• Most H. pylori infections are asymptomatic (~80%)
• Incidental finding on testing for dyspepsia

Symptomatic

• Dyspepsia (epigastric pain, bloating, nausea)
• Peptic ulcer disease symptoms (see PUD entry)
• Iron deficiency anaemia (unexplained — H. pylori impairs iron absorption)
• Idiopathic thrombocytopaenic purpura (ITP) — association recognised

Red Flags

• Alarm symptoms (dysphagia, weight loss, GI bleeding, anaemia) — require OGD
• Symptoms persisting despite H. pylori eradication — consider alternative diagnosis
• Family history of gastric cancer in H. pylori-positive patient

Bedside

• ¹³C-Urea breath test (UBT): first-line non-invasive test; sensitivity/specificity >95%; must stop PPI ≥2 weeks, antibiotics ≥4 weeks before testing
• Stool antigen test (monoclonal): alternative first-line; sensitivity/specificity ~95%; same preparation requirements

Bloods

• H. pylori serology (IgG): indicates exposure but NOT active infection — does not distinguish current from past infection; NOT recommended for diagnosis or eradication confirmation
• FBC: iron deficiency anaemia

Imaging

• OGD: not first-line for H. pylori testing alone; indicated if alarm features or age ≥55 with new dyspepsia

Special Tests

• CLO test (rapid urease test): performed on gastric biopsy at OGD; results within 1-24 hours
• Histology: Sydney protocol biopsies — identifies H. pylori organisms, gastritis pattern, atrophy, intestinal metaplasia
• Culture and sensitivity: for antibiotic resistance testing (mainly research; increasingly used for clarithromycin resistance)
• PCR: emerging for resistance gene detection

Non-pharmacological

• Test-and-treat strategy (NICE CG184): for patients with dyspepsia without alarm features and age <55
• Test and treat: if positive, eradicate; retest to confirm eradication

Pharmacological

• First-line eradication (7 days):
  • PPI (omeprazole 20 mg BD or lansoprazole 30 mg BD) + amoxicillin 1 g BD + clarithromycin 500 mg BD
  • If penicillin allergic: PPI + clarithromycin 500 mg BD + metronidazole 400 mg BD
• Second-line (if first-line fails — 7 days):
  • PPI + amoxicillin 1 g BD + metronidazole 400 mg BD
  • OR bismuth quadruple therapy: PPI + bismuth subsalicylate 524 mg QDS + metronidazole 400 mg TDS + tetracycline 500 mg QDS for 14 days
• Third-line: guided by culture and sensitivity if available
• Confirm eradication: UBT or stool antigen ≥4 weeks after completing eradication and ≥2 weeks off PPI
• Gastric MALT lymphoma: H. pylori eradication alone achieves complete remission in >75% of early-stage gastric MALT lymphoma

Surgical/Interventional

• Not applicable for H. pylori infection itself
• Surgery for complications (perforation, bleeding, malignancy)

Referral Criteria

• Gastroenterology referral for eradication failure after 2 courses
• OGD for alarm symptoms or age ≥55 with new dyspepsia
• Gastric cancer MDT if malignancy detected
• Consider screening first-degree relatives of gastric cancer patients

Eradication success rate is ~85% with first-line triple therapy, ~90%+ with bismuth quadruple therapy. Clarithromycin resistance is rising in the UK (~15-20%) and is the main cause of treatment failure. Successful eradication cures >95% of H. pylori-associated duodenal ulcers. Reinfection rate in the UK is <1% per year. H. pylori eradication reduces gastric cancer risk by approximately 30-40% in infected individuals. Early-stage gastric MALT lymphoma has >75% complete remission with eradication alone.

H. Pylori Eradication Regimens Summary

Testing Summary