Internal Diseases and Therapy · MU Sofia

91. Helicobacter pylori infection

Covers Helicobacter pylori as a gram-negative organism linked to peptic ulcers, chronic gastritis and gastric cancer risk, and how it damages the stomach and duodenal lining through urease, ammonia, toxins and inflammation. Also outlines diagnosis by stool antigen testing and first-line and quadruple eradication regimens, with a summary of triple and second-line treatment including penicillin-allergy alternatives. A four-step diagram of the infection process is included.

Inside: 2 sections · 1 labelled picture · 15 flashcards · 3 min

Topic 92 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 2 sections, about 443 words (3 min of reading), with 15 flashcards.

In this note

  1. Helicobacter pylori infection
  2. Treatment of Helicobacter pylori infection

Helicobacter pylori infection

Chronic gastritis and gastric and duodenal ulcers are a result (commonly) of H.pylori. First we will consider H.pylori as an organism and the methods for analysis and eradication, before considering gastritis in all forms.

Helicobacter pylori in the GI tract has a very close association with ulcer diseases (85% of patients with ulcers have H.pylori), however most persons with H.pylori infection are unaware they have it. The population risk of H.pylori is about 50%, of which 5-15% will form a peptic acid disease (chronic gastritis or ulcers). Furthermore, H.pylori infection confers a 2% risk of gastric adenocarcinoma!

Helicobacter pylori is a gram negative, microaerophilic bacterium usually found in eh stomach (rather than the duodenum). It is helical and motile, as well as oxidase, catalase and urease +ve. The bacteria burrow into the mucus lining of the stomach to reach the

epithelial cells, which it adheres to with adhesins. H.pylori also produces lots of urease which neutralizes the acid in the stomach allowing it to survive.

H.pylori affects the stomach and duodenal linings in several ways:

  • Ammonia production which is toxic to epithelial cells, as are proteases and cytotoxins it produces
  • H.pyloris presents triggers an inflammatory response, which causes mucosal damage
  • These changes mean that the peptic acid of the stomach is able to break through the mucosal barrier and damage the epithelial cells direct
  • H.pyloris ability to promote cancer is thought to be one of two mechanisms:
  • Production of free radicals near H.pylori increase cell mutation
  • The epigenetic pathway proposed suggests that there is enhancement of the transformed host cell phenotype meaning alterations in cell proteins

Image: “H pylori ulcer diagram en” by Y_tambe, CC BY-SA 3.0, via Wikimedia Commons.

Diagnosis

  • Testing is done in peptic acid diseases, or those with first-degree relatives who have had gastric adenocarcinoma
  • Stool tests are the most common test (stool antigen test)
  • These can be immunochromatography or enzyme immunoassay methods

H.pylori eradication protocols

  • First line
  • Oral proton pump inhibitor (e.g. omeprazole 20-40mg) + clarithromycin (500mg) and amoxicillin (1g) OR metronidazole (500mg) if allergic to penicillin
  • Twice daily for 7 days
  • Alternate first line (where high clarithromycin and metronidazole resistance)
  • Quadruple therapy: PPI (e.g. omeprazole) + bismuth (525mg) + tetracycline (500mg) + metronidazole (250mg) OR tinidazole
  • Four times daily, 10-14 days (97% eradication at 14 days)

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