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Who’s Afraid of the Big Bad GERD?

Leontiadis, Grigoris I MD*; Howden, Colin W MD

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Journal of Clinical Gastroenterology: October 2004 - Volume 38 - Issue 9 - p 731-732
doi: 10.1097/01.mcg.0000139176.56372.eb
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The relationship—if any—between Helicobacter pylori (H. pylori) infection and gastroesophageal reflux disease (GERD) has been extremely difficult to define.1 Because studies from different parts of the world have reached differing conclusions, one could be left with the impression that H. pylori predisposes to GERD, protects against GERD and its complications2 or has no net effect. In the United States, some primary care physicians have even expressed concern about treating H. pylori infection for fear of precipitating or exacerbating GERD,3 although an analysis of controlled studies from the US has shown no such effect.4 There is clearly widespread confusion regarding this difficult area. In this issue of the Journal of Clinical Gastroenterology, there is a small but potentially important study from Turkey5 that adds to the current controversy.

Guliter and Kandilci enrolled 34 H. pylori–positive GERD patients with mild esophagitis into their study of the effects of H. pylori eradication.5 Eighteen patients were cured of H. pylori infection and were further studied. (As an aside, the overall eradication rate following a 14-day course of PPI-based triple therapy was 68%, which seems disappointingly low by current standards.) Three months after the eradication of H. pylori infection, 24-hour intra-esophageal pH values and esophageal manometric findings did not change significantly, although there were significant reductions in heartburn and regurgitation scores, and improved endoscopic appearances in some patients.

What should be made of the above observations? Can GERD always be expected to improve when H. pylori infection is eradicated? Unfortunately, the answer to the second question must be a qualified “No.” Most of the H. pylori-infected GERD patients in this study had antral-predominant gastritis. Such patients would be expected to have relative hyperchlorhydria from the effects of many years of antral inflammation and hypergastrinemia. Once H. pylori infection is eradicated, antral inflammation resolves, gastrin levels revert toward baseline, and acid secretion eventually falls toward the levels found in uninfected patients.6 Thus, although the eradication of H. pylori infection does not influence gastroesophageal reflux, the reduced acid output (at least in those who had antral-predominant gastritis with sparing of the acid-secreting gastric corpus) might be expected to lead to some improvement in GERD symptoms. It would have been preferable, however, if these investigators had compared their results in a control group of infected GERD patients who were left—temporarily at least—with untreated H. pylori infection. The patients in this study were not apparently “blinded” to the effects of their H. pylori treatment regimen and may have reported subjective symptom improvement based solely on this therapeutic intervention. The improvement in GERD symptoms must, therefore, be interpreted cautiously.

There are, however, different possible distributions of H. pylori-related gastritis. Although the antral-predominant form is the more prevalent in the United States, corpus-predominant gastritis or pangastritis (ie, involvement of the entire stomach) are seen more frequently in developing nations. In patients with marked corpus involvement, acid secretion is reduced because of the effects of chronic inflammation on the acid-secreting mucosa of the stomach. As long as patients have not developed irreversible gastric atrophy from this process, eradication of H. pylori infection can lead to an increase in gastric acid secretion.6 If such patients already had a tendency to GERD, it is possible that their symptoms could worsen. If such patients had latent GERD but were previously asymptomatic, it is possible that GERD symptoms may manifest for the first time.

What should be done, therefore, for elderly patients with corpus-predominant gastritis or pangastritis? Can a case be made for leaving H. pylori infection untreated for fear of inducing GERD? That would be a controversial and difficult position to defend because H. pylori is officially a “definite” carcinogen. However, the risks of gastric cancer developing in an elderly patient who does not already have it are probably extremely low. If the patient was asymptomatic and had no past history of ulcer disease, a case might be made for leaving the H. pylori infection untreated—but a better case could be made for not testing the patient for the infection in the first place! If the eradication of H. pylori infection did happen to lead to the development of de novo GERD symptoms, it would hardly be a disaster for the patient or the physician because there are effective treatments available—albeit at some cost—to manage such symptoms.

What implications do the findings of the recent study5 have for clinical practice in the United States? First, and as already noted, most H. pylori-infected individuals in the United States—particularly those who acquired the infection in this country—will have the antral-predominant form of gastritis. That means that—in all likelihood—acid secretion would fall with the eradication of H. pylori infection. Among GERD sufferers, this might mean an improvement in symptoms (although that is by no means guaranteed). The more important point, however, is that there is no reason to believe that GERD would worsen in those already afflicted or would be precipitated in those who did not have it. Therefore, physicians in the United States should continue to follow current guidelines7,8 and treat H. pylori infection when it has been detected. Physicians should not “be afraid” of GERD in those patients; the benefits of eradicating H. pylori infection will continue to outweigh any theoretical disadvantages.


1. Pandolfino JE, Howden CW, Kahrilas PJ. H. pylori and GERD: Is less more? Am J Gastroenterol. 2004;99:1222–1225.
2. Sharma VK, Crowell MD, Howden CW. Infection with H. pylori or cagA+H. pylori is protective against Barrett’s esophagus and esophageal adenocarcinoma: A meta-analysis. Gastroenterology. 2004;128:A-87.
3. Chey WD, Inadomi JM, Booker AK. What do primary care physicians think about Barrett’s esophagus, the relationship between GERD and H. pylori, and treatment of nocturnal heartburn? Gastroenterology. 2003;124:A-108.
4. Laine L, Sugg J. Effect of Helicobacter pylori eradication on development of erosive esophagitis and gastroesophageal reflux disease symptoms: A post hoc analysis of eight double-blind prospective studies. Am J Gastroenterol. 2002;97:2992–2997.
5. Guliter S, Kandilci U. The effect of Helicobacter pylori eradication on gastroesophageal reflux disease. Journal of Clinical Gastroenterology. 2004;38:750–755.
6. Calam J, Gibbons A, Healey ZV, et al. How does Helicobacter pylori cause mucosal damage? Its effect on acid and gastrin physiology. Gastroenterology. 1997;113(Suppl):S43–S49.
7. Peura DA. The report of the Digestive Health Initiative International Update Conference on Helicobacter pylori. Gastroenterology 1997;113(Suppl.):S4 –S8.
8. Howden CW, Hunt RH. Guidelines for the management of Helicobacter pylori infection. Am J Gastroenterol. 1998;93:2330–2338.
© 2004 Lippincott Williams & Wilkins, Inc.