H. Pylori

Introduction

Helicobacter pylori is a gram-negative, spiral-shaped bacterium that colonises the gastric mucosa. It is a major cause of gastritis, peptic ulcer disease, and is associated with an increased risk of gastric cancer and MALT lymphoma.

Peak Incidence

• Most commonly affects individuals aged 40 years and above.
• Higher prevalence in low socioeconomic and overcrowded environments, often acquired in childhood.

Pathophysiology

• H. pylori produces urease, which hydrolyses urea into ammonia, neutralising gastric acid and allowing bacterial survival.
• Chronic infection triggers mucosal inflammation, leading to gastritis, peptic ulceration, and, in some cases, metaplastic or neoplastic transformation of gastric epithelium.

Symptoms

H. pylori infection is often asymptomatic but may present with:

• Dyspepsia – Indigestion with upper abdominal discomfort
• Epigastric pain – Burning or gnawing, often worse on an empty stomach
• Bloating
• Nausea and vomiting
• Loss of appetite
• Unintentional weight loss – Red flag symptom
• Gastro-oesophageal reflux-like symptoms – In some cases

Signs

• Epigastric tenderness on abdominal examination
• Features of anaemia, including:
  • Pallor
  • Angular cheilitis
  • Glossitis
  • Koilonychia
• Signs of perforation (in complicated ulcers):
  • Severe abdominal pain
  • Guarding and rebound tenderness

Diagnosis

First-Line Non-Invasive Tests

• Urea breath test
  • Detects urease activity.
  • Proton pump inhibitors (PPIs) must be stopped at least 2 weeks before testing to avoid false negatives.
• Stool antigen test
  • Detects H. pylori antigen in faeces.
  • Also requires cessation of PPIs for at least 2 weeks.

Endoscopic Evaluation (for high-risk patients)

• Rapid urease test (CLO test) – Performed on gastric biopsy samples.
• Histology and culture – Allows visual confirmation and testing for antibiotic resistance.
• Indications for urgent (2-week wait) endoscopy:
  • Red flag symptoms (e.g. unexplained weight loss, GI bleeding, persistent vomiting, dysphagia, family history of gastric cancer)
  • New-onset dyspepsia in patients aged >55 years

Complications

• Peptic ulcer disease – H. pylori is implicated in ~90% of duodenal ulcers and ~75% of gastric ulcers
• Gastric cancer – Especially adenocarcinoma, via chronic gastritis and atrophic changes
• MALT lymphoma – Low-grade B-cell lymphoma associated with chronic H. pylori infection
• Atrophic gastritis – Chronic inflammation leading to loss of acid-producing cells
• Iron-deficiency anaemia – From chronic mucosal bleeding
• Vitamin B12 deficiency – Secondary to impaired intrinsic factor production from mucosal damage

Management

Lifestyle Modifications

• Improve hygiene and sanitation to reduce faeco-oral transmission
• Avoid unnecessary NSAID use
• Reduce alcohol consumption and stop smoking, as both can exacerbate gastritis

First-Line Treatment (Triple Therapy) – 7 to 14 days

• If no penicillin allergy:
  • Proton pump inhibitor (e.g. omeprazole or lansoprazole)
  • Amoxicillin
  • Clarithromycin or metronidazole (avoid repeating metronidazole if recently used)
• If penicillin allergic:
  • Proton pump inhibitor
  • Clarithromycin
  • Metronidazole

Second-Line Treatment

• Repeat triple therapy with an alternative antibiotic (e.g. switch from clarithromycin to metronidazole or vice versa)

Third-Line Treatment (Refractory Cases)

• Consider antibiotic susceptibility testing
• Refer to gastroenterology if infection persists after two eradication attempts

Follow-Up

• Test for eradication 4–8 weeks after completing therapy

  • Preferred method: urea breath test
  • Ensure PPIs have been discontinued at least 2 weeks before testing