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Helicobacter Pylori Infection Treatment & Management

  • Author: Luigi Santacroce, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Mar 15, 2016
 

Medical Care

Only treat patients who have a positive test result for H pylori infection. Carefully educate patients regarding the importance of completing the prescription and about the potential adverse effects of the medications. Importantly, consider possible antibiotic resistance when selecting the treatment regimen. Note that surgery is not required for patients with H pylori infection, but it may be considered in patients with severe complications, such as cancer.

The US Food and Drug Administration has approved some regimens, which are now accepted internationally, for the treatment of H pylori infection in patients with peptic ulcer disease, both gastric and duodenal. These regimens are also known as triple therapies and have reported cure rates from 85-90%. Unfortunately, with the increasing rise in antimicrobial resistance there has been an associated increase in the failure rate of standard triple therapy for H pylori infection.[11]

Administer triple therapies for 10-14 days. The treatment regimens are omeprazole, amoxicillin, and clarithromycin (OAC) for 10 days; bismuth subsalicylate, metronidazole, and tetracycline (BMT) for 14 days; and lansoprazole, amoxicillin, and clarithromycin (LAC), which has been approved for either 10 days or 14 days of treatment.

A trial of empiric therapy for H pylori infection in 7 Latin American sites found higher eradication rates with 14 days of standard triple therapy (LAC) than with shorter 4-drug therapies. Neither 5 days of concomitant lansoprazole, amoxicillin, clarithromycin, and metronidazole nor 10-day sequential treatment (5 days of LA, then 5 days of LCM) was significantly better than the standard therapy at any site.[12]

H pylori eradication rates were higher for a 7-day antibiotic regimen containing lansoprazole, amoxicillin, and clarithromycin (LAC), when used as first-line therapy compared with levofloxacin, amoxicillin, and lansoprazole (LAL).[13] Additionally, LAC did not achieve a higher rate of eradication than LAL as second-line therapy; thus, consideration of the sequence of administering antibiotic regimens for H pylori is important.

Hsu et al reported that 7-day concomitant therapy is superior to the 7-day standard triple therapy for H pylori eradication, and it is also simpler to administer than the 10-day sequential therapy, because the drugs are not changed halfway through the treatment course.[11]  Similarly, Apostolopoulos et al reported 10-day comcomitant quadruple therapy resulted in statistically significant higher eradication of H pylori than 10-day sequential quadruple therapy in an area of Greece with a greater than 20% local resistance to clarithromycin.[14]

A study by Yoon et al investigated the efficacy of a moxifloxacin-containing triple therapy as second-line therapy for H pylori infection as well as the effect of treatment duration and antibiotic resistance on the eradication rate.[15] In 2004, 41 patients who had persistent H pylori infection were given a 7-day course of 400 mg qd moxifloxacin, 1000 mg bid amoxicillin, and 20 mg bid esomeprazole; the intention-to-treat (ITT) rate was 75.6% with a per-protocol (PP) eradication rate of 83.8% and a moxifloxacin resistance rate of 5.6%. During 2005-2006, 139 patients were treated to a 10-day course of this regimen, with an ITT rate of 71.9%, PP eradication rate of 82.6%, and moxifloxacin resistance rate of 12%. One-hundred eight-one patients treated in 2007-2008 received a 14-day triple-therapy regimen: ITT rate, 68%; PP eradication rate, 79.9%; moxifloxacin resistance rate: 28.2%.[15]

Despite the increased duration of treatment in each successive group of patients, there was no statistical difference in efficacy among the 3 treatment groups.[15] The investigators attributed the low eradication rate despite increased duration of therapy to a coincident, marked increase in moxifloxacin resistance and concluded that when rapid antibiotic resistance occurs, tailored treatment based on antibiotic susceptibility testing may achieve higher eradication rates.[15]

Macrolide resistance in patients with H pylori infection is an important problem. Although the molecular mechanisms of nitroimidazole resistance are very complex and still unclear, resistance has been shown to be due to a single point mutation (usually in the RDXA gene, although other genes may also be involved, eg, FRDXA) in 1 of 4 positions of the bacterial 23S rDNA. Such mutations also determine cross-resistance to other macrolides.

An emerging and increasing problem in many Western countries is the fact that some H pylori strains in children are resistant to the antibiotic clarithromycin.[16] The causes are not known.

All the eradication treatments have a high incidence of certain adverse effects (eg, nausea, metallic taste). If skin rash, vomiting, or diarrhea occurs, discontinue treatment.

The links between H pylori and nonulcer dyspepsia are debated; however, some patients with nonulcer dyspepsia benefit from eradication. Patients with symptoms have a higher eradication rate than patients with nonulcer dyspepsia disease. Eradication of H pylori in patients without peptic ulcer disease has resolved the dyspepsia in a few cases.

Diet and activity

No dietary restrictions are usually needed, and no limitations of physical activity are needed if patients do not have complications.

Posttreatment monitoring

Consider performing a urea breath test (UBT) 4-12 weeks after the end of treatment. An esophagogastroduodenoscopy (EGD) with biopsy and a urease test also may be useful, but, importantly, remember that this test does have a significant rate of false-negative results.

Next

Prevention

Note that the risk is increased in patients who have an H pylori infection and whose first-degree relatives have a history of gastric cancer, even if they are asymptomatic.

Persons emigrating from geographic areas with a high incidence of gastric cancer have an increased risk.

Consider any patient with precancerous lesions of the stomach (ie, intestinal metaplasia) for treatment of H pylori infection.

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Contributor Information and Disclosures
Author

Luigi Santacroce, MD Assistant Professor, Medical School, State University at Bari, Italy

Disclosure: Nothing to disclose.

Coauthor(s)

Manoop S Bhutani, MD Professor, Co-Director, Center for Endoscopic Research, Training and Innovation (CERTAIN), Director, Center for Endoscopic Ultrasound, Department of Medicine, Division of Gastroenterology, University of Texas Medical Branch; Director, Endoscopic Research and Development, The University of Texas MD Anderson Cancer Center

Manoop S Bhutani, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Institute of Ultrasound in Medicine, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

David Greenwald, MD Professor of Clinical Medicine, Fellowship Program Director, Department of Medicine, Division of Gastroenterology, Montefiore Medical Center, Albert Einstein College of Medicine

David Greenwald, MD is a member of the following medical societies: Alpha Omega Alpha, New York Society for Gastrointestinal Endoscopy, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

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An antral gland of the stomach with a large Giemsa-stained colony of Helicobacter pylori in the lumen (arrow) at 250X power. Courtesy of Pantaleo Bufo, University of Foggia, Italy.
Helicobacter pylori infection. Lamina propria of the stomach is shown with 2 mast cells overlapping each other. Note the upper part the degranulating process with the release of granules of inflammation mediators (Giemsa staining, 250X). Courtesy of Pantaleo Bufo, University of Foggia, Italy.
Helicobacter pylori infection. A transverse section of the gastric lamina propria is shown. In the lower part, an antral gland of the stomach is present with some Helicobacter pylori in the lumen (red-blue arrow). In the upper part, a mast cell (yellow arrow) is present (Giemsa staining, 250X). Courtesy of Pantaleo Bufo, University of Foggia, Italy.
An antral gland of the stomach is shown with a large colony of Helicobacter pylori in the lumen (Giemsa staining, 425X). Courtesy of Pantaleo Bufo, University of Foggia, Italy.
 
 
 
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