56. Peptic ulcer disease. Helicobacter pylori infection

Page created on October 15, 2021. Last updated on April 20, 2022 at 18:22

Peptic ulcer disease


For introduction, etiology, and pathomechanism, see the corresponding pathology 2 topic.

Clinical features

70% of peptic ulcers are asymptomatic, but they may still develop complications like bleeding or perforation.

Symptomatic peptic ulcers present with epigastric pain or discomfort, as well as other non-specific symptoms like bloating, abdominal fullness, and nausea. The symptoms of duodenal ulcers frequently improve with eating and worsen a few hours after meals and at night. The symptoms of gastric ulcers worsen with eating.

Bleeding ulcer presents with features of upper GI bleeding, like haematemesis, melena, or anaemia. Perforated ulcers are the most common cause of GI perforation and cause peritonitis. Duodenal ulcers may penetrate through the wall into adjacent organs, forming fistulas.

Diagnosis and evaluation

The diagnosis is suspected in patients with typical risk factors (chronic NSAIDs use, previous H. pylori infection) and typical symptoms, but definite diagnosis is based on upper endoscopy. All patients with suspected PUD should undergo this examination. Upper endoscopy allows not only direct visualisation but biopsy of ulcers which malignant features. Biopsy should also be taken from the gastric antrum to look for H. pylori.

Testing for H. pylori may be necessary as well if biopsy is negative or the patient does not undergo endoscopy.

Patients with features of complicated PUD require more thorough workup.


Treatment involves treating the underlying cause, removing risk factors, and giving PPIs.

Surgical treatment is necessary for the treatment of complications like perforation, bleeding (if endoscopic haemostasis fails), pyloric stenosis, cases which don’t respond to conservative therapy, or if malignancy is discovered. For surgical treatment, see topic B17 of surgery-traumatology.

Helicobacter pylori infection


For introduction, etiology, and pathomechanism, see the corresponding pathology 2 topic.

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.


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.

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