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Helicobacter pylori: An Update

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Helicobacter pylori: An Update
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Helicobacter pylori: An Update

PATHCHAT Edition No. 54
April 2019
Please contact your local Ampath pathologist for more information.

Author: Dr. Ebrahim Hoosien (Clinical Microbiologist)

Introduction

What is Helicobacter pylori?

  • H. pylori is a highly prevalent curved gram-negative bacterium.
  • Seropositivity rates in South Africa range from 60% to 100%.
  • Causes >90% of duodenal ulcers and up to 80% of gastric ulcers.
  • Atrophic gastritis due to H. pylori can progress to gastric cancer.
  • The World Health Organization (WHO) classifies H. pylori as a Group I carcinogen (same category as tobacco and asbestos).
  • Environmental, host, and bacterial factors influence progression to malignancy.

📌 H. pylori infection is common, but only a subset of patients develop severe complications.

Pathogenesis & Clinical Implications

Key Pathogenic Mechanisms of H. pylori:

  1. Adheres to gastric epithelial cells.
  2. Secretes urease, converting urea into ammonia, neutralizing gastric acid, and promoting bacterial survival.
  3. Produces virulence factors (e.g., CagA, VacA) that disrupt epithelial integrity.
  4. Triggers chronic gastritis and, in some cases, leads to atrophy, intestinal metaplasia, and gastric cancer.

🔹 Possible Outcomes of H. pylori Infection:

  • Asymptomatic carriage (most common).
  • Chronic gastritis (majority of infected individuals).
  • Peptic ulcer disease (10–15%).
  • Gastric cancer (1–3%).
  • Gastric MALT lymphoma (<1%).

📌 H. pylori infection increases the risk of gastric malignancies but does not cause symptoms in all patients.

Indications for H. pylori Testing

Who Should Be Tested?

  • Patients with active peptic ulcer disease (gastric or duodenal ulcer).
  • Patients with a history of documented ulcers (unless H. pylori eradication has been confirmed).
  • Unexplained dyspepsia in high-prevalence regions.
  • Family history of gastric cancer.
  • Gastric MALT lymphoma.
  • Persistent iron deficiency anaemia with no other known cause.
  • Idiopathic thrombocytopenic purpura (ITP).

📌 Routine population screening is NOT recommended.

Diagnostic Methods for H. pylori

Non-Invasive Tests (Preferred for Initial Diagnosis & Post-Treatment Follow-Up):

  1. Urea Breath Test (UBT) (Highly Accurate):
    • Detects urease activity from H. pylori.
    • Sensitivity: ~95%
    • Specificity: ~95%
    • Requires fasting and no recent antibiotics or PPIs (stop PPIs 2 weeks prior).
  2. H. pylori Stool Antigen Test (SAT) (Alternative to UBT):
    • Detects bacterial antigens in stool.
    • Sensitivity: ~90%
    • Specificity: ~90%
    • Affected by recent antibiotics, bismuth, and PPIs (stop PPIs 2 weeks prior).
  3. Serology (Not Recommended for Active Infection):
    • Detects IgG antibodies against H. pylori.
    • Cannot distinguish between past and current infections.

Invasive Tests (Endoscopy-Based, Used If Endoscopy Is Clinically Indicated):

  1. Histology (Gold Standard for Gastritis & Cancer Risk Assessment):
    • Detects H. pylori directly.
    • Identifies atrophic gastritis, metaplasia, dysplasia.
    • Requires endoscopic biopsy.
  2. Rapid Urease Test (CLO Test):
    • Detects urease activity in biopsy tissue.
    • Sensitivity: ~90%, specificity: ~95%.
    • False negatives occur with recent antibiotic/PPI use.
  3. H. pylori Culture & Antibiotic Susceptibility Testing:
    • Rarely performed, reserved for cases of treatment failure.

📌 Urea breath test and stool antigen test are the best non-invasive diagnostic options.

Treatment of H. pylori Infection

First-Line Eradication Therapy (Triple Therapy):

  • PPI (e.g., omeprazole, esomeprazole) twice daily.
  • Clarithromycin 500 mg twice daily.
  • Amoxicillin 1 g twice daily (or metronidazole 500 mg twice daily if penicillin-allergic).
  • Duration: 14 days.

Alternative Regimens (For Regions With High Clarithromycin Resistance or Treatment Failure):

  • Bismuth-Based Quadruple Therapy:
    • PPI twice daily.
    • Bismuth subsalicylate 525 mg 4× daily.
    • Tetracycline 500 mg 4× daily.
    • Metronidazole 500 mg 3× daily.
    • Duration: 14 days.
  • Levofloxacin-Based Therapy (For Treatment Failures):
    • PPI twice daily.
    • Levofloxacin 500 mg once daily.
    • Amoxicillin 1 g twice daily.
    • Duration: 14 days.

📌 First-line therapy should be chosen based on local antibiotic resistance patterns.

Follow-Up & Confirmation of Eradication

Who Requires Post-Treatment Testing?

  • All patients treated for peptic ulcer disease.
  • Patients with gastric MALT lymphoma.
  • Patients with a history of gastric cancer or strong family history.
  • Persistent dyspeptic symptoms after treatment.

Recommended Tests for Eradication Confirmation:

  • Urea Breath Test (preferred).
  • Stool Antigen Test (alternative).
  • Timing: Perform at least 4 weeks after completing therapy.
  • Avoid PPIs for 2 weeks before testing.

📌 Routine follow-up is unnecessary for asymptomatic patients unless high-risk factors are present.

Key Takeaways for Clinicians

H. pylori is a major cause of peptic ulcer disease, gastric cancer, and MALT lymphoma.
Diagnosis should be based on Urea Breath Test or Stool Antigen Test in most cases.
Endoscopic biopsy is required for histology, CLO test, and culture in selected cases.
Triple therapy remains the first-line treatment, but resistance to clarithromycin is rising.
Bismuth-based or levofloxacin-based regimens should be considered for treatment failures.
Post-treatment eradication testing is essential in high-risk patients.

📌 Accurate diagnosis and effective treatment strategies can reduce H. pylori-related complications.