<i>Helicobacter pylori</i>

Helicobacter pylori

Helicobacter pylori is a Gram-negative bacteria associated with a variety of gastrointestinal problems, principally peptic ulcer disease.

Pathophysiology

• Helicobacter pylori has 2 main mechanisms to survice in the acidic gastric environment:
  • chemotaxis away from low pH areas, using its flagella to burrow into the mucous lining to reach the epithelial cells underneath
  • secretes urease
    urease
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    → urea converted to NH₃ → alkalinization of acidic environment → increased bacterial survival
• pathogenesis mechanism:
  • Helicobacter pylori releases bacterial cytotoxins (e.g. CagA toxin) → disruption of gastric mucosa

Associations

• peptic ulcer disease
  • 95% of duodenal ulcers
  • 75% of gastric ulcers
• gastric cancer
• B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
• atrophic gastritis

The role of H pylori in Gastro-oesophageal reflux disease (GORD) is unclear - there is currently no role in GORD for the eradication of H pylori

Helicobacter pylori eradication may be achieved with a 7-day course of a proton pump inhibitor (PPI) + 2 antbiotics:

• first-line: PPI + amoxicillin + (clarithromycin OR metronidazole)
  H. pylori eradication: - PPI + amoxicillin + clarithromycin, or - PPI + metronidazole + clarithromycin
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  Importance: 92
  • if ongoing symptoms after first line treatment: PPI + amoxicillin+ (clarithromycin OR metronidazole, whichever was not used first line)
    if ongoing symptoms after first line treatment: PPI + amoxicillin+ (clarithromycin OR metronidazole, whichever was not used first line)
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• if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin

+PassMedicine Notes

Helicobacter pylori is a Gram-negative bacteria associated with a variety of gastrointestinal problems, principally peptic ulcer disease.

Pathophysiology

• Helicobacter pylori has 2 main mechanisms to survice in the acidic gastric environment:
• chemotaxis away from low pH areas, using its flagella to burrow into the mucous lining to reach the epithelial cells underneath
• secretes urease --> urea converted to NH3 --> alkalinization of acidic environment --> increased bacterial survival
• pathogenesis mechanism:
• Helicobacter pylori releases bacterial cytotoxins (e.g. CagA toxin) --> disruption of gastric mucosa

Associations

• peptic ulcer disease
• 95% of duodenal ulcers
• 75% of gastric ulcers
• gastric cancer
• B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
• atrophic gastritis

The role of H pylori in Gastro-oesophageal reflux disease (GORD) is unclear - there is currently no role in GORD for the eradication of H pylori

Helicobacter pylori eradication may be achieved with a 7-day course of a proton pump inhibitor (PPI) + 2 antbiotics:

• first-line: PPI + amoxicillin + (clarithromycin OR metronidazole)
• if ongoing symptoms after first line treatment: PPI + amoxicillin+ (clarithromycin OR metronidazole, whichever was not used first line)
• if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin