This common gastric pathogen is associated with peptic ulcer disease, nonulcer dyspepsia, chronic gastritis, gastric cancer (adenocarcinoma of the distal stomach) and low-grade mucosa-associated lymphoid tissue (MALT) lymphomas.  When infection is associated with peptic ulcer disease or chronic gastritis, treatment of Helicobacter pylori infection may result in a decrease in gastric symptoms and a decrease in recurrence rates thus eliminating the need for maintenance antisecretory therapy.  Appropriate treatment of H. pylori may also decreases the risk of developing gastric cancer.  It is estimated that approximately 50% of the world’s population are infected, and there is an increase in the incidence of infection in lower socioeconomic groups.  However, not all infected patients require treatment.  Current recommendations for groups who require diagnostic testing and treatment include patients with documented active ulcer disease, patients with a past history of ulcer disease who have never undergone testing for H. pylori and require ongoing antisecretory therapy, patients with symptoms suggestive of active ulcer disease or chronic gastritis who do not require endoscopy (lack of warning signs: weight loss, anemia, or guiac positive stools), patients with a family history of gastric cancer, patients who have undergone prior gastric resection for cancer, and patients with MALT lymphoma.  In essence, screening for infection in asymptomatic patients is not necessary.  Also, patients with symptoms of gastroesophageal reflux disease (GERD) do not require screening or treatment as eradication of H. pylori often worsens GERD symptoms.

     There are many tests available to confirm the presence of infection.  Biopsy specimens obtained during esophagogastricduodenoscopy may be subjected to Giemsa or Genta staining methods or the rapid urease test.  However, this involves an invasive procedure which is often unnecessary in patients younger than 50 years of age with uncomplicated peptic ulcer disease and no warning signs (weight loss, anemia, or guiac positive stools).  Enzyme-linked immunosorbent assay (ELISA) testing of patients sera for antibodies may be performed in the laboratory or via office based tests.  ELISA testing can not distinguish between prior or current infection.  Urea breath tests using 13C- or 14C- labeled urea can detect infection when H. pylori hydrolyzes the radiolabeled urea and results in an increased excretion of radiolabeled CO2.  Urea breath tests are less reliable in patients on antisecretory therapy (proton pump inhibitors or H2 receptor antagonists), bismuth, antimicrobials, or antacids.  Urea breath testing should be performed at least two weeks after antisecretory therapy and four weeks after antimicrobials have been discontinued.  The urea breath tests may be used to determine if infection eradication therapy was successful.  H. pylori infection may also be detected via a stool immunoassay.

     If a negative result is obtained on initial testing, then a confirmatory H. pylori test may prove useful especially when there is endoscopic or radiographic evidence of ulcer disease.  If confirmatory testing is negative, then no therapy is required.  Effective anti-H. pylori therapy is imperative when diagnostic testing confirms the presence of infection in symptomatic patients.  Repeat testing with either the urea breath test, biopsy, or stool antigen testing should be performed to confirm successful eradication of infection following treatment in patients whose symptoms persist after therapy.  Repeat testing to confirm eradication is not required in patients whose symptoms resolve following therapy.

     There are many successful therapies for H. pylori eradication.  If symptoms persist after a full course of therapy, repeat testing for H. pylori infection should be performed, and if infection is still present, repeat treatment with a different course of therapy should be instituted.  Testing to confirm eradication should occur at least two weeks after cessation of antisecretory therapy and a minimum of at least four weeks after completion of antibiotic therapy. Standard triple regimens include a PPI, clarithromycin, with either amoxicillin or metronidazole for 7-10 days. Single day quadruple therapy entails a PPI, bismuth (524 mg 2 tablets QID), amoxicillin (500 mg 4 tab QID) and metronidazole (500 mg QID) all for one day with PPI therapy continued until acute symptoms resolve. In resistent cases, 14 days of sequential therapy may be employed in which amoxicillin therapy for one week precedes triple therapy based regimens.