Diagnosis and Management of H pylori Infection

Laurie Barclay, MD

April 28, 2010

April 28, 2010 — A clinical review in the April 29 issue of the New England Journal of Medicine provides information on how to detect, diagnose, treat, and manage Helicobacter pylori infection.

"Infection with H. pylori is a cofactor in the development of three important upper gastrointestinal diseases: duodenal or gastric ulcers (reported to develop in 1 to 10% of infected patients), gastric cancer (in 0.1 to 3%), and gastric mucosa-associated lymphoid-tissue (MALT) lymphoma (in <0.01%)," writes Kenneth E. L. McColl, MD, from the Division of Cardiovascular and Medical Sciences, University of Glasgow, Gardiner Institute, Glasgow, United Kingdom. "The risk of these disease outcomes in infected patients varies widely among populations. The great majority of patients with H. pylori infection will not have any clinically significant complications."

Methods of Testing

Routine testing for H pylori infection is not recommended because the vast majority of patients with this infection do not have any associated clinical disease. However, confirmed gastric or duodenal ulcers and gastric MALT lymphoma are definite indications for detecting and treating H pylori infection. After surgical removal of early gastric cancers, it may also be reasonable to test for and eradicate H pylori infection.

For younger patients with upper gastrointestinal tract symptoms but without alarm symptoms such as weight loss, persistent vomiting, or gastrointestinal tract bleeding, it is reasonable to use a noninvasive test-and-treat strategy for H pylori infection. Options for noninvasive testing include the urea breath test, fecal antigen test, and serologic test. Of these options, the least accurate is the serologic test. Patients with positive test results should undergo eradication therapy.

For patients with alarm symptoms, or for older patients with new-onset dyspepsia, endoscopy is recommended. Depending on the specific set of guidelines used, older patients are defined as those 45 years or older or 55 years or older. Because nonsteroidal anti-inflammatory drugs can cause ulcers in the absence of H pylori infection, endoscopy is warranted for patients with dyspepsia associated with use of these drugs.

Treatments

Unless there is a high local rate of resistance to clarithromycin, appropriate first-line treatment is triple therapy using a proton-pump inhibitor plus clarithromycin and amoxicillin, each given twice per day for 7 to 14 days. Patients with a penicillin allergy should receive metronidazole instead of amoxicillin. When the prevalence of clarithromycin-resistant H pylori infection exceeds 20%, an alternative initial treatment regimen is quadruple therapy with a proton-pump inhibitor, tetracycline, metronidazole, and a bismuth salt for 10 to 14 days. However, bismuth salts are not available in the United States and in some other countries.

Another option is 10-day sequential therapy with a proton-pump inhibitor plus amoxicillin for 5 days, followed by a proton-pump inhibitor plus clarithromycin and tinidazole for 5 more days. However, the efficacy of this regimen needs to be confirmed before it is widely used.

"Data are lacking to inform the optimal management of recurrent or persistent dyspepsia after noninvasive testing and treatment of H. pylori infection," Dr. McColl writes. "Options include symptomatic acid-inhibitory therapy, endoscopy to check for underlying ulcer or another cause of symptoms, and repeat of the H. pylori test-and-treat strategy; other potential reasons for the symptoms should also be reconsidered."

After Eradication therapy: What Next?

When gastrointestinal tract symptoms recur or persist after eradication therapy without first testing for H pylori, the most likely explanation is that the symptoms are unrelated to H pylori infection, rather than treatment failure. Unless persistent H pylori infection is confirmed, further eradication therapy should not be considered.

Eradication of H pylori infection should be confirmed in patients who have had an H pylori–associated ulcer or gastric MALT lymphoma or who have undergone resection for early gastric cancer. Tests for eradication may include a urea breath test or fecal antigen test performed at least 4 weeks after treatment is completed, so that false-negative results from suppression of H pylori are avoided. For patients requiring endoscopy, eradication can also be confirmed by testing during this procedure.

When treatment fails to eradicate H pylori infection, therapeutic options include empiric acid-inhibitory therapy, endoscopy to detect underlying ulcer or another cause of symptoms, and subsequent use of the noninvasive test-and-treat strategy. Clinicians should also consider another cause for the symptoms, such as biliary tract, pancreatic, musculoskeletal, or cardiac disease or psychosocial stress. Poor compliance with initial treatment may also be implicated and mandates adherence to the second treatment regimen.

Treatment failure may be caused by H pylori resistance to clarithromycin or metronidazole, or both. Bismuth-based quadruple therapy is often used as second-line therapy if initial treatment did not include a bismuth salt. In patients previously treated with a proton-pump inhibitor, amoxicillin, and clarithromycin, a proton-pump inhibitor used in combination with metronidazole and either amoxicillin or tetracycline is recommended.

"Data from randomized trials are lacking to guide the care of patients whose symptoms persist after completion of H. pylori eradication therapy for uninvestigated dyspepsia," Dr. McColl concludes. "The effect of eradication of H. pylori infection on the risk of gastric cancer is unclear but is currently under study."

Dr. McColl has received lecture fees from AstraZeneca and Nycomed and consulting fees from Sacoor.

N Engl J Med. 2010;362:1597-1604.

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