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Helicobacter pylori gastritis

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Infection by H. pylori causes H. pylori gastritis, sometimes called B (bacterial) gastritis or environmental metaplastic atrophic gastritis (EMAG). This is a form of chronic atrophic gastritis and present in a whopping 2/3 of the population worldwide. The prevalence is decreasing due to sanitation and antibiotics, but it is still 90% in developing countries. While the infection usually occurs in childhood in developing countries, it usually occurs in adulthood in industrialized countries.

In most cases, the infection is asymptomatic and lasts the whole life. In those that have symptoms can the consequences however be fatal. The infection gives a 15-20 % lifetime risk of peptic ulcer disease. It has also been linked to 70 % of gastric cancers, especially intestinal types and gastric MALT lymphoma.

Microbiology

Helicobacter pylori is a spiral shaped bacterium which resides in the gastric mucus, adhering to the epithelial cells of the gastric mucosa and causing local inflammation. This bacterium produces the virulence factor urease, which forms ammonia, a base which neutralises the acid around the bacterium, allowing it to survive in the acidic environment of the stomach. However, this urease activity is toxic to the epithelial cells. Other bacterial toxins, like e.g. cagA, VacA and ammonia are also toxic to the epithelial cells

Pathology

H. pylori destroys the somatostatin-producing D-cells in the gastric antrum, leading to decreased somatostatin production, which leads to decreased inhibition of gastrin production, which leads to increased production of gastric acid. This may predispose to the formation of duodenal ulcers.

The inflammation eventually causes atrophy of the local mucous membrane (including the acid-producing parietal cells) and intestinal metaplasia, which predisposes to development of cancer. Inflammation predominantly affects the gastric antrum but may spread to other parts of the stomach if left untreated. Gastric ulcers may also develop due to inflammation and intestinal metaplasia, but in the context of normal or reduced gastric acid secretion.

Clinical features

H. pylori gastritis is present in 2/3 of the world’s population. In most cases, the infection is asymptomatic. However, it may cause:

  • Atrophic gastritis
  • Peptic ulcer disease (especially duodenal ulcers)
  • Gastric cancer
  • Gastric MALT lymphoma

>90% of patients with duodenal ulcers are H. pylori positive.

Diagnosis and evaluation

Diagnosis can be made based upon either of these:

  • Histology (direct visualisation or urease test)
  • H. pylori antigen test on stool
  • IgG antibodies on serology
  • Urea breath test

Testing for H. pylori is not recommended for asymptomatic patients who have no close relatives at high risk for gastric cancer. Testing should only be performed if the clinician plans to offer eradication if the result is positive. Therefore, the indications for testing are the same as for eradication. See below.

Treatment

Without treatment, H. pylori infection is lifelong. H. pylori is a difficult bacterium to eradicate, and it’s asymptomatic in most cases. For these reasons, guidelines (Maastricht consensus) were made to determine who should be treated and who shouldn’t:

  • Testing and eradication strongly suggested
    • Peptic ulcer disease
    • Active gastritis
    • Gastric cancer (after surgery)
    • First degree relatives of patients with gastric cancer
    • MALT lymphoma
  • Testing and eradication should be considered
    • Functional dyspepsia
    • GERD
    • Before long term NSAID therapy
  • Testing and eradication not suggested
    • Asymptomatic patients with no high cancer risk close relatives

Eradication is also known as triple therapy, due to the requirement of a combination of three drugs to eradicate the bacterium. The first line is a PPI + clarithromycin + amoxicillin for 14 days. Second line uses metronidazole + tetracycline or levofloxacin + amoxicillin instead. The PPI increases the efficacy of the antibiotics.

After treatment, eradication should be confirmed by testing, mostly by stool antigen test. If first- and second-line treatments fail the bacterium should be cultured for antibiotic resistance. Antibiotic resistance is an increasing problem with regards to H. pylori. First line antibiotics may differ geographically based on local resistance rates.