Treatment aims to eradicate H. pylori, reduce the risk of peptic ulcer disease, ulcer bleeding and gastric malignancy, and the recurrence of gastritis and peptic ulcers.
About
- First discovered by Barry Marshall in 1982
- Commonest cause of peptic ulceration and carriage is often asymptomatic
- Studies show that it is present with 95% of duodenal and 70–80% of gastric ulcers associated with it.
- NSAIDs may have an additive effect if there is co-existent H. pylori infection
- Associated with acute and chronic gastritis, gastric cancer, and gastric mucosa associated lymphoid tissue (MALT) lymphoma.
Electron Microscopy
Source
- It is likely spread person to person through touch or oral to oral or Faeco oral spread is possible.
- Commoner in older patients and in poor socioeconomic environments
- Reservoir is humans with faeco-oral and oral routes but also found in cats
Characteristics
- HP is a slow-growing spiral-shaped gram-negative highly motile bacillus and microaerophilic organism
- Possesses 4 to 6 unipolar flagella and has Urease production
- Attaches to human gastric epithelial cells and exists below the mucous layer
Virulence
- The bacterium sets off a localised neutrophilic gastritis
- Presence of cagA gene+ strain are more associated with disease [cAg= cytotoxin associated gene]
Pathogenicity
- Antral gastritis - achlorhydria and raised gastrin with increased acid secretion
- Chronic duodenal ulcer in over 95%
- Gastric ulcer in over 80%
- Gastric adenocarcinoma in over 80%
- Mucosal associated lymphoid tissue (MALT) lymphoma - regression with eradication
Investigations
- Serology to IgG however it gives no timing as to the infection whether it was recent or longstanding otherwise cheap and sensitive. Serology cannot differentiate new from an old infection
- Carbon urea breath test using 13C or 14C - urease is present in the stomach causes the formation of labelled carbon dioxide when urea is split which is absorbed into the circulation, where its presence can be determined by analysis of expired breath [overall best test] [14 C - radioactivity, 13C needs expensive mass spectrometer]. Acute H. pylori is diagnosed by a positive urea breath test and negative IgG anti-H. pylori antibodies
- Stool Helicobacter Antigen Test (SAT) can also confirm infection
- Histology - high sensitivity and specificity
- Rapid urease tests - done at endoscopy. CLO test. Cheap and quick and specific
- Culture - highly specific - slow and labourious but gold standard
Management
- First line
- Clarithromycin 500 mg BD for 1 week
- Amoxicillin 1 g BD for 1 week
- Omeprazole 20 mg BD for 2 weeks
- Second line
- Metronidazole for 1 week
- Amoxicillin 1 g BD for 1 week
- Omeprazole 20 mg BD for 2 weeks
- Treatment indicated for peptic ulcer disease and MALT lymphoma
- Routine screening for H. pylori in asymptomatic individuals is not indicated in low-risk patients
References