Skip to main content

Advertisement

Log in

Helicobacter pylori and gastroesophageal reflux disease

  • Published:
Current Treatment Options in Gastroenterology Aims and scope Submit manuscript

Opinion statement

Since the rediscovery of Helicobacter pylori two decades ago, it has become increasingly clear that the true relationships between this organism and diseases of the upper gastrointestinal tract are highly complex. H. pylori colonization is a strong risk factor for peptic ulceration and distal gastric cancer; however, gastritis has no adverse consequences for most hosts, and the prevalence of H. pylori is inversely related to gastroesophageal reflux disease (GERD) and its sequelae, which include Barrett’s esophagus and esophageal adenocarcinoma. One clinical implication stemming from these data is that H. pylori eradication may not be appropriate in certain human populations due to potential beneficial effects conferred by persistent gastric inflammation. However, the majority of published intervention trials indicate that H. pylori treatment neither leads to the development of clinically significant de novo esophagitis nor exacerbates existing reflux disease. Superimposed upon these observations are reports that long-term acid suppression induced by proton-pump inhibitors (PPIs) in conjunction with H. pylori colonization may enhance the development of atrophic gastritis, a well-recognized histologic step in the progression to intestinal-type gastric cancer. Therefore, current evidence-based recommendations regarding management of H. pylori-positive individuals with GERD include the following. H. pylori should not be treated with the intent to either improve reflux symptoms or prevent the development of reflux complications. However, if patients are to receive long-term acid suppressive therapy, they should be tested for H. pylori and treated if positive, due to the potential for PPIs to accelerate atrophy within H. pylori-infected mucosa. Optimal first-line regimens in this country consist of a PPI in combination with clarithromycin and either amoxicillin or metronidazole (triple therapy) for at least 7, but preferably 10, days. Because the most effective second-line regimens contain metronidazole, it is advisable to use amoxicillin instead of metronidazole as first-line therapy in order to optimize results should subsequent therapy be required. If first-line regimens fail to eliminate H. pylori, patients should receive quadruple therapy consisting of a PPI, bismuth subsalicylate, metronidazole, and tetracycline for 14 days. Due to the availability and accuracy of noninvasive diagnostic tests for H. pylori, it is recommended that successful cure be confirmed after intervention.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References and Recommended Reading

  1. Everhart JE: Recent developments in the epidemiology of Helicobacter pylori. Gastroenterol Clin North Am 2000, 29:559–578.

    Article  PubMed  CAS  Google Scholar 

  2. Ernst PB, Gold BD: The disease spectrum of Helicobacter pylori: the immunopathogenesis of gastroduodenal ulcer and gastric cancer. Annu Rev Microbiol 2000, 54:615–640.

    Article  PubMed  CAS  Google Scholar 

  3. Peek RM, Blaser MJ: Helicobacter pylori and gastrointestinal tract adenocarcinomas. Nat Rev Cancer 2002, 2:28–37.

    Article  PubMed  CAS  Google Scholar 

  4. Parsonnet J: The incidence of Helicobacter pylori infection. Aliment Pharmacol Ther 1995, 9:45–51.

    PubMed  Google Scholar 

  5. Howson CP, Hiyama T, Wynder EL: The decline in gastric cancer: epidemiology of an unplanned triumph. Epidemiol Rev 1986, 8:1–27.

    PubMed  CAS  Google Scholar 

  6. Devesa SS, Blot WJ, Fraumeni JF: Changing patterns in the incidence of esophageal and gastric carcinoma in the United States. Cancer 1998, 83:2049–2053.

    Article  PubMed  CAS  Google Scholar 

  7. Werdmuller BF, Loffeld RJ: Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis. Dig Dis Sci 1997, 42:103–105.

    Article  PubMed  CAS  Google Scholar 

  8. Varanasi RV, Fantry GT, Wilson KT: Decreased prevalence of Helicobacter pylori infection in gastroesophageal reflux disease. Helicobacter 1998, 3:188–194.

    Article  PubMed  CAS  Google Scholar 

  9. Weston AP, Badr AS, Topalovski M, et al.: Prospective evaluation of the prevalence of gastric Helicobacter pylori infection in patients with GERD, Barrett’s esophagus, Barrett’s dysplasia, and Barrett’s adenocarcinoma. Am J Gastroenterol 2000, 95:387–394.

    Article  PubMed  CAS  Google Scholar 

  10. Haruma K, Hamada H, Mihara M, et al.: Negative association between Helicobacter pylori infection and reflux esophagitis in older patients: case-control study in Japan. Helicobacter 2000, 5:24–29.

    Article  PubMed  CAS  Google Scholar 

  11. Vicari JJ, Peek RM, Falk GW, et al.: The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology 1998, 115:50–57.

    Article  PubMed  CAS  Google Scholar 

  12. Chow WH, Blaser MJ, Blot WJ, et al.: An inverse relation between cagA+ strains of Helicobacter pylori infection and risk of esophageal and gastric cardia adenocarcinoma. Cancer Res 1998, 58:588–590.

    PubMed  CAS  Google Scholar 

  13. Loffeld RJ, Werdmuller BF, Kuster JG, et al.: Colonization with cagA-positive Helicobacter pylori strains is inversely associated with reflux esophagitis and Barrett’s esophagus. Digestion 2000, 62:95–99.

    Article  PubMed  CAS  Google Scholar 

  14. Warburton-Timms VJ, Charlett A, Valori RM, et al.: The significance of cagA(+) Helicobacter pylori in reflux oesophagitis. Gut 2001, 49:341–346.

    Article  PubMed  CAS  Google Scholar 

  15. Raghunath A, Hungin AP, Wooff D, et al.: Prevalence of Helicobacter pylori in patients with gastro-oesophageal reflux disease: systematic review. BMJ 2003, 326:737–743.

    Article  PubMed  Google Scholar 

  16. Sharma P, Vakil N: Review article: Helicobacter pylori and reflux disease. Aliment Pharmacol Ther 2003, 17:297–305. Excellent review delineating the effects of H. pylori colonization on reflux-mediated diseases.

    Article  PubMed  CAS  Google Scholar 

  17. El-Serag HB, Sonnenberg A, Jamal MM, et al.: Corpus gastritis is protective against reflux oesophagitis. Gut 1999, 45:181–185.

    Article  PubMed  CAS  Google Scholar 

  18. Koike T, Ohara S, Sekine H, et al.: Helicobacter pylori infection prevents erosive reflux oesophagitis by decreasing gastric acid secretion. Gut 2001, 49:330–334.

    Article  PubMed  CAS  Google Scholar 

  19. Labenz J, Blum AL, Bayerdorffer E, et al.: Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology 1997, 112:1442–1447.

    Article  PubMed  CAS  Google Scholar 

  20. Sasaki A, Haruma K, Manabe N, et al.: Long-term observation of reflux oesophagitis developing after Helicobacter pylori eradication therapy. Aliment Pharmacol Ther 2003, 17:1529–1534.

    Article  PubMed  CAS  Google Scholar 

  21. Schwizer W, Thumshirn M, Dent J, et al.: Helicobacter pylori and symptomatic relapse of gastro-oesophageal reflux disease: a randomised controlled trial. Lancet 2001, 357:1738–1742.

    Article  PubMed  CAS  Google Scholar 

  22. Moayyedi P, Bardhan C, Young L, et al.: Helicobacter pylori eradication does not exacerbate reflux symptoms in gastroesophageal reflux disease. Gastroenterology 2001, 121:1120–1126. Large, well-performed, prospective randomized trial evaluating the effects of H. pylori treatment on relapse of GERD.

    Article  PubMed  CAS  Google Scholar 

  23. Tefera S, Hatlebakk JG, Berstad A: The effect of Helicobacter pylori eradication on gastro-oesophageal reflux. Aliment Pharmacol Ther 1999, 13:915–920.

    Article  PubMed  CAS  Google Scholar 

  24. Porro GB, Pace F: Should we eradicate Helicobacter pylori in patients with recurrent gastro-oesophageal reflux disease? Eur J Gastroenterol Hepatol 2000, 12:S7-S10.

    Article  Google Scholar 

  25. Kuipers EJ, Uyterlinde AM, Pena AS, et al.: Increase of Helicobacter pylori-associated corpus gastritis during acid suppressive therapy: implications for long-term safety. Am J Gastroenterol 1995, 90:1401–1406.

    PubMed  CAS  Google Scholar 

  26. Falk GW: The possible role of Helicobacter pylori in GERD. Semin Gastrointest Dis 2001, 12:186–195. A well-written, comprehensive, and clinically oriented review of the role of H. pylori and GERD.

    PubMed  CAS  Google Scholar 

  27. Kuipers EJ, Lundell L, Klinkenberg-Knol EC, et al.: Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication. N Engl J Med 1996, 334:1018–1022.

    Article  PubMed  CAS  Google Scholar 

  28. Correa P: Helicobacter pylori and gastric cancer: state of the art. Cancer Epidemiol Biomarkers Prev 1996, 5:477–481.

    PubMed  CAS  Google Scholar 

  29. Eissele R, Brunner G, Simon B, et al.: Gastric mucosa during treatment with lansoprazole: Helicobacter pylori is a risk factor for argyrophil cell hyperplasia. Gastroenterology 1997, 112:707–717.

    Article  PubMed  CAS  Google Scholar 

  30. Klinkenberg-Knol EC, Nelis F, Dent J, et al.: Long-term omeprazole treatment in resistant gastroesophageal reflux disease: efficacy, safety, and influence on gastric mucosa. Gastroenterology 2000, 118:661–669.

    Article  PubMed  CAS  Google Scholar 

  31. Stolte M, Meining A, Schmitz JM, et al.: Changes in Helicobacter pylori-induced gastritis in the antrum and corpus during 12 months of treatment with omeprazole and lansoprazole in patients with gastrooesophageal reflux disease. Aliment Pharmacol Ther 1998, 12:247–253.

    Article  PubMed  CAS  Google Scholar 

  32. Lundell L, Miettinen P, Myrvold HE, et al.: Lack of effect of acid suppression therapy on gastric atrophy. Nordic Gerd Study Group. Gastroenterology 1999, 117:319–326.

    Article  PubMed  CAS  Google Scholar 

  33. Schenk BE, Kuipers EJ, Klinkenberg-Knol EC, et al.: Helicobacter pylori and the efficacy of omeprazole therapy for gastroesophageal reflux disease. Am J Gastroenterol 1999, 94:884–887.

    Article  PubMed  CAS  Google Scholar 

  34. Kuipers EJ, Nelis GF, Klinkenberg-Knol EC, et al.: Helicobacter pylori eradication for the prevention of atrophic gastritis during omeprazole therapy: a prospective randomized trial. Gastroenterology 2001, 120:A14.

    Article  Google Scholar 

  35. Labenz J, Tillenburg B, Peitz U, et al.: Helicobacter pylori augments the pH-increasing effect of omeprazole in patients with duodenal ulcer. Gastroenterology 1996, 110:725–732.

    Article  PubMed  CAS  Google Scholar 

  36. Miehlke S, Bayerdorffer E, Graham DY: Treatment of Helicobacter pylori infection. Semin Gastrointest Dis 2001, 12:167–179. An important review of current treatment regimens available for eradication of H. pylori.

    PubMed  CAS  Google Scholar 

  37. Malfertheiner P, Megraud F, O’Morain C, et al.: Current concepts in the management of Helicobacter pylori infection—the Maastricht 2-2000 Consensus Report. Aliment Pharmacol Ther 2002, 16:167–180. This consensus statement is regarded as the international standard for prioritization of anti-H. pylori therapies.

    Article  PubMed  CAS  Google Scholar 

  38. Ulmer HJ, Beckerling A, Gatz G: Recent use of proton pump inhibitor-based triple therapies for the eradication of Helicobacter pylori: a broad data review. Helicobacter 2003, 8:95–104.

    Article  PubMed  CAS  Google Scholar 

  39. Vaira D, Holton J, Ricci C, et al.: Review article: Helicobacter pylori infection from pathogenesis to treatment —a critical reappraisal. Aliment Pharmacol Ther 2002, 16:105–113. An excellent critical review of current advances in both diagnosis and treatment of H. pylori.

    Article  PubMed  Google Scholar 

  40. Basset C, Holton J, Ricci C, et al.: Diagnosis and treatment of Helicobacter: a 2002 updated review. Aliment Pharmacol Ther 2003, 17:89–97. This manuscript not only reviews recent studies focused on optimizing traditional therapeutic modalities against H. pylori, but also discusses novel regimens that may be useful in the near future.

    Article  PubMed  Google Scholar 

  41. Bazzoli F, Zagari RM, Pozzato P, et al.: Low-dose lansoprazole and clarithromycin plus metronidazole vs. full-dose lansoprazole and clarithromycin plus amoxicillin for eradication of Helicobacter pylori infection. Aliment Pharmacol Ther 2002, 16:153–158.

    Article  PubMed  CAS  Google Scholar 

  42. Choi IJ, Jung HC, Choi KW, et al.: Efficacy of low-dose clarithromycin triple therapy and tinidazole-containing triple therapy for Helicobacter pylori eradication. Aliment Pharmacol Ther 2002, 16:145–151.

    Article  PubMed  CAS  Google Scholar 

  43. Vallve M, Vergara M, Gisbert JP, et al.: Single vs. double dose of a proton pump inhibitor in triple therapy for Helicobacter pylori eradication: a meta-analysis. Aliment Pharmacol Ther 2002, 16:1149–1156.

    Article  PubMed  CAS  Google Scholar 

  44. Qasim A, O’Morain CA: Review article: treatment of Helicobacter pylori infection and factors influencing eradication. Aliment Pharmacol Ther 2002, 16:24–30.

    Article  PubMed  CAS  Google Scholar 

  45. Givens RC, Watkins PB: Pharmacogenetics and clinical gastroenterology. Gastroenterology 2003, 125:240–248.

    Article  PubMed  CAS  Google Scholar 

  46. Macfarlane GT, Cummings JH: Probiotics, infection and immunity. Curr Opin Infect Dis 2002, 15:501–506.

    PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Peek, R.M. Helicobacter pylori and gastroesophageal reflux disease. Curr Treat Options Gastro 7, 59–70 (2004). https://doi.org/10.1007/s11938-004-0026-0

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/s11938-004-0026-0

Keywords

Navigation