see also clinically important bacteria; gastro-oesophageal reflux; peptic ulcer disease; Dyspepsia;

• H. pylori is the dominant factor in the multifactorial disease peptic ulceration & its eradication should decrease incidence of DU in humans by over 90%;
• Most people infected with H. pylori are asymptomatic but infection confers a lifetime risk of peptic ulcer disease of 15% to 20%, and of gastric cancer of up to 2%.
  • Gastric cancer prevalence is falling in Australia in parallel with a long-term decline in H. pylori prevalence.
  • High-risk subgroups for developing gastric cancer are those with a greater risk of infection (especially migrants from high prevalence areas, older people and those with a family history).
  • Gastric mucosa-associated lymphoid tissue (MALT) lymphomas are uncommon but most are caused by H. pylori infection. Eradication of the organism when the lymphoma is still at a low-grade stage usually results in regression and cure.
• All people infected develop active chronic gastritis, although there is an inconstant relationship between the presence of H. pylori gastritis and symptoms.
• unlike patients with ulcers, only a minority of people with H. pylori gastritis and symptoms (nonulcer dyspepsia) will have sustained relief of their symptoms after eradication therapy.
• Colonisation is specific to mucous layer covering gastric epithelial cells resulting in chronic gastritis in 20-40% & if duodenum has undergone metaplasia to a gastric-like epith. ? due to hyperacidity, then DU may result as H.pylori is found in 95% of DU;
• H. pylori appear to bind to gastric lining via adhesin protein called SabA
• H.pylori induces hypochlorhydria that can persist > 8months after infection & can remain chronically, causing atrophic gastritis.
• hypochlorhydria is an important risk factor for cholera in developing countries.
• it is thought that H. pylori is transmitted by oral route amongst toddlers who then become life long carriers.
• the only consistent source of H.pylori is gastric mucosa & thus spread is likely to be by vomitus including gastro-oesophageal reflux; ?? role of house fly???
• Culture for H. pylori and testing for antibiotic sensitivity have little role in clinical decision making (but remains important for surveillance purposes)

• in developing countries up to 80% of children under age 10yrs are infected, compared with 10-50% in developed countries.
• adults < 30 yrs: 10-20% in developed countries;
• infection risk increases with family contacts (esp. number of infected siblings - ie. usually are the older siblings), instituitional care, poor socioeconomic conditions
• although ~60% of 60 yr old adults are infected, adults rarely become infected with seroconversion rates of ~0.4% per person-year
• children > 5yrs & adults rarely become reinfected (2%/yr) after successful treatment despite their being a high prevalence of infection in siblings/families of 65-75%, this could be due to either:
  • immunity
  • improved sanitary habits with age ⇒ less exposure to vomitus

• peptic ulcer disease - past or present - Rx heals ulcers and reduces relapse
• Dyspepsia - Rx may reduce symptoms and long-term risks of peptic ulcer disease and gastric cancer
• non-steroidal anti-inflammatory drugs (NSAIDs) and aspirin (acetylsalicylic acid) users - Rx reduces risks of peptic ulcer disease and gastric bleeding
• atrophic gastritis and intestinal metaplasia - Rx reduces long-term risk of gastric cancer
• patients requiring long-term acid suppression - Rx reduces progression of intestinal metaplasia
• close relatives of patients with gastric cancer - Rx reduces long-term risk of gastric cancer
• patients with treated early gastric cancer - Rx reduces risk of further gastric cancer
• low-grade gastric MALT lymphoma - Rx induces regression of lymphoma

• Assessment of the outcome of eradication therapy is mandatory in cases of complicated ulcer disease or where cessation of maintenance therapy for ulcer disease is contemplated. In other situations, assessment of the outcome of therapy is recommended as this guides subsequent management, provides reassurance when negative, and has medicolegal implications.
• Post-treatment testing is best done with a C^13- or C^14-urea breath test. The C^13-urea breath test is not radioactive and is preferable for women of childbearing age and children. Prior to breath testing, no antibiotics or bismuth should be taken for at least 1 month and proton pump inhibitors should be suspended for 2 weeks if possible to minimise the chance of false negative results.
• Follow-up endoscopy is usually not required. The exceptions are for gastric ulcers (to exclude malignancy and to document healing), and for some complicated duodenal ulcers such as ulcers that were clinically silent before presentation with bleeding.

• use a 7 day combination pack containing:
  • PPI (either omeprazole or esomeprazole) 20mg bd for 7 days, PLUS,
  • amoxycillin 1g bd for 7 days, PLUS
  • clarithromycin 500mg bd for 7 days
• if penicillin hypersensitive:
  • as above but substitute metronidazole 400mg for 7days instead of amoxycillin (gives 80% eradication success)
  • or, use 2nd line Rx

• secondary clarithromycin resistance is very common after failure of first-line therapy THUS avoid clarithromycin
• PPI in standard dose bd for 7-14 days, PLUS
• colloidal bismuth subcitrate 120 mg orally, 4 times daily for 7 or 14 days, PLUS
• tetracycline 500 mg orally, 4 times daily for 7 or 14 days, PLUS
• metronidazole 400 mg orally, 3 times daily for 7 or 14 days
• Reported success rates for this combination are about 80% to 85%. These results are unaffected by pre-treatment metronidazole resistance.
• Adverse effects are common and include nausea, loose or discoloured stools and taste disturbance.

• PPI (either omeprazole or esomeprazole) 20mg bd for 10 days, PLUS,
• amoxycillin 1g bd for 10 days, PLUS
• rifabutin 150 mg orally, twice daily for 10 days
• Eradication rates of about 60% to 70% have been reported.
• This combination should only be used by prescribers familiar with rifabutin.